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Emotion regulation and psychopathology in children and adolescents ( PDFDrive )

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672 276 Emotion Dysregulation in Adolescents with Borderline Personality Disorder Dixon-G​ ordon, K. L., Chapman, A. L., Lovasz, N., & Walters, K. (2011a). Too Upset to Think: The Interplay of Borderline Personality Features, Negative Emotions, and Social Problem Solving in the Laboratory. Personality Disorders-​Theory Research and Treatment, 2(4), 243–​260. doi:10.1037/​ A0021799 Dixon-​Gordon, K. L., Chapman, A. L., Lovasz, N., & Walters, K. (2011b). Too upset to think: the interplay of borderline personality features, negative emotions, and social problem solving in the laboratory. Personal Disord, 2(4), 243–2​ 60. doi:10.1037/​a0021799 Domes, G., Schulze, L., & Herpertz, S. C. (2009). Emotion Recognition in Borderline Personality Disorder—​a Review of the Literature. Journal of Personality Disorders, 23(1), 6–1​ 9. Donegan, N. H., Sanislow, C. A., Blumberg, H. P., Fulbright, R. K., Lacadie, C., Skudlarski, P., … Wexler, B. E. (2003). Amygdala hyperreactivity in borderline personality disorder: implications for emotional dysregulation. Biol Psychiatry, 54(11), 1284–1​ 293. doi:S000632230300636X [pii] Dziobek, I., Fleck, S., Kalbe, E., Rogers, K., Hassenstab, J., Brand, M., … Convit, A. (2006). Introducing MASC: a movie for the assessment of social cognition. J Autism Dev Disord, 36(5), 623–​636. doi:10.1007/s​ 10803-0​ 06-0​ 107-​0 Fonagy, P., Gergely, G., Jurist, E. L., & Target, M. (2002). Affect regulation, mentalization, and the development of self. New York: Other Press. Fonagy, P., Gergely, G., & Target, M. (2007). The parent-​infant dyad and the construction of the subjective self. [Review]. Journal of Child Psychology and Psychiatry and Allied Disciplines, 48(3-4​ ), 288–​328. doi:10.1111/​j.1469-​7610.2007.01727.x Fonagy, P., & Luyten, P. (2009). A developmental, mentalization-b​ ased approach to the understanding and treatment of borderline personality disorder. Dev Psychopathol, 21(4), 1355–​1381. Fonagy, P., Rossouw, T., Sharp, C., Bateman, A., Allison, L., & Farrar, C. (2014). Mentalization-b​ ased treatment for adolescents with borderline traits. In C. Sharp & J. L. Tackett (Eds.), Handbook of borderline personality disorder in children and adolescents (pp. 313–​332). New York, NY: Springer. Fonagy, P., Rosssouw, T., Sharp, C., Bateman, A., Allisson, L., & Farrar, C. (2014). Mentalization-​based treatment for adolescents with borderline traits. In C. Sharp & J. L. TAckett (Eds.), The handbook of borderline personality disorder in children and adolescents. New York: Springer. Fossati, A. (2014). Borderline Personality Disorder in Adolescence: Phenomenology and Construct Validity. In C. Sharp & J. Tackett (Eds.), Handbook of borderline personality disorder in children and adolescents. New York: Springer. Frick, C., Lang, S., Kotchoubey, B., Sieswerda, S., Dinu-​Biringer, R., Berger, M., … Barnow, S. (2012). Hypersensitivity in Borderline Personality Disorder during Mindreading. Plos One, 7(8). doi:ARTN e41650 10.1371/j​ ournal.pone.0041650 Garnefski, N., Kraaij, V., & Spinhoven, P. (2002). Manual for the use of the Cognitive Emotion Regulation Questionnaire. Leiderdorp, The Netherlands: DATEC. Glenn, C. R., & Klonsky, E. D. (2009). Emotion Dysregulation as a Core Feature of Borderline Personality Disorder. Journal of Personality Disorders, 23(1), 20–2​ 8. Gratz, K. L., Dixon-​Gordon, K. L., & Tull, M. T. (2014). Self-​injurious behaviors in adolescents wtih Borderline Personality Disorder. In C. Sharp & J. L. Tackett (Eds.), Handbook of Borderline Personality Disorder in Children and Adolescents (pp. 195–​210). New York: Springer. Gratz, K. L., & Roemer, L. (2004). Multidimensional assessment of emotion regulation and dysregulation: Development, factor structure and initial validation of the Difficulties in Emotion Regulation Scale. Journal of Psychopathology and Behavioral Assessment, 26(1), 41–5​ 4. Gratz, K. L., Rosenthal, M. Z., Tull, M. T., Lejuez, C. W., & Gunderson, J. G. (2006). An experimental investigation of emotion dysregulation in borderline personality disorder. Journal of Abnormal Psychology, 115(4), 850–8​ 55. doi:10.1037/​0021-​843x.115.4.850 Gratz, K. L., Tull, M. T., Baruch, D. E., Bornovalova, M. A., & Lejuez, C. W. (2008). Factors associated with co-​occurring borderline personality disorder among inner-c​ ity substance users: the roles of childhood maltreatment, negative affect intensity/​reactivity, and emotion dysregulation. Comprehensive Psychiatry, 49(6), 603–​615. doi:10.1016/​j.comppsych.2008.04.005

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872 278 Emotion Dysregulation in Adolescents with Borderline Personality Disorder children. [Evaluation Studies Research Support, N.I.H., Extramural Research Support, Non-U​ .S. Gov’t]. Personality Disorders: Theory, Research, and Treatment, 4(1), 15–​22. doi:10.1037/​a0027948 Miller, A. L., Muehlenkamp, J. J., & Jacobson, C. M. (2008). Fact or fiction: Diagnosing borderline personality disorder in adolescents. Clinical Psychology Review, 28(6), 969–​981. doi:10.1016/​ j.cpr.2008.02.004 Minzenberg, M. J., Fan, J., New, A. S., Tang, C. Y., & Siever, L. J. (2007). Fronto-​limbic dysfunction in response to facial emotion in borderline personality disorder: An event-​related fMRI study. Psychiatry Research-​Neuroimaging, 155(3), 231–​243. doi:10.1016/​j.pseychresns.2007.03.006 Minzenberg, M. J., Poole, J. H., & Vinogradov, S. (2006). Social-​emotion recognition in borderline personality disorder. Compr Psychiatry, 47(6), 468–4​ 74. doi:S0010-​440X(06)00050-​2 [pii] 10.1016/​ j.comppsych.2006.03.005 Monk, C. S., McClure, E. B., Nelson, E. E., Zarahn, E., Bilder, R. M., Leibenluft, E., … Pine, D. S. (2003). Adolescent immaturity in attention-​related brain engagement to emotional facial expressions. Neuroimage, 20(1), 420–4​ 28. doi:10.1016/​S1053-​8119(03)00355-​0 National Health and Medical Research Council. (2013). Clinical practice guideline for the management of borderline personality disorder 2012. Melbourne, Australia: National Health and Medical Research Council. National Institute for Health and Clinical Excellence. (2009). Borderline personality disorder: Treatment and management. Clinical guideline 78. London, UK: National Institute for Health and Clinical Excellence. Nica, E. I., & Links, P. S. (2009). Affective instability in borderline personality disorder: experience sampling findings. [Review]. Curr Psychiatry Rep, 11(1), 74–​81. Normandin, L., Ensink, K., Yeomans, F., & Kernberg, O. F. (2014). Transference-​focused psychotherapy for personality disorders in adolescence. In C. Sharp & J. L. Tackett (Eds.), Handbook of child and adolesent borderline personality disorder (pp. 333–3​ 59). New York, NY: Springer. Perez, J., Venta, A., Garnaat, S., & Sharp, C. (2012). The Difficulties in Emotion Regulation Scale: Factor Structure and Association with Nonsuicidal Self-I​njury in Adolescent Inpatients. Journal of Psychopathology and Behavioral Assessment, 34(3), 393–4​ 04. doi:10.1007/s​ 10862-0​ 12-​9292-​7 Robin, M., Pham-​Scottez, A., Curt, F., Dugre-​Le Bigre, C., Speranza, M., Sapinho, D., … Kedia, G. (2012). Decreased sensitivity to facial emotions in adolescents with Borderline Personality Disorder. Psychiatry Research, 200(2) 417–​421. Roisman, G. I., Masten, A. S., Coatsworth, J. D., & Tellegen, A. (2004). Salient and emerging developmental tasks in the transition to adulthood. Child Development, 75(1), 123–​133. Rossouw, T. I., & Fonagy, P. (2012). Mentalization-​Based Treatment for Self-H​ arm in Adolescents: A Randomized Controlled Trial. Journal of the American Academy of Child and Adolescent Psychiatry, 51(12), 1304–1​ 313. doi: 10.1016/​i.jaac.2012.09.018 Ruocco, A. C., Medaglia, J. D., Tinker, J. R., Ayaz, H., Forman, E. M., Newman, C. F., … Chute, D. L. (2010). Medial prefrontal cortex hyperactivation during social exclusion in borderline personality disorder. Psychiatry Research-N​ euroimaging, 181(3), 233–2​ 36. doi:10.1016/​j.pscychresns.2009.12.001 Ryle, A., & Kerr, I. B. (2002). Introducing cognitive analytic therapy: Principles and practice. Chichester, UK: John Wiley and Sons. Salsman, N. L., & Linehan, M. M. (2012). An Investigation of the Relationships among Negative Affect, Difficulties in Emotion Regulation, and Features of Borderline Personality Disorder. Journal of Psychopathology and Behavioral Assessment, 34(2), 260–2​ 67. doi:10.1007/​s10862-0​ 12-9​ 275-​8 Schramm, A. T., Yenta, A., & Sharp, C. (2013). The Role of Experiential Avoidance in the Association Between Borderline Features and Emotion Regulation in Adolescents. Personality Disorders-T​ heory Research and Treatment, 4(2), 138–​144. doi:10.1037/​A0031389 Schuppert, H. M., Giesen-B​ loo, J., van Gemert, T. G., Wiersema, H. M., Minderaa, R. B., Emmelkamp, P. M., & Nauta, M. H. (2009a). Effectiveness of an emotion regulation group training for adolescents—​a

972 Conclusion 279 randomized controlled pilot study. [Multicenter Study Randomized Controlled Trial Research Support, Non-U​ .S. Gov’t]. Clin Psychol Psychother, 16(6), 467–4​ 78. doi: 10.1002/​cpp.637 Schuppert, H. M., Giesen-​Bloo, J., van Gemert, T. G., Wiersema, H. M., Minderaa, R. B., Emmelkamp, P. M., & Nauta, M. H. (2009b). Effectiveness of an emotion regulation group training for adolescents—​a randomized controlled pilot study. [Multicenter Study Randomized Controlled Trial Research Support, Non-​U.S. Gov’t]. Clinical Psychology and Psychotherapy, 16(6), 467–4​ 78. doi: 10.1002/c​ pp.637 Schuppert, H. M., Timmerman, M. E., Bloo, J., van Gemert, T. G., Wiersema, H. M., Minderaa, R. B., … Nauta, M. H. (2012). Emotion regulation training for adolescents with borderline personality disorder traits: a randomized controlled trial. [Randomized Controlled Trial Research Support, Non-​U.S. Gov’t]. J Am Acad Child Adolesc Psychiatry, 51(12), 1314–1​ 323 e1312. doi: 10.1016/​ j.jaac.2012.09.002 Scott, L. N., Stepp, S. D., Hallquist, M. N., Whalen, D. J., Wright, A. G. C., & Pilkonis, P. A. (2015). Daily Shame and Hostile Irritability in Adolescent Girls With Borderline Personality Disorder Symptoms. Personality Disorders-T​ heory Research and Treatment, 6(1), 53–6​ 3. doi:10.1037/​Per0000107 Selby, E. A., Anestis, M. D., & Joiner, T. E. (2008). Understanding the relationship between emotional and behavioral dysregulation: emotional cascades. Behav Res Ther, 46(5), 593–​611. doi:10.1016/​ j.brat.2008.02.002 Selby, E. A., & Joiner, T. E. (2009). Cascades of Emotion: The Emergence of Borderline Personality Disorder From Emotional and Behavioral Dysregulation. Review of General Psychology, 13(3), 219–2​ 29. doi:10.1037/​A0015687 Selby, E. A., Kranzler, A., & Panza, E. (2014). Development of emotional cascades in borderline personality disorder. In C. Sharp & J. L. Tackett (Eds.), Handbook of borderline personality disorder in children and adolescents (pp. 159–1​ 76). New York: Springer. Sharp, C. (2015). Hypermentalizing in adolescent BPD compared to psychiatry and healthy controls: Introducing a new measure. Paper presented at the Annual Meeting of the American Psychiatric Association, Montreal. Sharp, C., & Fonagy, P. (2008). Social cognition and attachment-r​ elated disorders. In C. Sharp, P. Fonagy & I. M. Goodyer (Eds.), Social cognition and developmental psychopathology. Oxford: Oxford University Press. Sharp, C., & Fonagy, P. (in press). Practitioner review: Emergent borderline personality disorder in adolescence:—​Recent conceptualization, intervention, and implications for clinical practice. Journal of Child Psychology and Psychiatry 56(12), 1266–1​ 288. Sharp, C., Ha, C., Carbone, C., Kim, S., Perry, K., Williams, L., & Fonagy, P. (2013). Hypermentalizing in adolescent inpatients: treatment effects and association with borderline traits. J Pers Disord, 27(1), 3–​18. doi: 10.1521/p​ edi.2013.27.1.3 Sharp, C., Ha, C., Michonski, J., Venta, A., & Carbonne, C. (2012). The diagnosis of Borderline Personality Disorder in adolescents: Evidence in support of the CI-​BPD in a sample of adolescent inpatients. Comprehensive Psychiatry, 53(6), 765–7​ 74. Sharp, C., & Kalpakci, A. (2015). If it looks like a duck and quacks like a duck: Evaluating the validity of borderline personality disorder in adolescents. The Scandinavian Journal of Child and Adolescent Psychology and Psychiatry, 3(1), 49–​62. Sharp, C., Kalpakci, A., Mellick, W., Venta, A., & Temple, J. R. (2014). First evidence of a prospective relation between avoidance of internal states and borderline personality disorder features in adolescents. Eur Child Adolesc Psychiatry, doi: 10.1007/​s00787-​014-​0574-3​ Sharp, C., & Kim, S. (2015). Recent advances in the developmental aspects of borderline personality disorder. Current Psychiatry Reviews, 17(21), 1–9​ . Sharp, C., Pane, H., Ha, C., Venta, A., Patel, A. B., Sturek, J., & Fonagy, P. (2011). Theory of Mind and Emotion Regulation Difficulties in Adolescents With Borderline Traits. Journal of the American Academy of Child and Adolescent Psychiatry, 50(6), 563–5​ 73. doi:10.1016/​j.jaac.2011.01.017

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182 Chapter 14 Emotion Regulation in Severe Irritability and Disruptive Mood Dysregulation Disorder Katharina Kircanski, Ellen Leibenluft, & Melissa A. Brotman Disruptive mood dysregulation disorder By definition, dysfunction in normative emotion regulation is central to disruptive mood dys- regulation disorder (DMDD), a new diagnosis in the Diagnostic and Statistical Manual of Mental Disorders, fifth edition (DSM-5╉ ; American Psychiatric Association [APA], 2013). The hallmark characteristic of DMDD is chronic, severe, and functionally impairing irritability. Here, irritabil- ity refers to a propensity toward anger and is specifically operationalized as: 1) Recurrent severe temper outbursts occurring at least three times per week, which are out of proportion to the situation and inconsistent with developmental level; and 2) persistently irritable or angry mood between outbursts, for most of the day, nearly every day. These core symptoms must be present for at least one year across at least two of three settings (i.e., home, school, peers) and must begin before age ten years; however, the diagnosis of DMDD cannot be made before age six years. Given the recency with which DMDD was established as a formal diagnosis, data on its preva- lence, clinical correlates, and outcomes are limited. In the first and largest epidemiological study of the disorder, three-m╉ onth prevalence estimates ranged from 0.8–â3•‰ .3% across three community samples of children and adolescents ages two to 17 years, notwithstanding the exclusion of chil- dren younger than six years of age by the DSM-5╉ criteria (Copeland, Angold, Costello, & Egger, 2013). More recently, the three-m╉ onth prevalence rate in a sample of six-ây•‰ ear-âo•‰ lds (N = 462) was reported to be 8.2% (Dougherty et al., 2014). No sex differences in prevalence rates were found in either study. Importantly, these investigations also found DMDD to be associated with significant functional impairment, particularly social role impairment, high rates of comorbid emotional and behavioral disorders (Copeland et al., 2013; Dougherty et al., 2014), and high rates of service use (e.g., mental health, school system; Copeland et al., 2013). Irritability itself in adolescence has been associated with risk for suicidality in adulthood (Pickles et al., 2010). Therefore, the current state of knowledge situates DMDD as a severe mood disorder that has serious consequences for the health and daily functioning of those affected. Severe mood dysregulation The DSM-â5•‰ formulation of DMDD relied strongly on the syndrome of severe mood dysregulation (SMD), operationalized by Leibenluft and colleagues (2003) for research purposes to examine if chronic, severe irritability was a developmental presentation of bipolar disorder (reviewed in

28 282 Emotion Regulation in Severe Irritability and Disruptive Mood Dysregulation Disorder Leibenluft, 2011; Stringaris & Taylor, 2015). Unlike DMDD, SMD also included hyperarousal symptoms such as insomnia, agitation, and distractibility, and required an onset of both chronic irritability and hyperarousal symptoms before age 12 years. Consistent with prevalence estimates of DMDD (Copeland et al., 2013), the lifetime prevalence of SMD was estimated to be 3.3% in a community sample of children ages nine to 19 years (Brotman et al., 2006). In a series of studies, SMD was compared to narrow phenotype bipolar disorder (NP-âB•‰ D; i.e., a history of strictly defined, distinct episode(s) of euphoric mania/h╉ ypomania) in youth with respect to pathophysiology, family history, and longitudinal outcomes. Evidence generally did not support the conceptualization of SMD as a phenotype of bipolar disorder (see Leibenluft, 2011). In fact, SMD (Brotman et al., 2006) and chronic irritability (Savage et al., 2015; Stringaris, Cohen, Pine, & Leibenluft, 2009)  in children and adolescents were found to predict the development of unipolar depressive and anxiety disorders, but not bipolar disorder, in adulthood. Additive genetic factors were found to explain a substantial portion of the relation between irritability and anxiety/âd•‰ epression (Savage et al., 2015). In addition, risk for future manic/h╉ ypomanic episodes was documented to be 50 times higher in youth who met criteria for NP-âB•‰ D than in youth with SMD (Stringaris et al., 2010). Finally, youth who met criteria for SMD were significantly less likely than those with NP-âB•‰ D to have a parent diagnosed with bipolar disorder (Brotman et al., 2007). Thus, although some youth with NP-âB•‰ D may exhibit irritability while euthymic and/âo•‰ r increases in irritability during mood episodes, evidence strongly suggests that chronic, severe irritability is not a developmental precursor of bipolar disorder. Further, any history of manic/h╉ ypomanic episodes is exclusionary for the diagnosis of DMDD, such that NP-B╉ D and DMDD cannot be comorbid. Distinctions from associated conditions DMDD is placed in the mood disorders section of the DSM-â5•‰ in recognition of its primary affec- tive features and clinical associations with unipolar depression and anxiety, and to further dif- ferentiate DMDD from other disorders (e.g., oppositional defiant disorder [ODD]). However, the symptom criteria for DMDD and SMD do exhibit areas of overlap with those for ODD and atten- tion deficit hyperactivity disorder (ADHD) (APA, 2013), and a sizeable proportion of youth with DMDD or SMD meet concurrent criteria for ODD, ADHD, and/âo•‰ r conduct disorder (Brotman et al., 2006; Dougherty et al., 2014; Roy et al., 2013). Supporting the conceptualization of irritabil- ity as distinct from the full ODD syndrome, research by Stringaris and Goodman (2009ab) docu- mented that the “irritable” dimension of ODD symptoms (in contrast to the “headstrong” and “hurtful” dimensions) was the only feature of ODD to exhibit concurrent and prospective associa- tions with major depressive disorder (MDD) and generalized anxiety disorder (GAD), consistent with the pattern of associations observed for SMD. In addition, the range of clinical severity that is seen in ODD does not correspond to the necessarily high level of severity that defines DMDD (Leibenluft, 2011). Therefore, DSM-â5•‰ specifies that the DMDD diagnosis “trumps” ODD, such that ODD should not be diagnosed in the context of DMDD. With respect to ADHD, whereas SMD included hyperarousal symptoms in its definition, DMDD does not. Therefore, clinically significant symptoms of hyperarousal, impulsivity, and/âo•‰ r inattention that accompany DMDD should be designated as a comorbid diagnosis of ADHD when these features are present. Finally, irritability is a symptom criterion of both GAD and MDD (APA, 2013). Irritability within the syndrome of GAD must be associated with several other symptoms, including the cardinal fea- ture of excessive and pervasive worry, which are not part of the criteria for DMDD or SMD; fur- ther, irritability can present in GAD at varying levels of severity. Although DMDD can co-âo•‰ ccur with depression in children and adolescents (Copeland et al., 2013; Dougherty et al., 2014), the

382 The role of emotion (dys)regulation 283 expression of irritability in MDD is episodic by definition, and the diagnosis of DMDD should not be made if irritability occurs only within the context of a depressive episode (APA, 2013). The role of emotion (dys)regulation General empirical approach Research on the pathophysiological correlates of irritability has begun in the past decade. As described earlier, the majority of empirical work in this area has focused on SMD and initially examined whether youth with SMD could be distinguished from those with NP-B╉ D. Further stud- ies also have compared youth who met criteria for SMD to youth with other disorders and/âo•‰ r youth with no history of psychiatric disorder. Integrating behavioral and biological metrics, this research has aimed to identify the behavioral anomalies and dysfunctional neural circuitry that differentiate SMD from both healthy functioning and other clinical syndromes, with the ultimate goal of pinpointing biomarkers to facilitate diagnosis and intervention (Leibenluft, 2011). DMDD is now the focus of ongoing and concerted research. Currently, it is unknown the extent to which findings for SMD will generalize to DMDD; however, the vast majority of research participants with SMD would have met diagnostic criteria for DMDD, suggesting that the pattern of findings would be similar. The field of affective neuroscience views the construct of emotion regulation broadly, as “any process that maintains, accentuates, or attenuates emotional responses” (Davidson, Jackson, & Kalin, 2000, p.  903). In this context, brain-b╉ ased methodologies such as functional magnetic resonance imaging (fMRI) have been used to characterize the neural mechanisms mediating emotional processing as individuals with SMD engage in behaviors relevant to their condition. In line with the knowledge that different neural pathways may mediate the same behavioral deficits observed on tasks (Wilkinson & Halligan, 2004), neuroimaging techniques have been particularly effective in elucidating neural circuit mechanisms of SMD that appear to differ from those of NP-âB•‰ D, even when behavioral impairments on the paradigms are similar across these two groups. Working model of pathologic irritability Based on this research to date, we review below three domains of emotion regulation that have been implicated in the pathophysiology of SMD: decreased context-s╉ensitive regulation; dys- regulated attention-âe•‰ motion interactions; and misinterpretation of social-e╉ motional stimuli. For each domain, we describe the correlates of SMD with respect to 1) cognitive/b╉ ehavioral impair- ments and 2) neural function; we then integrate the results from these two levels of analysis in summarizing each domain. Finally, we end our review with the most recent findings of pref- erential processing of threat in SMD, which link with several findings in the other domains to motivate new lines of ongoing research. Together, these contributing psychological processes and neural circuits can be organized within an overarching systems neuroscience framework for pathologic irritability, which both derives from the existing empirical literature and gener- ates additional hypotheses to be tested (see Figure 14.1; revised from Leibenluft, 2011, Figure 2). Critically, underlying this framework is the conceptualization of irritability as a low (relative to normative) threshold for experiencing negative affect in the context of frustration, in which frustration refers to the emotional response when goal attainment is blocked or an action does not produce the expected outcome (Blair, 2010; Leibenluft, 2011; Leibenluft et al., 2003). This is consistent with the observed emphasis on anger as included in the clinical definition of DMDD (APA, 2013).

482 284 Emotion Regulation in Severe Irritability and Disruptive Mood Dysregulation Disorder Amplification of Frustration Dysregulated attention-emotion interactions Decreased Threshold Blocked goal Frustration Misinterpretation Increased irritability attainment of social-emotional Behavioral dyscontrol Increased stimuli probability Decreased context-sensitive regulation Figure 14.1╇ Working etiopathological model of emotion dysregulation in chronic irritability, based on reviewed empirical findings Reproduced from Ellen Leibenluft, Severe Mood Dysregulation, Irritability, and the Diagnostic Boundaries of Bipolar Disorder in Youths, The American Journal of Psychiatry, pp. 129–1╉ 42, Figure 2 doi.org/â1•‰ 0.1176/âa•‰ ppi.ajp.2010.10050766 © American Psychiatric Association, 2011, with permission. Decreased context-s╉ ensitive regulation The human environment involves ever-c╉hanging situations and contingencies, and “context-╉ sensitive regulation” (Ochsner, 2008; p. 53), or the ability to detect and flexibly shift behaviors in accord with such changes, promotes adaptive social functioning and emotion regulation. This construct can be measured in the laboratory using response reversal tasks. In such tasks, over a series of trials, participants initially learn to associate a particular stimulus (e.g., a geometric shape on a computer screen) with the experience of reward (e.g., winning points by selecting that shape among others presented simultaneously). Subsequently, reversal trials occur in which the previously-âr•‰ ewarded stimulus is no longer followed by reward. Instead, participants must learn a new set of contingencies (e.g., selecting a different geometric shape to continue obtaining points). The task can be graded by utilizing a range of difficulty of contingency changes (e.g., using a previously-i╉rrelevant aspect of the stimuli as a new basis on which to reward responses), so that correct responses on difficult trials require not only cognitive flexibility, but also the ability to attend selectively and ignore irrelevant information. Impairments in mechanisms mediating these abilities could increase the likelihood of experiencing blocked goal attainment, or of encounter- ing situations in which outcomes are different than expected, causing more frequent or persistent experiences of frustration (Blair, 2010; Leibenluft, 2011; Figure 14.1). Behavioral findings In the first investigation of reversal learning in SMD, Dickstein and colleagues (2007) compared children and adolescents who met criteria for SMD to youth who met criteria for NP-B╉ D and

582 The role of emotion (dys)regulation 285 non-p╉ sychiatric control participants. Compared to controls, participants with SMD and NP-B╉ D both made more errors on the difficult response reversal trials. However, the two clinical groups did not differ from one another on these trials, suggesting that impairment in cognitive flexibility is common to both syndromes. Dickstein et al. (2010) further examined the diagnostic specific- ity of response reversal deficits by comparing groups of participants who met criteria for SMD, NP-B╉ D, unipolar depression, and anxiety disorders, as well as healthy controls. The probabilistic response reversal task that was used in this study included both reward and punishment (point loss) contingencies. In contrast to the earlier findings, participants with SMD did not differ sig- nificantly from controls (or other clinical groups) on the primary performance metrics that were assessed. However, the effect size associated with the comparison between SMD and control par- ticipants was medium-t╉ o-âl•‰arge, so that the lack of a significant group difference may have reflected insufficient statistical power. In secondary analyses, youth with SMD and NP-B╉ D both exhibited greater difficulty than did controls in using reward and punishment expectancies (i.e., learning on previous trials) to facilitate adaptive responding to this task. Neural findings Adleman and colleagues (2011) used fMRI to assess the neural correlates of response reversal learning in children and adolescents with SMD, NP-B╉ D, and no history of psychiatric disorder. The paradigm employed in the scanner was similar to that used by Dickstein et al. (2010) and had been adapted previously for fMRI in a study of youth with ODD and conduct disorder (Finger et al., 2008). Behaviorally, participants with SMD performed more poorly than did both the NP-╉ BD and control groups throughout the task, suggestive of a generalized deficit in contingency learning. With respect to patterns of neural activation, on incorrect versus correct trials, both the SMD and NP-âB•‰ D groups failed to exhibit an increase in activity in the caudate nucleus that was shown by healthy comparison youth. The caudate, a component of the striatum, supports motor learning to enable behavioral adjustment following errors (Packard & Knowlton, 2002). Thus, findings for this region directly implicate difficulty learning from errors in both SMD and NP-B╉ D. Interestingly, however, only the SMD group exhibited dysfunction in frontal activity when com- pared to both the NP-âB•‰ D and healthy comparison groups. Specifically, youth with SMD exhib- ited hypoactivation in the inferior frontal gyrus, which supports the resolution of error-r╉elated conflict through motor response selection and mediates key sub-âp•‰ rocesses, such as maintenance of attention and cognitive representation of goals and contingencies (Budhani, Marsh, Pine, & Blair, 2007). Activity in other regions, including frontal and cerebellar regions, was also found to distinguish the SMD group and further implicated dysfunction in detecting and adapting to errors in SMD. Summary of findings Therefore, across both behavioral and neural metrics, youth with SMD show impairments in the ability to detect and flexibly respond to changing environmental contingencies of reward and punishment. Whereas the behavioral deficits appear to be shared with NP-B╉ D, the two conditions differ in their mediating neural circuitry. In particular, SMD has been characterized by a unique and pervasive pattern of frontostriatal dysfunction in the context of reversal learning, which may increase the probability of experiencing blocked goal attainment or other unexpected outcomes and heighten the resultant frustration response (Blair, 2010; Leibenluft, 2011). Dysregulated attention-e╉ motion interactions As noted earlier, adaptive functioning requires the ability to selectively attend to motivation- ally salient information in the environment while ignoring irrelevant information (Desimone & Duncan, 1995). In addition, the recruitment of attentional strategies, such as flexibly shifting

682 286 Emotion Regulation in Severe Irritability and Disruptive Mood Dysregulation Disorder attention toward or away from particular stimuli, can facilitate emotion regulation (Posner & Rothbart, 1998) and behavioral self-c╉ ontrol (Mischel, Shoda, & Rodriguez, 1989). Such norma- tive attention-âe•‰ motion interactions appear to be disrupted in children and adolescents with SMD, especially in the context of frustration (see Figure 14.1). One commonly used task in this domain is the affective Posner paradigm, which experimentally manipulates demands on participants’ attention and elicits frustration through the use of rigged performance feedback (Perez-âE•‰ dgar & Fox, 2005). On each trial, participants view two display frames on opposing sides of the computer screen. Next, a cue (e.g., blue illumination) appears inside one of the frames, followed quickly by a target in one of the two locations. Participants are instructed to indicate its location as quickly and accurately as possible. A cue validity effect is typically observed, i.e., responses are relatively slower on “invalid” trials, when the cue and target are presented in opposing locations. The affec- tive adaptation of this task includes an initial baseline phase in which participants complete the trials as described; a second phase in which participants win or lose money based on their perfor- mance; and a critical third phase entailing blocked goal attainment in which participants receive noncontingent negative performance feedback that results in monetary loss on a substantial pro- portion of trials (i.e., frustration trials). Behavioral findings The affective Posner task has been conducted with SMD samples in three separate investigations, all of which included both behavioral and neural assessments (Deveney et al., 2013; Rich et al., 2007, 2011). Behaviorally, children and adolescents with SMD were found to differ consistently from non-âp•‰ sychiatric comparison participants in their affective responses to the frustration trials. As expected, SMD participants reported higher levels of arousal (Rich et al., 2007), unhappiness (Rich et al., 2011), and frustration (Deveney et al., 2013) than did the comparison participants. In the two studies that also included participants with NP-B╉ D, these youth were similarly char- acterized by heightened negative affect in response to frustration (Rich et al., 2007, 2011). With respect to task performance, the pattern of findings is less consistent. In one study, participants with both SMD and NP-B╉ D were less accurate in their responses than healthy comparison youth (Rich et al., 2007); however, another study did not document any group differences in behavioral performance (Rich et al., 2011). Further, two findings were unique to SMD: These youth reported greater arousal in response to negative performance feedback than did both NP-B╉ D and healthy comparison participants (Rich et al., 2011), and SMD youth were slower than healthy comparison youth in responding to invalid trials during the frustration phase (Deveney et al., 2013). This lat- ter effect, which we will return to in the neural findings, suggests decreased flexibility in spatial attention in the context of frustration. Neural findings An electroencephalographic investigation by Rich and colleagues (2007) compared youth with SMD, NP-B╉ D, and no history of disorder in their event-âr•‰elated potentials (ERPs) to targets pre- sented within the affective Posner paradigm. Despite similarities in the behavioral responses of SMD and NP-âB•‰ D participants in this study, ERP profiles diverged between these two syndromes. Most notably, across all phases of the task, the SMD group exhibited lower N1 and P1 amplitudes than did both the NP-B╉ D and healthy comparison groups. The N1 and P1 components occur very quickly following the presentation of a stimulus and reflect initial attentional orienting. Similar reductions in N1/âP•‰ 1 amplitude have been reported for ADHD (Jonkman et al., 2000) and sug- gest a generalized deficit in attentional orienting in SMD. In a follow-âu•‰ p study, Rich et al. (2011) used magnetoencephalography to evaluate the neural responses of SMD, NP-âB•‰ D, and typically-╉ developing participants to the performance feedback portion of the frustration trials. When

782 The role of emotion (dys)regulation 287 contrasting responses to negative feedback versus positive feedback, participants with SMD uniquely showed heightened activity in the anterior cingulate cortex and medial frontal gyrus relative to healthy comparison participants. Previous research has documented activity in these brain structures to be associated with frustration (Moadab, Gilbert, Dishion, & Tucker, 2010), which is consistent with the elevated arousal that was reported by SMD participants in response to negative feedback in this study. Moreover, these results provide direct neurobiological evidence for heightened frustration to blocked goal attainment in SMD. Deveney and colleagues (2013) further explored the neural circuitry mediating frustration by adapting the affective Posner task for fMRI with SMD and healthy comparison participants. In response to frustration trials on which participants received negative feedback, SMD youth were characterized by widespread neural deactivations, both relative to comparison youth in this con- dition (i.e., between-g╉ roup differences) and relative to their own responses to positive feedback (i.e., within-âg•‰ roup differences). In particular, SMD youth showed deactivations in the left and right striatum, left amygdala, posterior cingulate cortex, and parietal cortex. Striatal deactiva- tion is known to occur frequently in conjunction with negative prediction error, or conditions in which an outcome is worse than expected (Schultz, Dayan, & Montague, 1997; Schultz, 2010). Extrapolating from this knowledge and consistent with the response reversal findings, greater deactivation in this region suggests that SMD youth experience blocked goal attainment as more unexpected and/o╉ r unpleasant than do healthy youth. Deactivations in the amygdala and poste- rior cingulate are more difficult to interpret, although as we review in the next section, Thomas et  al. (2013) similarly found in SMD attenuated amygdala and posterior cingulate activity to high levels of facial anger intensity. Finally, the parietal cortex plays a key role in spatial attention (Corbetta, Kincade, Ollinger, McAvoy, & Shulman, 2000), and deactivation in this area suggests that frustration reduces attentional flexibility for youth with SMD, which may have contributed to their slowed performance on invalid trials when frustrated. Summary of findings The affective Posner paradigm has generated both behavioral and neural data to support the pro- posed pathophysiology of SMD. In response to blocked goal attainment, children and adolescents with SMD show heightened activity in brain structures associated with frustration and, corre- spondingly, they report elevated levels of negative affective arousal. In addition, unique striatal and parietal cortex dysfunctions suggest that, relative to healthy comparison youth, youth with SMD experience blocked goal attainment as more unexpected and have limited attentional flex- ibility to regulate their frustration. Misinterpretation of social-âe•‰ motional stimuli As a third domain of emotion regulation, motivationally salient cues in one’s environment are frequently social, i.e., others’ emotional expressions that directly or indirectly signal information about current circumstances, such as an angry expression communicating hostility or a fearful expression communicating the presence of a threat. The ability to identify such cues promotes self-r╉egulation and social adaptation (Ochsner, 2008). This construct has been translated to the laboratory using a variety of experimental paradigms. Most of these tasks involve the presenta- tion of controlled visual stimuli (e.g., facial expressions of emotions) over a series of trials in order to characterize behavioral and neural responses as a function of varying stimulus char- acteristics (e.g., the specific emotion expressed, the intensity of the emotion). Misinterpretation of such social-âe•‰ motional information is another process that has been found to broadly charac- terize youth with SMD and is postulated to amplify their frustration (see Figure 14.1). Perhaps especially for children and adolescents, the experience of blocked goal attainment often occurs

82 288 Emotion Regulation in Severe Irritability and Disruptive Mood Dysregulation Disorder during social interactions (e.g., being told by one’s parents to stop playing a video game or another preferred activity). Misinterpretations of others’ emotion cues in the setting of these interactions (e.g., failing to identify the parent’s angry expression or, conversely, mislabeling the parent’s neu- tral expression as angry) might exacerbate frustration in response to the precipitating events. Behavioral findings Guyer and colleagues (2007) conducted the first study of face emotion labeling in SMD, compar- ing these youth to NP-B╉ D, anxiety and/âo•‰ r unipolar depressive disorders, ADHD and/o╉ r conduct disorder, and non-p╉ sychiatric comparison youth. Participants viewed child and adult faces dis- playing angry, fearful, sad, or happy emotions. On each trial, participants indicated the emotion being expressed. The SMD and NP-âB•‰ D groups both made more identification errors than did all other groups, and did not differ from one another. Further, in both SMD and NP-B╉ D this impair- ment was generalized across child and adult faces and across all emotions. In a subsequent eye tracking study, Kim et al. (2013) replicated this broad deficit in face emotion labeling in SMD and NP-âB•‰ D relative to healthy comparison participants. However, whereas NP-B╉ D was characterized by reduced visual attention to the eyes in the facial stimuli, the pattern of visual attention to the eyes in youth with SMD fell in between that in NP-B╉ D and comparison participants. These data suggest that, in SMD, the observed deficit in face emotion labeling is not fully explained by insuf- ficient visual attention to emotion-r╉ elevant cues in others’ eyes. In a more fine-âg•‰ rained examination of face emotion labeling in SMD, NP-B╉ D, and healthy com- parison participants, Rich et al. (2008) assessed the intensity of expression that was required to label emotions correctly. Each trial began with the presentation of a neutral facial expression, which gradually increased in emotional intensity to result in anger, fear, disgust, sadness, happi- ness, or surprise. Participants were instructed to indicate, once they were aware, the specific emo- tion being expressed by each face, and they were allowed to change their responses as each trial progressed further. Across most emotions, both SMD and NP-âB•‰ D participants required greater intensity of facial expressions than did the comparison participants in order to label the emo- tions correctly. In addition, within the SMD group, greater impairment in face emotion identifica- tion was associated with poorer family functioning, including general relationships with family members and typical interactions surrounding family rules, chores, and solving problems. Finally, Deveney and colleagues (2012) examined children’s ability to label nonverbal emotional cues con- veyed vocally. Extending the earlier findings for emotions presented visually, both the SMD and NP-B╉ D groups were found to perform more poorly than a healthy comparison group in identify- ing the emotion in others’ speech. Neural findings Brotman and colleagues (2010) used an fMRI paradigm to investigate functional activity of the amygdala to facial expressions in youth with SMD, NP-âB•‰ D, ADHD, and no history of disorder. On each trial participants used a rating scale to respond to one of four questions about the face being presented. Importantly, some responses engaged attention to its emotional aspects (e.g., “How afraid are you of this face?”) while other responses engaged attention to its non-âe•‰ motional aspects (e.g., “How wide is the nose?”). Behaviorally, participants with both SMD and NP-B╉ D reported being more afraid of the neutral faces than did ADHD and healthy participants. However, amyg- dala responses to the neutral faces distinguished SMD and NP-B╉ D. Specifically, participants with SMD exhibited hyperactivity in the left amygdala when rating the nose width of the faces (i.e., dur- ing implicit emotional processing), but hypoactivity in the left amygdala when rating their fear of the faces (i.e., during explicit emotional processing). This response pattern was not shown in the NP-âB•‰ D, ADHD, or healthy comparison group. The amygdala is critical to detecting the emotional

982 The role of emotion (dys)regulation 289 salience of environmental stimuli, particularly in terms of threat value (Davis, 1992). Thus, in direct contrast to the findings for SMD, greater amygdala activity is normative when attending to the emotional versus non-e​ motional aspects of a stimulus. Similarly aberrant findings of amyg- dala hypoactivity to face emotion have been reported in children diagnosed with MDD (Beesdo et al., 2009; Thomas et al., 2001), which is intriguing in light of the reviewed cross-s​ ectional and longitudinal associations between SMD/D​ MDD and unipolar depression (Brotman et al., 2006; Copeland et al., 2013; Dougherty et al., 2014; Savage et al., 2015; Stringaris et al., 2009). The brain-b​ ased assessment of face emotion processing in SMD was recently advanced through three programmatic studies by Thomas and colleagues (2012, 2013, 2014), all of which included participants diagnosed with SMD, NP-B​ D, and no history of disorder. First, Thomas et al. (2012) examined the modulation of neural activity to faces that varied systematically along intensity gradients of neutral to angry expressions and neutral to happy expressions; participants processed faces both implicitly and explicitly in this task. In response to increasing intensity of anger expres- sions, typically-​developing participants exhibited parametric increases in activity in the amygdala and posterior cingulate cortex, the latter of which similarly activates to emotional stimuli and participates in motivation-d​ riven allocation of spatial attention (Mohanty, Gitelman, Small, & Mesulam, 2008). Both SMD and NP-B​ D participants, however, failed to modulate amygdala or posterior cingulate activity in this manner, indicating impoverished neural responsivity to higher levels of anger intensity. With respect to increasing intensity of happy expressions, SMD partici- pants exhibited a distinct frontoparietal pattern that entailed low initial activity (i.e., in response to neutral faces) coupled with increasing activity in several regions that implement attention (Kanwisher & Wojciulik, 2000), face processing (Kanwisher, 2000), and emotion processing in a social context (Beer & Ochsner, 2006). Considered with the behavioral deficits in face emo- tion labeling that typify SMD, increasing frontoparietal activity to happiness intensity may reflect greater effort required to correctly identify others’ happy expressions. Thomas et al. (2013) focused on implicit emotional processing of angry, fearful, and neutral facial expressions, utilizing a common fMRI paradigm in which participants indicated the gender of each of a series of faces. Across all emotion types, participants with both SMD and NP-B​ D exhibited hyperactivity in the right amygdala (i.e., increased activity during implicit emotional processing); this finding for SMD is notably similar to that in Brotman et al. (2010). In response to fearful expressions, only participants with SMD showed deactivation in several medial brain regions that comprise a “default mode network” (Raichle & Snyder, 2007), which, among several formulated functions, monitors information about one’s internal state. Extrapolating from cur- rent knowledge of this network, the findings suggest that youth with SMD may not appropriately monitor interoceptive cues in response to fearful stimuli to facilitate their identification. Thomas et  al. (2014) integrated the assessment of automatic face emotion processing that occurs outside of one’s conscious awareness. The authors used a backwards masking paradigm in which, on a portion of trials (“non-​aware” trials), facial expressions were presented subliminally. On other trials the faces were presented quickly but supraliminally, or of sufficient duration for awareness (“aware” trials). Youth with both SMD and NP-B​ D exhibited greater activity in occipi- tal regions during “non-a​ ware” than “aware” trials of all face types, which was the opposite of the occipital response pattern shown in healthy comparison participants and implicates disruption in basic ventral visual stream functions (e.g., object recognition) in these two clinical syndromes (Goodale & Milner, 1992). However, collapsing across “aware” and “non-a​ ware” trials of angry faces, only youth with SMD showed elevated activity in several regions that support higher-o​ rder face processing and social cognition, including the posterior cingulate cortex, superior temporal gyrus, and middle occipital gyrus (Allison, Puce, & McCarthy, 2000; Gallagher & Frith, 2003). Finally, a recent replication study by Tseng and colleagues (2016) compared youth with SMD to

092 290 Emotion Regulation in Severe Irritability and Disruptive Mood Dysregulation Disorder healthy comparison participants in the neural correlates of masked and unmasked face emotion processing. Again, when viewing angry faces, youth with SMD exhibited hyperactivity relative to comparison youth in several brain regions associated with face and emotion processing, such as the parahippocampal gyrus and superior temporal gyrus. Hyperreactivity of these structures to both subliminal and rapid supraliminal anger expressions suggests heightened neural sensitivity toward anger. The threat system: A new research domain in DMDD Finally, two recent studies found youth with SMD or DMDD to preferentially process threaten- ing information (Hommer et al., 2014; Stoddard et al., 2016). This tendency may increase their likelihood of perceiving a goal as being blocked, further fueling frustration and problematic social interactions. In the first investigation, Hommer and colleagues (2014) found youth with SMD to demonstrate heightened attention toward threat. The authors used a dot-âp•‰ robe paradigm in which participants were presented simultaneously with one emotional facial expression (angry or happy) and one neutral expression over a series of trials. These face pairs were followed immedi- ately by a probe (asterisk) in one of the two locations where a face had been, and participants were instructed to indicate the location of the probe as quickly and accurately as possible. Biased alloca- tion of visual attention is indexed using latencies to respond to the probe. Participants with SMD exhibited a greater attentional bias toward angry faces, but not happy faces, compared to healthy comparison participants. Intriguingly, this same threat-âr•‰elevant attentional bias has been docu- mented reliably in youth with anxiety disorders (Waters, Henry, Mogg, Bradley, & Pine, 2010). Importantly, however, the significant difference between SMD and healthy participants was not driven by concurrent anxiety (or depression) within the SMD group. Most recently, Stoddard et  al. (2016, Study 1)  demonstrated that DMDD is associated with a hostile interpretation bias, or elevated tendency to interpret ambiguous facial expressions as angry. In this paradigm, participants viewed and classified as either “happy” or “angry” a series of facial expressions that varied along a continuum of happy to angry and were presented in random order. Critically, faces in the middle of the continuum were ambiguous in expression, as they represented morphed images of both happy and angry faces. Youth with DMDD were more likely than were healthy comparison participants to classify these ambiguous faces as angry. Taken together, these recent findings indicate that chronic, severe irritability is associated with both enhanced attention to, and interpretation of, threat in face emotion stimuli. In this context, it is intriguing to consider neurobiological formulations of an overarching threat-âr•‰esponse system, a circuit that includes the amygdala, hypothalamus, and periaqueductal gray and is posited to mediate the emotions of both anger and fear (Blair, 2010; Johansen, Tarpley, LeDoux, & Blair, 2010; Panksepp, 2006). The concept of threat system dysregulation in SMD also integrates some of the reviewed findings for other domains in which these youth reported height- ened fear of neutral faces (Brotman et al., 2006) and showed elevated neural sensitivity to anger expressions that were presented subliminally or rapidly (Thomas et al., 2014; Tseng et al., 2016). Further, threat system dysregulation may underlie the concurrent and prospective associations between SMD/âD•‰ MDD and anxiety disorders (Brotman et al., 2006; Copeland, Shanahan, Egger, Angold, & Costello, 2014; Savage et al., 2015; Stringaris et al., 2009). For all of these reasons, the threat system is a focus of ongoing pathophysiological research in DMDD. Summary of findings In sum, SMD is characterized by extensive perturbations in face emotion processing. Behaviorally, youth with SMD show broad deficits in identifying others’ emotional expressions

192 PSYCHOTHERAPEUTIC INTERVENTIONS 291 and detecting subtle expressions. NP-B╉ D shares these behavioral impairments and evidence for basic neural dysfunction in the ventral visual stream; however, other neural disruptions appear unique to SMD. Although the precise findings have varied across studies (and these response patterns may not generalize to non-âf•‰acial emotional stimuli; see Rich et  al., 2007, 2010), an overall pattern emerges in which youth with SMD seem to miscalibrate neural activity to faces with respect to the appropriate depth of emotional processing (implicit versus explicit) and the intensity or salience of emotional expression (neutral versus highly expressive). In addi- tion, recent findings indicate that irritable youth preferentially process threatening face emo- tions (Hommer et al., 2014; Stoddard et al., 2016). In the setting of everyday family and social interactions, such miscalibrations may result in inappropriate responses, such as anger, toward others. Evidenced-‰•bâ ased interventions State of the literature Currently, there are no well-âe•‰stablished, evidence-âb•‰ ased treatments specifically developed for SMD or DMDD. However, a number of psychotherapeutic and psychopharmacological interven- tions have been developed for related clinical syndromes (e.g., disruptive behavior disorders) or selected symptoms that are common in SMD/âD•‰ MDD (e.g., aggression, noncompliant behavior). Below, we review these interventions and their evidence base with respect to the clinical symp- toms or syndromes for which they were tested. Given the independent contributions of chronic, severe irritability in youth to adverse outcomes, and the dearth of empirically-s╉upported treat- ments, there is a great need for the development of novel therapeutic approaches (Leibenluft, 2011; Stoddard et  al., 2016; Waxmonsky et  al., 2013). At the end of this section, we highlight several novel approaches with promising initial findings. Psychotherapeutic interventions Numerous psychotherapeutic interventions have been tested for disruptive behavior and conduct problems (Weisz, Jensen-D╉ oss, & Hawley, 2006). Extant approaches fall into two general catego- ries: Parent management training and cognitive-âb•‰ ehavioral therapy. These may be delivered as stand-a╉ lone treatments or in combination with one another. In this section, we briefly highlight these interventions. In the final section of the chapter, we describe in greater detail two therapeu- tic methods that may specifically target emotion dysregulation in SMD/D╉ MDD. Parent management training Parent management training (PMT) is a type of behavioral treatment in which parents learn to no longer engage in dysfunctional interactions with their children. The goal is to reduce child disruptive behaviors, chiefly noncompliance and aggression, as manifested prototypically in ODD and conduct disorder (reviewed in Kazdin, 2010; Sukhodolsky, Smith, McCauley, Ibrahim, & Piasecka, 2016). Given its strong evidence base developed over several decades of research, PMT has achieved the status of a “well-âe•‰ stablished” treatment (Chambless et al., 1996, 1998) for disruptive behavior disorders (Eyberg, Nelson, & Boggs, 2008). Indeed, group-b╉ ased PMT for parents of children ages three to 11 years with oppositional defiant disorder and conduct dis- order is included in the United Kingdom’s National Institute for Health and Clinical Excellence official guidelines. However, the immediate benefits reported by parents may not generalize to other contexts (e.g., with teachers) and may be difficult to sustain over the long term (e.g., one year) (Pilling et al., 2013).

29 292 Emotion Regulation in Severe Irritability and Disruptive Mood Dysregulation Disorder Typically conducted with the parent(s) only, PMT techniques are grounded in parent-âc•‰hild interaction research by Patterson and colleagues (Patterson, 1982; Patterson, DeBaryshe, & Ramsey, 1989; Patterson, Reid, & Dishion, 1992). This work draws heavily on operant condi- tioning (i.e., instrumental learning), in which behavior is shown to be shaped by the positive and negative outcomes that follow it. Specific PMT techniques include instructing parents in the use of positive reinforcement, selective attention and ignoring, and mild negative con- sequences (reviewed in Kazdin, 2010; Sukhodolsky et al., 2016). Numerous clinician protocols are available, including Kazdin’s (2005) 12-s╉ession and Barkley’s (2013) ten-s╉ession manuals. In addition, a number of broader treatment programs for childhood disruptive behavior disorders have a parent training component (e.g., Incredible Years, Webster-S╉ tratton & Reid, 2010; Parent-╉ Child Interaction Therapy, Zisser & Eyberg, 2010; Positive Parenting Program/T╉ riple-P╉ , Sanders, 1999). A  large meta-a╉nalysis reported that, across numerous treatment packages that entailed some degree of parent training, factors associated with the largest effect sizes included a focus on enhancing parental consistency, positive interactions, and affective communication, and the use of in-s╉ ession practice with the child (Kaminski, Valle, Filene, & Boyle, 2008). Efforts are underway to adapt PMT to disruptive behavior in the context of other diagnoses, such as autism spectrum disorders (reviewed in Sukhodolsky et al., 2016). Cognitive-â‰b• ehavioral therapy In contrast to PMT, cognitive-âb•‰ ehavioral therapy (CBT) is conducted directly with the child, aim- ing to help the child learn skills to reduce maladaptive responses to everyday situations (reviewed in Kazdin, 2010; Sukhodolsky et  al., 2016). Several CBT protocols have been developed for school-âa•‰ ge children and adolescents with disruptive behavior. Evidence supports these treatments as “probably efficacious” (Eyberg et al., 2008), consistent with a meta-a╉ nalysis by Sukhodolsky and colleagues (2004) that reported a medium effect size of these interventions on outcomes. CBT involves both in-âs•‰ ession therapeutic techniques and out-o╉ f-âs•‰ ession practice by the child, often with monitoring of practice by the parent. The skills taught in CBT for disruptive behavior draw on several theories, but most centrally the work of Dodge and colleagues regarding chil- dren’s social information processing (Crick & Dodge, 1994; Dodge, 1980, 2003). In this frame- work, cognitive processing of social cues comprises a series of steps: Encoding the cues of others, interpreting these cues, searching for a response, selecting a response, and engaging in the chosen response. Dysfunction in one or more of these processes is posited to underlie anger and aggres- sive responding. Notably, the first two steps of this model (implicating impairments in encoding and interpreting social cues) align with the findings, reviewed above, for misinterpretation of social-âe•‰ motional stimuli in SMD/âD•‰ MDD, particularly in terms of heightened sensitivity to threat cues (Stoddard et al., 2016; Thomas et al., 2014; Tseng et al., 2016). CBT emphasizes more adap- tive ways to think about, and respond to, social situations that elicit anger and aggression. Specific CBT protocols, among others, include Kazdin’s (2010) 20-╉to 25-âs•‰ession Problem-âS•‰ olving Skills Training (PSST), Sukhodolsky and Scahill’s (2012) ten-s╉ ession treatment, and Lochman and col- leagues’ (2010) group-âb•‰ ased Anger Control Training. In the meta-a╉ nalysis of CBT for disruptive behavior, clinician techniques associated with the largest effect sizes were training in social skills, modeling appropriate behaviors, providing direct feedback to the child, and assigning homework to be done outside of the session (Sukhodolsky et al., 2004). Psychopharmacological interventions As described earlier, clinical and pathophysiological research has strongly suggested that SMD is not a developmental presentation of bipolar disorder. This work has important treatment

392 Psychotherapeutic interventions 293 implications, particularly with respect to psychopharmacological interventions. First-l╉ine treat- ments for NP-B╉ D include mood stabilizers and atypical antipsychotics, which have considerable side effect burden (Correll et al., 2009). Indeed, a major impetus of the research on SMD was con- cern over the increasing use of these medications to treat nonepisodic irritability (Olfson, Blanco, Liu, Moreno, & Laje, 2006). Dickstein et al. (2009) investigated the use of lithium to treat youth with SMD in a small, six-âw•‰ eek double-b╉ lind placebo-âc•‰ontrolled trial. There was no significant advantage of lithium over placebo, consistent with findings that the pathophysiology of SMD is distinct from that of NP-B╉ D. Divalproex, an antiepileptic medication that also may be used as a mood stabilizer in NP-âB•‰ D, has received slightly stronger support to target irritability and aggres- sion, especially in youth with ADHD, although it has not been tested for SMD or DMDD directly (Blader, Schooler, Jensen, Pliszka, & Kafantaris, 2009; Donovan et  al., 2000; Steiner, Petersen, Saxena, Ford, & Matthews, 2003). Further, whereas stimulants and selective serotonin reuptake inhibitors (SSRIs) are contraindi- cated for NP-âB•‰ D, these medications might be effective to treat SMD (or DMDD with co-o╉ ccurring ADHD) as the syndrome is conceptualized as irritability and hyperarousal symptoms that are lon- gitudinally and genetically associated with unipolar depression and anxiety (Savage et al., 2015). Two such treatment trials are underway to test the efficacy of stimulant plus SSRI versus stimulant plus placebo (clinicaltrials.gov identifiers NCT00794040, NCT01714310). These studies reflect the growing attention of the field to chronic, severe irritability as a broader clinical phenotype (Hulvershorn, Fosselman, Dickstein, & Janicak, 2012ab). Previous studies of stimulant medication for ADHD reported a decrease in aggression as a secondary outcome. A meta-a╉ nalysis of these studies indicated a medium-ât•‰o-âl•‰arge effect size on reductions in aggressive behavior (Connor, Glatt, Lopez, Jackson, & Melloni, 2002). Finally, it is notable that irritability in the context of autism spectrum disorders has been the symptom target in previous medication trials. As a result of such trials, risperidone and aripipra- zole, second-g╉ eneration antipsychotics, received FDA indication for the treatment of irritability in autism (Marcus et al., 2009; McCracken et al., 2002). Development of novel interventions The review of extant treatment options makes clear the need for novel, pathophysiologically-╉ driven interventions specifically designed for DMDD. Several investigations have reported promising preliminary findings. First, Stoddard et  al. (2016, Study 3)  furthered their inves- tigation of hostile interpretation bias in DMDD by testing the efficacy of a computer-âb•‰ ased program to train away this bias. In an open trial, 14 youth with DMDD viewed a series of facial expressions that were visually morphed along a continuum of happy to angry. As in the origi- nal paradigm (Study 1), participants classified each face as either happy or angry. However, in response to ambiguous faces in the middle of the continuum, participants were given feedback from the computer. Specifically, participants were trained to classify faces that they originally identified as “angry” as “happy.” Thus, youth with DMDD learned to make less hostile and more benign interpretations of the ambiguous faces. Training over the course of four days was associ- ated with a decrease in irritability symptoms and changes in lateral orbitofrontal activation to happy versus angry faces. Together with another published trial in youth at-âr•‰ isk for aggressive behavior (Penton-âV•‰ oak et  al., 2013), these results provide the justification for a randomized controlled trial of interpretation bias training in DMDD that is currently being conducted by our group. Second, Miller and colleagues (2015) have adapted empirically-s╉upported interpersonal ther- apy (IPT) for mood disorders to adolescents with SMD, based on the significant social-âe•‰ motional

492 294 Emotion Regulation in Severe Irritability and Disruptive Mood Dysregulation Disorder impairments documented in this population. A recent proof-o╉ f-âc•‰oncept study indicated excel- lent participant attendance, high participant satisfaction, and overall improvement in core SMD symptoms. A randomized controlled trial is presently being conducted by this research group. Third, Waxmonsky and colleagues (2013) have developed a novel group therapy for youth with ADHD and co-o╉ ccurring SMD. The multimodal treatment incorporates elements of both PMT and CBT. In a pilot trial, all 7 participants also were taking stimulant medication. Reductions in mood lability, depressive symptoms, and overall child functioning were observed, although the effect sizes for changes in disruptive behavior were not as large. Selected psychotherapeutic techniques Therapeutics through the lens of emotion regulation As discussed earlier, the pathophysiology of chronic, severe irritability involves several disrup- tions in normative emotion regulation. First, children and adolescents with SMD are less able to regulate their behavior to changing environmental contingencies of reward and punishment (Dickstein et al., 2007, 2010), and they exhibit pervasive frontostriatal dysfunction in this context relative to healthy comparison youth (Adleman et al., 2011). Second, when an expected reward is omitted, youth with SMD show hyperactivity in brain regions associated with frustration (Rich et al., 2011), and hypoactivity in brain regions that mediate spatial attention, suggesting lim- ited attentional flexibility to regulate frustration (Deveney et al., 2013). Third, youth with SMD or DMDD miscalibrate their neural and behavioral responses to social-âe•‰motional stimuli, and are especially sensitive to threatening facial expressions (Hommer et al., 2014; Stoddard et al., 2016; Thomas et al., 2014; Tseng et al., 2016), which may lower their threshold for anger in social situations. Given that pathophysiological research on SMD began only in the past decade, it is not surpris- ing that interventions specifically indicated for SMD/D╉ MDD remain under development. Rather, it is promising that several lines of psychotherapeutic and psychopharmacological research are already underway. Notwithstanding future advances in treatment, it may be useful to consider extant therapeutic techniques and how they might help to address the deficits in emotion regula- tion that characterize chronic, severe irritability. Here, we examine two different psychotherapeu- tic techniques through this lens. Labeling irritable emotion The “Feeling Thermometer” is one of the first tools introduced to patients in many CBT protocols for disruptive behavior (e.g., Sukhodolsky & Scahill, 2012, p. 30), as in CBT packages for other disorders (e.g., anxiety disorders; Kendall & Hedtke, 2006). In this technique, the clinician visu- ally presents a thermometer or scale that has a simple numerical range (e.g., zero to ten) and describes that the scale can be used to rate the intensity of angry, frustrated, or irritable feelings. Through clinician prompts and discussion, the child learns to label his emotions verbally and assign numerical values to different intensities of emotion that are elicited in different situations. For example, a child may assign a “five” out of ten (moderate anger, irritability, or frustration) to a scenario in which his parent asks him to stop playing a video game and come to the dinner table. Some youth may be able to generate such scenarios independently, whereas others may require the clinician to provide examples. The Feeling Thermometer also is useful to rate emotional inten- sity when the child is actively experiencing irritability or anger in session. With regard to emotion regulation, a growing literature supports the neural and behav- ioral benefits of verbalizing negative emotions (reviewed in Lieberman, 2011). Neuroimaging

592 Selected psychotherapeutic techniques 295 studies document that assigning verbal labels to emotionally evocative images, versus viewing those images, serves to decrease activity in the amygdala and increase activity in the right ventrolateral prefrontal cortex (Lieberman et al., 2007; Tabibnia, Lieberman, & Craske, 2008). Moreover, clinical analog studies have shown that labeling one’s emotions during exposure to a feared stimulus reduces physiological arousal relative to a variety of comparison conditions (Kircanski, Lieberman, & Craske, 2012; Niles, Craske, Lieberman, & Hur, 2015). Given the emotion dysregulation and aberrant patterns of prefrontal and amygdala activity that char- acterize SMD and DMDD (Adleman et al., 2011; Brotman et al., 2010; Thomas et al., 2014; Tseng et  al., 2016), it is possible that verbally labeling irritable emotion may be helpful for these youth. In addition, Feeling Thermometer ratings can be used to measure the success of other emotion regulation strategies (e.g., cognitive restructuring) to decrease their irritability, anger, or frustration. Consistency in parental contingencies for behavior As reviewed earlier, PMT teaches parents to be more consistent in delivering positive and mild negative consequences for child behaviors, in order to shape these behaviors through instrumen- tal learning. Typically, the clinician introduces specific therapeutic techniques in a prescribed order; for detailed descriptions, see Kazdin (2005) and Barkley (2013). In general, however, early sessions focus on enhancing positive reinforcement for adaptive and desired behaviors. For exam- ple, in the case of a child asked to stop playing a video game and come to the dinner table, the parent may positively attend to, praise, and/o╉ r provide a secondary reward (e.g., token or point) in response to the child complying with this request. In later sessions, parents learn to administer mild negative parental consequences or time-o╉ ut from reinforcement in response to maladaptive behaviors. For instance, if the child were to respond argumentatively to the request to come to the dinner table, the parent may ignore this behavior or fail to provide the secondary reward. The clinician works with the parent(s) intensively to achieve greater consistency in their responses while minimizing negative, punitive reactions to the child. Researchers have long recognized the influence of parental attention and contingencies on children’s emotional and behavioral regulation (reviewed in Morris, Silk, Steinberg, Myers, & Robinson, 2007). Given the deficits in instrumental learning that have been documented in youth with SMD (Adleman et al., 2011; Dicksten et al., 2007, 2010), these deficits may be exac- erbated by parental inconsistency in positive and negative consequences for behavior. Further, as SMD and DMDD have been associated with the preferential processing of threat stimuli, these youth may be particularly sensitive to their parents’ negative emotional expressions and punitive consequences (Hommer et al., 2014; Stoddard et al., 2016). Indeed, Patterson and col- leagues’ early research on the “coercive family process” (Patterson, 1982) in youth with conduct problems demonstrated that parents’ negative, punitive reactions to child disruptive behaviors tended to increase rather than decrease the frequency of problem behaviors. Additional studies by Eisenberg and Fabes (1994) and Snyder et al. (2003) have shown that dismissing and punitive parental responses to child expressions of anger are associated with anger amplification and poor behavioral coping (e.g., escaping from the situation). Therefore, enhancing parental consistency and minimizing punitive parenting through positive parent training techniques may be useful components of treatment. Finally, it is important in this context to recall the heightened neural and affective responses to blocked goal attainment that characterize SMD (Deveney et al., 2013; Rich et al., 2007, 2011); failure to receive an expected reward from parents may be particularly frustrating for these youth. This potential to elevate frustration will be an important area for future work to address in adapting parent training techniques to chronic, severe irritability.

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503 Chapter 15 Children of Abuse and Neglect Faye Riley, Anna Bokszczanin, & Cecilia A. Essau Abuse and neglect Violence against children dates back to ancient civilisations, with infanticide, child abuse and cruelty routinely noted in ancient Greece, Rome, Egypt and China (Ten, Bensel, Rheinberger, & Radbill, 1997). For example, in ancient Rome a child was viewed as the possession of the father, who had the legal right to sell, mutilate or kill their child at will. It was also forbidden to rear deformed children; thus, making infanticide or abandonment the only option (Zigler & Hall, 1989). Throughout history, children have also been forced to work in poor conditions and histori- cal accounts have emerged of neglect and sexual abuse (Krug, Mercy, Dahlberg, & Zwi, 2002). However, the issue of child protection remained largely unacknowledged until 1874 with the landmark case of nine-y╉ ear-o╉ ld Mary Ellen Wilson in the United States, who had been severely abused and neglected by her guardian. This case gained widespread media attention and led to the acknowledgement of child abuse and the founding of the New York Society for the Prevention of Cruelty to Children, believed to be the first child protective agency in the world (Myers, 2008). Even with the knowledge of such abuse and the existence of charitable groups concerned with the protection of children, the issue did not receive widespread attention until 1962, with the publication of “The battered child syndrome” (Kempe, Silverman, Steele, Droegemueller, & Silver, 1962). The term “battered child syndrome” refers to serious physical abuse in children and it was after this seminal work that parents and caregivers began to be held responsible for these injuries (Kempe et al., 1962). Kempe and colleagues further asserted that healthcare professionals were responsible for the protection of children and preventing continued abuse, and made recommen- dations on how to identify and report maltreatment. Definition Following the publication of this seminal volume, awareness of other forms of abuse such as child sexual abuse and neglect also increased, along with an increased understanding of the physical, emotional and behavioral consequences of all forms of abuse. However, it was not until 1999 that the World Health Organisation Consultation on Child Abuse Prevention gave a definition of child abuse as, “all forms of physical and/âo•‰ r emotional ill-t╉reatment, sexual abuse, neglect or negligent treatment, or commercial or other exploitation of children, resulting in actual or potential harm to a child’s health, survival, development, or dignity in the context of a relationship of responsibil- ity, trust or power.” Forms of child abuse and neglect are generally recognised to fall into four main categories (Higgins & McCabe, 2001). Firstly, physical abuse which involves hitting, shaking, throwing, poi- soning, burning or scalding, suffocating, or otherwise causing the child actual physical harm or creating the potential for harm. The second form is sexual abuse which involves forcing or entic- ing a child to take part in sexual activities, not necessarily involving a high level of violence,

603 306 Children of Abuse and Neglect irrespective of whether or not the child is cognizant of what is happening to them. The third from is emotional abuse, which is defined as the persistent emotional maltreatment of a child and includes the failure of a caregiver to provide an appropriate and supportive environment. It includes acts that have an adverse effect on the emotional health and development of a child, such as denigration, ridicule, threats, intimidation, discrimination, rejection and other nonphysical forms of hostile treatment. The final form is neglect, which has been defined as the persistent failure to meet a child’s basic physical and/âo•‰ r psychological needs and is likely to result in the serious impairment of the child’s health or development. Neglect may result when a caregiver fails to provide adequate food, clothing and shelter (including exclusion from the home or abandon- ment), fails to protect a child from physical and emotional harm or danger, fails to respond to a child’s basic emotional needs, does not provide adequate supervision, or does not ensure access to appropriate medical care or treatment. Prevalence Child maltreatment is complex and difficult to study, consequently current estimates of preva- lence can vary widely depending on a variety of factors such as differing legal and cultural defi- nitions of child maltreatment used between countries; the type of child maltreatment studied; the population studied and how the sample was recruited; the methods of research used; the breadth and quality of official statistics and the extent of mandatory reporting; the breadth and quality of population-b╉ased self-âr•‰eport surveys collected from victims, parents or caregivers (Finklehor, 1994). Prevalence estimates of abuse and neglect in the child population vary considerably depending on the country of study. For example, in a review of international studies, Radford et al. (2011) showed prevalence rates for different forms of abuse ranging from 1.8% to 34% for physical vio- lence; 1.1% to 32% for sexual abuse; 5.4% to 37.5% for emotional abuse; and 6% to 41.5% for neglect. Prevalence rates can also vary depending on the age of the population studied. In the UK, a National Society for the Prevention of Cruelty to Children (NSPCC) prevalence study found that 2.5% of children under 11 years of age and 6% of 11 to 17 year olds had experienced mal- treatment by a parent or caregiver in the past year. For lifetime rates, it was found that one in 17 (5.9%) children under 11 years and one in five 11–â1•‰ 7 year olds (18.6%) had experienced severe maltreatment during childhood. A further issue is that abuse and neglect are often hidden from view and therefore large numbers of cases are not detected, reported or recorded, even where mandatory reporting exists (Theodore & Runyan, 1999). Consequently, official statistics often reveal little about the true rates of child abuse. There are currently over 50,000 children identified that are in need of protection from abuse in the UK, yet the NSPCC estimates that for every child identified as needing protection from abuse, another eight may be suffering abuse (Harker et al., 2013). In part this may be because children do not disclose what is happening to them out of fear of the repercussions or due to fear that they will not be believed. In addition, some victims may be too young to realise that what is happening to them is wrong, or abuse may not be officially reported even if other family members or adults know about it. Moreover, in many countries, there are no legal or social systems with specific responsibility for recording, or responding to, reports of child abuse and neglect (Bross, Miyoshi, Miyoshi, & Krugman, 2000). Therefore, prevalence rate estimates gathered through research studies and official statistics in particular, may often only represent the “tip of the iceberg” in terms of the extent of child abuse and neglect. However, such data are useful to gain a picture of the general patterns of abuse and have shown a global trend that has significant, deleterious consequences for public health (Krug et al., 2002).

703 RISK FACTORS FOR ABUSE AND NEGLECT 307 Assessment Early detection and intervention of abuse is important in limiting the damage done to the devel- opment of the child. When early intervention does not occur, approximately one in three children will suffer continued abuse (Seifert et  al., 2010). Child abuse and neglect is rarely detected or prevented before hospitalisation, most likely due to limited contact with non-f╉ amily members and because violent incidents often occur within or around the family, in “a circle of trust” (Finkelhor, 1994). It is estimated that 2% to 10% of children who visit hospital emergency departments are victims of child abuse and neglect (Holt, Buckley, & Whelan, 2008; Hussey, Chang, & Kotch, 2006; Palazzi, de Girolamo, & Liverani, 2005). Therefore, hospital staff may be the first contact and opportunity for physical abuse to be identified. However, recognising maltreated children in the everyday routine of an emergency department is a major challenge and detection rates of child abuse remain low, often going undetected by both clinical and nursing staff (Gilbert, Kemp, et  al., 2009; Louwers et  al., 2012; Oral, Blum, & Johnson, 2003). This is influenced by factors such as knowledge, training, attitude and the experience of health care professionals, and avail- able resources for referral to name a few (Flaherty et al., 2008; Fraser, Mathews, Walsh, Chen, & Dunne, 2010; Jones et al., 2008). Due to limitations associated with identifying abuse at emergency departments, other screen- ing assessments attempt to facilitate the detection of abuse before hospitalisation. For example, the “Tool for identifying families at risk of or with already established infant and toddler abuse and neglect problems” (INTOVIAN Tool), is a five-âi•‰tem checklist addressing risk indicators for physi- cal and/o╉ r psychological violence, neglect, and disordered/âa•‰ busive relationship patterns between the child and caregiver. This tool aims to prevent violence, or to break the cycle of violence in the family before children suffer more severe maltreatment. The tool can be used by professionals as part of routine observations in children’s centers and nurseries, or by medical staff during routine health examinations. Staff who have been trained in education and who work in nurseries and children’s centers will likely be in a better position to detect signs of neglect, because it is more long-ât•‰erm; whereas, staff in health and social services will be better placed to identify child abuse (Essau, 2015). Professionals can use the aforementioned tool to assess the quality of the caregiver and child interaction; levels of affection shown; and the psychological involvement of both the caregiver and child, in order to uncover any potential issues regarding the caregiver-c╉ hild rela- tionship, which may be indicative of maltreatment. Risk factors for abuse and neglect A variety of theories and models have been developed to explain the occurrence of child abuse. The most widely adopted explanatory model is the ecological model. This risk factor approach assumes that there is no single pathway to abuse and that risk factors occur across multiple devel- opmental domains or levels of a child’s social ecology (Bronfenbrenner, 1988). As applied to child abuse and neglect, the ecological model proposes a number of factors that contribute to the risk of maltreatment, covering characteristics of the individual child, those of the caregiver or family, parent-c╉ hild relationships, neighbourhood characteristics, and societal factors. Child factors A number of child characteristics have been associated with greater likelihood of being abused or neglected, which include age; being perceived as problematic; or having a disability or ill- ness. In terms of age, the risk of maltreatment is greater for children under four years of age or during adolescence. Fatal cases of physical abuse are more common among young infants (Damashek, Nelson, & Bonner, 2013; Klevens & Leeb, 2010), who are particularly vulnerable due

803 308 Children of Abuse and Neglect to their dependency, small size, and inability to defend themselves. In contrast, rates of sexual abuse tend to rise after the onset of puberty, with the highest rates occurring during adolescence (Finklehor, 1994). Caregivers who perceive their children as having more problem behaviors are more likely to physically abuse them (During & McMahon, 1991; Whipple & Webster-S╉ tratton, 1991). In addi- tion, difficult child temperament (as perceived by the parent) has been specifically associated with emotional neglect (Harrington, Black, Starr, & Dubowitz, 1998). Such behavior and perceptions may strain the parent-c╉ hild relationship, increasing the risk of maltreatment. Finally, it has been documented that children with disabilities are 1.8 times more likely to be neglected, 1.6 times more likely to be physically abused, and 2.2 times more likely to be sexually abused than are children without disabilities (Sullivan & Cork, 1996). It may be that due to the demands of raising a child with a disability caregivers become overwhelmed and respond with irritability, inconsistency, or punitive discipline. Furthermore, disabled children may be unre- sponsive or have limited ability to interact with, or show affection to their caregivers, which conse- quently may interfere with attachment and bonding (Hibbard & Desch, 2007). Compounding the issue further, children with disabilities may be less able to protect themselves and are also highly dependent on adults for their safety and well-âb•‰ eing, meaning they may be particularly vulnerable to abuse or neglect. Caregiver or family factors Research has linked certain characteristics of the caregiver and the wider family environment to child abuse and neglect. Such factors may compromise parenting, resulting in maltreatment. These factors include: The family structure and resources; family size and household composition; personality and behavioral characteristics of the caregiver; stress; lack of social support; failure to bond with and nurture the child; being maltreated themselves as a child; misusing alcohol or drugs; experiencing financial difficulties; and family breakdown or conflict. In terms of family structure and resources, physically abusive parents are more likely to be young, single, poor, unemployed and less educated than non-âa•‰ busing parents. For example, being in a single parent household increases the risk of child neglect by 87% (Connell-C╉ arrick, 2003) and single mothers are three times more likely to report using harsh physical discipline when com- pared with mothers in two-âp•‰ arent families (Straus & Gelles, 1990). For single parents there may be less time to accomplish household tasks, including child supervision, spending quality time with children and earning sufficient money to adequately provide for them (DePanfilis, 2006). With relation to family size and household composition, households of a larger size have been shown to present a greater risk of child abuse (Damashek et al., 2013). In part this may be due to unstable family environments, where the make-u╉ p of the household frequently changes as mem- bers move in and out (Dubowitz & Black, 2001). Furthermore, children living in households with adults who are not related to them, have 50 times greater risk of fatal injury as children living with two biological parents or a single parent (Schnitzer & Ewigman, 2005). Personality and behavioral characteristics of parents may also influence child abuse. Parents who are more likely to abuse their children tend to have lower self-âe•‰ steem and reduced mental well-b╉ eing. For example, research has shown that physically abusive parents have more negative self-âp•‰ erceptions than parents who are not physically abusive (Christensen et al., 1994) and have greater general emotional distress and unhappiness (Caliso & Milner, 1992; Milner & Robertson, 1990). These characteristics may compromise their parenting capabilities and may be associated with disrupted social relationships, an inability to cope with stress and difficulty in forming social support systems (Krug et al., 2002).

903 Risk factors for abuse and neglect 309 In relation to stress, it is believed that stress resulting from job changes, loss of income, health problems or other stressors can exacerbate characteristics in the family, such as hostility, anxi- ety, or depression, which in turn might increase levels of family conflict and child maltreatment (Goldman, Salus, Wolcott, & Kennedy, 2003). Indeed, abusive parents reported more stressful life events (Coohey & Braun, 1997)  and scored higher on perceived daily stress (Williamson, Borduin, & Howe, 1991), compared to non-​abusive parents. Physically abusive mothers also per- ceive themselves as using more inefficient coping strategies when faced with stress (Cantos, Neale, O’Leary, & Gaines, 1997). While families who are coping with such problems may also lack the time or emotional capacity to provide for the basic needs of their children, resulting in neglect (DePanfilis, 2006). Social support can also play a role in the occurrence of child abuse. Abusive mothers report receiving less social support, compared to non-a​busive mothers (Chan, 1994) and the support that is received, seems to be weaker with abusive mothers reporting they receive less emotional resources (e.g., listening, decision-m​ aking, companionship) from their social networks (Coohey & Braun, 1997). A lack of social support may mean parents or caregivers have less of a support net- work to act as alternative caregivers, or to provide additional support to the caregiver or the child. A further contributing factor is failure to bond with and nurture the child. Abusive parents show greater irritation and annoyance in response to their children’s moods and behavior and have been shown to be more controlling and hostile, and less supportive, affectionate, playful and responsive to their children (Bardi & Borgognini-T​ arli, 2001; National Research Council, 1993). Furthermore, abusive mothers have greater negative expectations of their children (Larrance & Twentyman, 1983) and are less likely to blame themselves for failed mother–​child interactions, and give less credit to their children for successful mother–​child interactions than other mothers (Bradley & Peters, 1991). Such characteristics can impact upon the successful formation of the parent-c​ hild relationship and thus, increase the risk for abuse. The caregivers’ own childhood can also serve as a risk factor, specifically if they have been mal- treated themselves as a child. Research has shown that abusive mothers are more likely to report having been physically victimized as children by their parents (Coohey & Braun, 1997) and expe- riencing corporal punishment as a teen has also been shown to be a significant predictor of per- petrating severe child abuse (Ross, 1996). Additionally, neglectful mothers are three times more likely to have been abused in childhood than mothers who did not neglect their children (Zuravin & DiBlasio, 1996). This can be explained by social learning theory, which suggests that children’s behavior is largely shaped by their parents via modelling and schedules of reinforcement such that exposure to abusive and maltreating parents during their own childhood encourages the caregiver to believe such behaviors are acceptable and effective, leading them to incorporate these into their own parenting styles as adults (Dodge, Bates, & Pettit, 1990). Substance abuse can also be a contributing factor. Research has demonstrated that physically abusive mothers are more likely to have a history of drug problems (Whipple & Webster-​Stratton, 1991) and, children whose parents abused alcohol and other drugs are more than four times more likely to be neglected than children whose parents did not (Jaudes, Ekwo, & Van Voorhis, 1995). Such substance abuse may limit the ability of the caregiver to provide adequate care for their children or to make appropriate decisions regarding their welfare (Slack et al., 2011), particularly when intoxicated, with one study reporting that 65% of maltreated children who had parents with substance abuse problems were maltreated while the parent was intoxicated (Donohue, 2004). Experiencing financial difficulties in the family has also been found to be a strong predictor of child neglect (Slack et al., 2011), with a lack of familial financial resources having serious negative consequences on the ability of the caregiver to meet even the most basic needs of their child. For

013 310 Children of Abuse and Neglect example, poverty can affect the ability of the caregiver to provide adequate supervision (e.g., can- not afford child care), housing, nutrition, medical care, clothing, and safety. Finally, family breakdown and conflict can be a further contributing factor. Straus and Gelles (1990) found that parents with higher rates of inter-âp•‰ arental verbal aggression were more likely to perpetrate severe child abuse. Additionally, physically abused adolescents are more likely to come from families experiencing high levels of family stress, and these adolescents perceived their families as being less adaptive and cohesive (Williamson et al., 1991). Family life with such stress and conflict may be so disorganized and hostile that caregivers are unable to meet the basic needs of their children on a consistent basis (Hornor, 2014). Community factors A number of community characteristics may increase the risk of child maltreatment. These factors include poverty; community disorganisation; and poor social cohesion. In relation to poverty, this has been shown to adversely affect children through its impact on parental behavior and the avail- ability of community resources (McLoyd, 1990). Communities with high levels of poverty tend to have weaker physical and social infrastructures and fewer resources and amenities in place to prevent and detect child abuse, such as accessible health care, social services, and affordable child care, which can reduce the ability of caregivers to appropriately care for their children (Corcoran & Nichols-âC•‰ asebolt, 2004). Community disorganization can be a further risk factor. Rates of child abuse and neglect are higher in communities characterized by high levels of unemployment, high population turnover and high availability of alcohol and drugs (DePanfilis, 2002; Gillham et al., 1998). Finally, children living in communities that lack social cohesion and solidarity have been found to be at greater risk of abuse (Runyan et al., 1998), due to the lack of positive informal and formal support systems for families (Cash & Wilke, 2003). Societal factors A range of society level factors are considered to have important influences on child maltreat- ment. Many of these broader cultural and social factors can influence how caregivers treat their children. These include factors such as the presence of policies and programs to prevent child abuse and neglect, and the responsiveness of the criminal justice system. In addition, cultural norms and the cultural definitions of generally accepted child-r╉ earing principles, may contribute to this issue. Specifically, social and cultural norms that promote or tolerate violence towards oth- ers and support the use of corporal punishment or certain cultural practices that may be viewed as abusive or neglectful to the larger society (e.g. genital mutilation). Moreover, social, economic, health and education policies that lead to poor living standards, or to socioeconomic instability, may also be a contributing factor to child abuse. Outcomes The consequences of child abuse and neglect can vary widely. Physical injuries and, in extreme cases, death are direct consequences; however, there are also a variety of psychological and behav- ioral outcomes. Various aspects of the maltreatment situation, such as duration, type and sever- ity of abuse, can directly impact the development of negative outcomes (Manly, Cicchetti, & Barnett, 1994). Chronically maltreated children appear to be at a high-âr•‰isk of developing clinical levels of psychological problems (Ethier, Lemelin, & Lacharité, 2004). Research has shown that there is a particularly strong association between childhood abuse and mood and anxiety disorders, including depression, bipolar disorder, generalized anxiety disorder, panic disorder, phobias, and

13 Emotion regulation 311 posttraumatic stress disorder (PTSD) (Gilbert, Widom, et al., 2009; Heim & Nemeroff, 2001; Hill, 2003; Katerndahl, Burge, & Kellogg, 2005; Kendler et al., 2000; Molnar, Buka, & Kessler, 2001). In addition, traumatic experiences early in life are associated with other psychological conditions, such as schizophrenia, reactive attachment disorder, eating disorders, and personality disorders (Ackard & Neumark-S╉ ztainer, 2003; Kaplan & Klinetob, 2000; Noll, Horowitz, Bonanno, Trickett, & Putnam, 2003; Zeanah et al., 2004). Heim, Shugart, Craighead, and Nemeroff (2010) conducted a meta-âa•‰nalysis of 124 studies that investigated the relationship between child physical abuse, emotional abuse, or neglect and various health outcomes. It was found that emotionally abused children were three times more likely to develop depression than non-âa•‰ bused individuals. Physically abused and neglected chil- dren also had a higher risk of developing a depressive disorder. Cicchetti and Rogosch (1997) examined the level of adaptation of school-âa•‰ ged maltreated children who were evaluated over a three-ây•‰ ear period. Over this period, the maltreated children exhibited more externalising and internalising behavior problems, less prosocial behavior, greater symptoms of depression, and more withdrawn behavior than the non-âm•‰ altreated children. This study confirms continuity in the difficulties experienced by abused children. In addition, research has shown children who experience maltreatment are also at increased risk for substance misuse, engagement in high-âr•‰ isk sexual behaviors, delinquency and poor academic performance (Dubowitz, 2009; Felitti et  al., 1998; Lansford et al., 2007). As well as causing immediate harm and later childhood impairment, abuse and neglect can have many long-ât•‰erm consequences that endure well into adulthood. A  longitudinal study revealed that as many as 80% of young adults who had been abused as a child met the diag- nostic criteria for at least one psychiatric disorder at age 21 (Silverman, Reinherz, & Giaconia, 1996). Adult psychological difficulties most frequently associated with child abuse include depression, anxiety, PTSD, low self-e╉ steem, poor adjustment, criminal behavior, risky sexual behavior and substance misuse (Afifi et al., 2008; Fergusson, Boden, & Horwood, 2008; Huang et al., 2011; Widom, Marmorstein, & White, 2006; Wilson & Widom, 2011). Moreover, chil- dren who experience maltreatment are also at increased risk for adverse health effects and certain chronic diseases as adults, including heart disease, cancer, chronic lung disease, liver disease, obesity, high blood pressure and high cholesterol (Danese et  al., 2009; Felitti et  al., 1998; Springer, Sheridan, Kuo, & Carnes, 2007). A further long-ât•‰ erm consequence of maltreat- ment is the heightened likelihood of abusing or neglecting one’s own children (Thornberry & Henry, 2013), which, therefore, contributes to the establishment of an intergenerational cycle of neglect and abuse. Emotion regulation Emotion regulation is generally defined as the internal and external processes by which the indi- vidual manages the occurrence, intensity, and expression of emotions to reach goals or situational demands (Cicchetti & Howes, 1991; Eisenberg & Morris, 2002; Thompson, 1994). The childhood years are thought to be a critical period for the development of emotion regulation skills, and suf- fering abuse and neglect during this time can interfere with the acquisition of these skills (Shields & Cicchetti, 1998). Maltreated children can experience conflicting feelings and impulses arising from being neglected and/o╉ r harmed by an adult who is often also an attachment figure. Abusive and neglectful caregivers also likely fail to engage in behaviors that enable children to develop optimal emotion regulation strategies. Consequently, maltreated children often exhibit a range of emotion regulation deficits, with nearly 80% of maltreated children displaying dysregulated emo- tion patterns, compared with only 36% of non-m╉ altreated children (Maughan & Cicchetti, 2002).

213 312 Children of Abuse and Neglect In the next section, we discuss how abuse and neglect can lead to the development of emotion regulation problems, how these problems manifest in abused children and how these problems can heighten the. risk of continued abuse and exacerbate negative outcomes and psychopathology. Development of emotion regulation problems Caregiver influence Individual differences in emotion regulation emerge from the quality of familial relationships and from caregiver socialisation of appropriate emotion related behaviors, through processes such as modelling, reinforcement, discipline, displays of positive or negative affect and sensitiv- ity (Calkins, 1994; Morris, Silk, Steinberg, Myers, & Robinson, 2007; Thompson & Meyer, 2007; Valiente & Eisenberg, 2006). Caregiver behavior can influence the child’s internal emotional expe- riences, emotional reactivity, and modulate their emotional arousal (van der Kolk & Fisler, 1994). From the perspective of attachment theory, securely attached children are able to use care- givers effectively to help regulate their emotions (Bowlby, 1969, 1982). However, in abusive and neglectful environments characterized by inconsistency and hostility, caregivers lack certain char- acteristics thought to be important to the development of their children’s emotion management skills (Howes, Cicchetti, Toth, & Rogosch, 2000). In particular, abusive caregivers socialize emo- tion management skills differently than non-a╉busive caregivers, by providing less support and acknowledgement in response to their children’s emotions, showing lower levels of emotional expression in the parent-c╉hild relationship, and providing less emotion-âr•‰elated information exchange (Bousha & Twentyman, 1984; Camras, Sachs-A╉ lter, & Ribordy, 1996; Gaudin, Polansky, Kilpatrick, & Shilton, 1996; Shipman, Zeman, Penza, & Champion, 2000; Shipman & Zeman, 2001). Such parenting practices are imbedded in the caregivers’ own attitudes towards emotion and have been found to correlate with children’s successful regulation of emotion (Gottman, Katz, & Hooven, 1996; Lunkenheimer, Shields, & Cortina, 2007). It is also believed that abusive caregivers tend to be more socially isolated, and in turn isolate their children from interactions with others, resulting in fewer opportunities for the child to engage in emotional communication (Salzinger, Feldman, Hammer, & Rosario, 1993). Abusive caregivers have additionally been found to show less positive and more negative emo- tion, than non-âa•‰busive caregivers (Bugental & Others, 1989; Kavanagh, Youngblade, Reid, & Fagot, 1988) and as such, abused children are exposed to frequent negative emotional experiences including anger, frustration, reactivity, and irritability (Alessandri, 1991; Shields & Cicchetti, 1998). This can place the child in a state of near constant arousal and vigilance. Such overwhelming emotional arousal can foster conditions that undermine the child’s ability to process and manage emotions effectively (Briere & Jordan, 2009; Maughan & Cicchetti, 2002) and may later manifest in problematic behavior, such as aggression or hypervigilance (Greenberg, Speltz, & Deklyen, 1993). For example, abused children may be more sensitive to anger from their abuser and fearful of those around them, because this could help them identify threat quickly and potentially avoid additional abuse (Masten et al., 2008). In other cases, the emotional regulatory problems of maltreated children arise from the incon- sistent emotional demands expected from the caregiver, which means a child can have difficulty predicting the consequences of their behavior (Dadds & Salmon, 2003). Thus, the same emo- tional signals from the child that can elicit nurturance from non-âa•‰ busive caregivers may result in hostile or angry reactions from an abusive caregiver. Consequently, children may learn that it is unacceptable or even dangerous to discuss their feelings and emotions, particularly negative ones (Beeghly & Cicchetti, 1994) and accordingly develop strategies of emotion regulation that

31 Development of emotion regulation problems 313 attempt to accommodate these conditions. Emotionally abusive environments in which children are told their emotional reactions are bad or inappropriate, or in which negative emotions are punished, ignored, or met with hostility, may elicit patterns of avoidance, suppression, and harm- ful attempts at managing emotions (Krause, Mendelson, & Lynch, 2003). For example, Shipman, Edwards, Brown, Swisher, and Jennings (2005) found support for this from the perspective of neglected children. Neglected children were more likely to inhibit the expression of negative emo- tion to their mothers and expected less support and more punishment or conflict from mothers in response to displays of negative emotion. Children who anticipate non-s╉ upportive or disparag- ing responses to their emotional displays are then likely to restrict emotional expressiveness as a learned response (Cole, Zahn-âW•‰ axler, & Smith, 1994). In summary, certain parenting practices and behavior associated with abuse and neglect may interfere with the normal acquisition of emotional understanding and emotion regulation skills in maltreated children. Neurobiology It is probable that the emotional difficulties displayed by maltreated children are not only a reflec- tion of caregiver influence, but also affected by changes in neurobiological structure and function- ing that occur as a result of abuse or neglect (Cicchetti & Tucker, 1994). These changes can reduce a child’s capacity to regulate affective states and modulate behavioral responses to stressors, and thus, may influence emotion regulation processes. Maltreatment in childhood appears to be associated with the reorganisation of neural circuits in ways that alter the processing of emotional information, which may underlie the emotion regula- tion deficits reported in maltreated children (Pollak, 2008). For instance, youth with histories of early-l╉ife abuse and trauma display greater amygdala activity to threatening cues and emotional conflict, showing a hypervigilance to threat stimuli and reduced ability to regulate emotional processing (Marusak, Martin, Etkin, & Thomason, 2015; McCrory et al., 2011). Engagement of the amygdala is thought to support preferential processing to emotional stimuli (Vuilleumier, Armony, Driver, & Dolan, 2001), in order to allow potential threats to be rapidly detected and evaluated (LeDoux, 1996). Thus, the alterations in the neural systems of abused children alter how they monitor the environment for threatening information. Pollak, Klorman, Thatcher, and Cicchetti (2001) found that the event-r╉elated potential amplitude responses of maltreated chil- dren exceeded those of non-m╉ altreated children in response to angry facial expressions, but not to fearful or happy expressions, reflecting a response bias for angry stimuli. These results suggest that the abusive experiences encountered by these children during their development may enhance the memory of salient stimuli, due to the stored mental representations that have been associated with that stimulus over time. As such, maltreated children are particularly sensitive to, and quick to detect, anger, as they develop an association between this emotion and abusive behavior from their caregiver. Furthermore, there is substantial evidence that amygdala reactivity is under inhibitory control of medial prefrontal regions (Ochsner & Gross, 2005), particularly Pregenual anterior cingulate cortex (pgACC) (Maier & di Pellegrino, 2012). Marusak et al. (2015) found an absence of nega- tive regulation-r╉ elated amygdala–p╉ gACC connectivity in maltreated youth, indicating an absence of effective inhibitory control. Maltreated children have also been found to exhibit dysregulation of the hypothalamic-p╉ ituitary-a╉ drenal axis following social interactions, signifying the impaired ability to cope with stressors and negative emotions (Tarullo & Gunnar, 2006). Collectively, these neurobiological findings imply abuse and neglect is associated with a simul- taneous heightened sensitivity to conflicting emotional information and a lack of regulatory

413 314 Children of Abuse and Neglect control over emotion processing. Thus, the combination of these factors is likely to limit the abil- ity of the maltreated child to master appropriate emotional skills. Expression of emotion regulation deficits The emotion regulatory deficits associated with abuse and neglect manifest through a range of expressions and behaviors, including the poor understanding and recognition of emotions (Cicchetti & Curtis, 2005; Shipman et al., 2005), greater negative affect (Gaensbauer, 1982), fewer adaptive emotion regulation skills (e.g., situational appropriateness of affective displays, empathy, and emotional self-a╉ wareness) (Shipman et al., 2005), heightened vigilance to threatening stimuli (Pollak, Vardi, Putzer Bechner, & Curtin, 2005; Rieder & Cicchetti, 1988), and poor regulation of emotions (Maughan & Cicchetti, 2002; Shipman et al., 2007). Behaviorally, maltreated children exhibit less self-c╉ ontrol and social competence (Shields, Cicchetti, & Ryan, 1994) and more irrita- bility, reactivity and anger (Alessandri, 1991). The atypical emotional development of maltreated children can become apparent from the first few months of life. Early-âl•‰ife abuse appears to be a particular risk for emotion regulation problems. Children who experienced maltreatment during early-âl•‰ife showed significantly reduced emotion regulation compared to non-âm•‰ altreated children; whereas, children who experienced a later onset did not (Kim & Cicchetti, 2010). Early-l╉ife abuse and neglect has been associated with high levels of negativity and anger in toddlers, and a lack of self-âc•‰ ontrol in pre-âs•‰ choolers (Erickson, Egeland, & Pianta, 1989). For example, Gaensbauer, Mrazek, and Harmon (1981) found that maltreated infants as young as three months of age displayed higher rates of fearfulness, anger, and sad- ness during mother-i╉nfant interactions, and expressed a reduced range of emotions and increased duration of negative affect, compared with non-âm•‰ altreated controls. Similarly, maltreated chil- dren aged one to three years, exhibited more anger and less positive affect compared to non-╉ maltreated children (Robinson et  al., 2008). Furthermore, Macfie, Cicchetti, and Toth (2001) studied dissociation in a sample of maltreated and non-m╉ altreated preschoolers and found that physically abused, sexually abused, and neglected children all demonstrated greater dissociation than non-âm•‰ altreated children. In primary school-a╉ ge children, Shields and Cicchetti (1998) found that abuse was associated with regulatory deficits characterized by emotional lability and negativity. In particular, physi- cally abused children were more likely than their non-âm•‰ altreated peers to be rated by counsellors as expressing greater emotional negativity when transitioning from one activity to the next (i.e., becoming anxious, angry, or distressed) and as having more difficulty recovering emotionally from exposure to stressful events. Similarly, school-âa•‰ged girls with sexual abuse histories have been found to display regulation difficulties. When compared to non-âm•‰ altreated peers, these abused children showed limited emotional awareness, a decreased capacity to regulate their emo- tions appropriately and greater affective lability (Shipman et al., 2000). Older children and adolescents with histories of abuse, or currently suffering abuse, often express emotion regulation problems through high levels of arousal, greater reactive aggres- sion, and have more difficulty regulating this response, when exposed to potentially threaten- ing situations, such as interpersonal anger and conflict (Cummings, Hennessy, Rabideau, & Cicchetti, 2008; Shackman & Pollak, 2014; Shields et al., 1994). Reactive aggression is emotion- ally driven and associated with a high degree of sympathetic arousal and angry reactivity, and is thought to be motivated by a desire to protect oneself from real or perceived threat. Physically abused adolescents in particular, seem especially prone to exhibiting this form of aggression, which can lead to poor social competence and difficulty with peer relationships (Shields & Cicchetti, 1998).

513 Propagation and maintenance of outcomes 315 Additionally, different forms of neglect and abuse have been associated with differential expres- sions of poor emotion regulation. For example, Pollak, Cicchetti, Hornung, and Reed (2000) reported that neglected children, who often suffer from an extremely limited emotional envi- ronment, had more difficulty in identifying and distinguishing between emotions, compared to physically abused or non-âm•‰ altreated children. Furthermore, a history of neglect has been found to relate more strongly to a bias toward sad facial expressions; whereas, physical abuse has been linked to a response bias to angry stimuli and a greater hostile attribution bias in ambiguous social situations (Pollak et al., 2000, 2005; Pollak & Sinha, 2002; Shackman, Shackman, & Pollak, 2007). This suggests physically abused children feel an exaggerated need to defend themselves from perceived threats, which is reflected in their emotional processing (Dodge et  al., 1990; Rieder & Cicchetti, 1989). Pollak et al. (2005) suggested that in physically abusive home environments children learn to associate anger with threat of harm and therefore, become better prepared at identifying threats. In contrast, neglect is typically associated with an emotionally impoverished environment, with few opportunities for meaningful social interactions. If children are deprived of interactive emotional experiences with others, their capacity to tolerate intense emotional states may be underdeveloped, which can manifest in problems discriminating between emotions. When examining additional types of maltreatment, childhood sexual abuse has been associated with lower impulse control, whereas emotional abuse has been linked to impulsivity and problems with behaving in accordance with desired goals (Oshri, Sutton, Clay-W╉ arner, & Miller, 2015). In summary, emotion regulation deficits manifest in various ways, including difficulties in iden- tifying, understanding, expressing and regulating emotions, and can be dependent on the devel- opmental stage of the child and the type of abuse experienced. Propagation and maintenance of outcomes The maladaptive emotion regulation strategies caused by abuse and neglect may leave children vulnerable to other risks, and has been suggested as one reason why maltreated children are more likely to develop clinical symptomatology and behavioral problems, both during childhood and in adulthood. Impairment in emotion regulation is, therefore, both a negative consequence, and an important mechanism connecting the experience of childhood abuse with subsequent difficulties (Choi, Choi, Gim, Park, & Park, 2014). Psychopathology As noted above, child abuse and neglect have been associated with internalising disorders includ- ing anxiety, depression, and PTSD (Cannon, Bonomi, Anderson, Rivara, & Thompson, 2010; Gilbert, Widom, et  al., 2009; Kaufman, Plotsky, Nemeroff, & Charney, 2000; Springer et  al., 2007), along with greater externalising problems, such as aggressive behavior and psychopathy (Bernstein & Watson, 1997; Kolla et al., 2013; Lang, Klinteberg, & Alm, 2002; Weiler & Widom, 1996). Evidence has also indicated that many such outcomes associated with childhood abuse are characterized by deficits in the processing and regulation of emotion (Burns, Jackson, & Harding, 2010; Etkin & Wager, 2007). Thus, child maltreatment may be linked with negative outcomes via ineffective emotion regulation strategies, which may lead to a domino effect of deficits, resulting in maladaptive functioning during childhood (Eberhart, Auerbach, Bigda-âP•‰ eyton, & Abela, 2011). Internalising problems, which can result from child abuse, have been linked with emotional processing and regulation deficits. For example, enhanced anxiety symptoms are associated with poorer emotional awareness and perception (Bradley, Mogg, White, Groom, & Bono, 1999; Eisenberg et al., 2001) and deficits in the regulation of emotions (Suveg, Morelen, Brewer, & Thomassin, 2010; Suveg & Zeman, 2004). In addition, PTSD has also been associated with a

613 316 Children of Abuse and Neglect lack of emotional clarity and acceptance, difficulty engaging in goal-​directed behavior when dis- tressed, and an attentional bias towards trauma related stimuli (Buckley, Blanchard, & Trammell Neill, 2000; Cloitre, Miranda, Stovall-M​ cClough, & Han, 2005; Tull, Barrett, McMillan, & Roemer, 2007). Similarly, depression is also characterized by deficits in regulating emotions (Joormann, Siemer, & Gotlib, 2007), perceiving emotion in others (Stuhrmann, Suslow, & Dannlowski, 2011), the inability to support oneself when experiencing negative emotions (Berking et al., 2011) and to modify negative emotions (Ehring, Fischer, Schnülle, Bösterling, & Tuschen-C​ affier, 2008; Kassel, Bornovalova, & Mehta, 2007). Finally, substance misuse is widely theorized as an effort to regulate or avoid negative emotions (Baker, Piper, McCarthy, Majeskie, & Fiore, 2004; Wupperman et al., 2012). For example, negative affect has been shown to predict increases in desire to drink and drinking levels in individuals treated for alcohol dependence (Birch et al., 2004; Falk, Yi, & Hilton, 2008; Gamble et al., 2010; Sinha et al., 2009) and deficits in emotion regulation skills have been shown to predict relapse during and after cognitive–​behavioral therapy for dependence (Berking et al., 2011). A number of studies have also reported emotional deficits in individuals with externalising symptoms (Blair, Peschardt, Budhani, Mitchell, & Pine, 2006; Eisenberg et al., 2001; Hill, Degnan, Calkins, & Keane, 2006), including deficits in empathy (Blair, 1995), experiencing emotion (Blair et al., 2006; Frick, Lilienfeld, Ellis, Loney, & Silverthorn, 1999), and identifying emotional expres- sions (Blair et  al., 2004; Iria & Barbosa, 2009; Pham & Philippot, 2010). For example, antiso- cial behavior has been linked with deficits in perceiving negative emotions in facial expressions and an inability to distinguish between emotions (Blair, Colledge, Murray, & Mitchell, 2001). Additionally, psychopathic traits reflect greater emotional desensitisation, and an inability to empathize or respond to the emotional needs of others (Weiler & Widom, 1996). The emotion regulation problems that characterize children of abuse and these disorders seem to be important for understanding linkages between maltreatment and maladjustment. The emotion-b​ ased deficits resulting from the abusive behavior of a caregiver and neurobiological changes related to abuse, may in turn influence the development and maintenance of maladap- tive psychological and behavioral outcomes (Dodge, 1991). This is supported by Kim-S​poon, Cicchetti, and Rogosch (2013) who showed that poor emotion regulation predicted a subsequent increase in internalising symptomatology. Early maltreatment was associated with high emotion lability at age seven, which contributed to poor emotion regulation at age eight, which in turn was predictive of increases in internalising symptomatology, from age eight to nine. In addition, numerous studies have established that the relationship between childhood abuse and various psychological symptoms is mediated by impairments in emotion regulation (Choi et al., 2014; Schwartz & Proctor, 2000; Shields & Cicchetti, 2001). For example, in women with a history of childhood abuse, emotion regulation difficulties mediated the relationship between abuse and current post-t​raumatic symptomology (PTS) (Burns et  al., 2010; Choi & Oh, 2014; Stevens et  al., 2013). Further to this, the relationship between specific dimensions of emotion regulation and PTS was investigated among undergraduates with a history of trauma exposure during childhood (Tull et  al., 2007). After controlling for negative affect, three dimensions of emotion regulation—​difficulties in impulse-​control, diminished access to effective emotion regu- lation strategies, and a lack of emotional clarity—​remained significant predictors of PTS symp- tom severity. These findings provide support for the notion that difficulties in emotion regulation could indirectly influence the maintenance of trauma symptoms. Specifically, abused or neglected children were more likely to experience difficulties in emotion regulation, which then served to exacerbate trauma symptoms. In turn, increased PTS resulted in increased physiological arousal, maintaining the cycle of dysregulation, as increased arousal is harder to regulate (Tull et al., 2007).

713 Adaptive outcomes of emotional regulation deficits 317 Interpersonal problems Emotion regulation also appears to be important for understanding linkages between abuse and neglect and subsequent problems forming relationships. Maltreated children are at greater risk of unpopularity among their peers (Anthonysamy & Zimmer-G╉ embeck, 2007; Bolger, Patterson, & Kupersmidt, 1998; Rogosch, Cicchetti, & Aber, 1995), and are more likely to be rejected by peers, not only on a single occasion, but also across multiple years from second through seventh grade (Bolger & Patterson, 2001). Evidence has indicated that children’s deficits in emotional under- standing mediated the link between earlier abuse and later interpersonal functioning and rejec- tion by peers (Briere & Rickards, 2007; Cloitre et al., 2005; Rogosch, Cicchetti, & Aber, 1995). Shipman et  al. (2005) found neglected children used avoidance strategies when responding to other’s emotion distress. Such strategies reflect an emphasis on self-r╉eliance when handling emotional distress, as opposed to seeking help and support. For example, when asked how they would respond to negative emotional displays in others, neglected children frequently indicated that they would ignore or remove themselves from the situation. In contrast, non-âm•‰ altreated children generally indicated that they would provide the other child with assistance or support. These avoidance strategies utilized by neglected children may hinder their ability to form and maintain positive interpersonal relationships and have profoundly negative consequences for self-╉ regulation, which could add to the continuation of their abuse in contexts outside the home. This is consistent with research, which demonstrates that emotional understanding is related to peer acceptance (Cassidy & Parke, 1991; Denham et al., 1990; Underwood, 1997). Children who have difficulty managing their negative emotions are more likely to become dis- ruptive, impulsive and reactively aggressive in social interactions, leading to lower acceptance and more rejection by peers (Maszk, Eisenberg, & Guthrie, 1999). Peer rejection can then place abused children at risk of subsequent adjustment problems, including internalising and externalising dis- orders (Kupersmidt & Coie, 1990; Ladd & Troop-G╉ ordon, 2003). Kim and Cicchetti (2010) found support for this mechanism. In this study early experiences of abuse and neglect were related to emotion dysregulation, which placed these children at a greater risk of peer rejection, which then contributed to internalising and externalising symptomology one year later, after controlling for initial symptomology. Kim and Cicchetti (2010) argued that in the absence of positive peer interactions and relationships, abused children may become more vulnerable to stress, which can manifest as internalising or externalising disorders. Maladaptive emotion regulation, therefore, may impede children’s abilities to establish positive peer relationships due to an underdevelop- ment of certain traits, such as perspective-ât•‰ aking and empathy, which are vital to the development of social competence. Adaptive outcomes of emotional regulation deficits Although these patterns of emotion regulation are typically viewed as maladaptive and may result in impaired functioning, in neglectful and abusive situations these strategies may serve cer- tain adaptive functions that enable children to protect themselves from further harm (Rogosch, Cicchetti, Shields, & Toth, 1995). For example, in a home environment in which the child’s emo- tional expressions elicit an aversive or punitive reaction from the caregiver, a child may suppress their future emotions in an attempt to avoid further harm and hostile reactions. Shipman et al. (2005) found that although neglected children did not understand emotion in a manner con- sistent with cultural norms, their understanding may be adaptive within the neglectful context. Therefore, in response to questions regarding self-a╉ wareness of emotional experience, neglected children tended to deny experiencing negative emotions (e.g., “I never feel mad at any one”). This

813 318 Children of Abuse and Neglect decreased self-a╉ wareness may help neglected children cope with a home environment which fails to support emotional expressiveness. Maltreated children’s hypervigilance to potential threats and overregulation of distress responses may also assist in reducing rates of abuse. For children who have experienced abuse, displays of anger in their environment are the strongest predictors of threat and therefore a selective attention to threat-r╉elated (i.e., angry) stimuli at the expense of attention to other emotional cues would be adaptive, as children are quickly able to detect signs of anger and remove themselves from a potentially dangerous situation (Pollak et al., 2005). Additionally, managing the intense emotions arising from physical abuse may also include cognitive strategies that enable the child to maintain a sense of control over their circumstances. However, although emotional withdrawal and hypervigilance during conflict can result in short-ât•‰erm relief for the abused child, it may also heighten the long-ât•‰ erm risk of future abuse both in the home and in other contexts. Thus, immediate goals may conflict with longer-t╉erm goals and the emotional strategies developed may be unsuccessful at accomplishing both, leaving the child vulnerable to further risks. In settings outside the home, these deviant strategies of emotion regulation may simultaneously create other problems, such as social difficulties and poor peer relations (Cicchetti & Schneider-âR•‰ osen, 1986). Ultimately, Thompson and Calkins (1996) suggest that although children may adapt by trying to cope with the emotional demands of abuse and neglect, there are likely to be no optimal approaches to emotion regulation available to them and efforts are likely to result in a problematic mixture of adaptive and maladaptive outcomes. In summary, emotion regulation strategies developed in the context of abusive homes may serve specific protective functions, while concurrently resulting in maladaptive outcomes, with evidence suggesting these emotional deficits play a role in the development and maintenance of psychopathology and interpersonal difficulties. In turn, such problems can make a child more vulnerable to future abuse and victimisation both in and outside the home. Implications for intervention The body of research on emotion regulation and child abuse and neglect has important implica- tions for the development and utilisation of intervention programs targeted at abusive caregiv- ers and their children. Difficulties with emotion regulation have become an important target of clinical interventions in maltreated children (Cloitre, Koenen, Cohen, & Han, 2002) and many approaches to individual psychotherapy with victims of abuse focus on improving emotion regu- lation skills (Leahy, Tirch, & Napolitano, 2011; Paivio & Laurent, 2001). These skills play a vital role in attaining successful social interactions and psychological adjustment and, therefore, may be a source of resiliency related to maltreatment and psychopathology (Chang, Schwartz, Dodge, & McBride-C╉ hang, 2003; Shields et al., 1994). If intervention programs can help abused children to develop such resiliency this may reduce the emotional, psychological and social problems asso- ciated with neglect and abuse. Several empirically supported group treatments emphasize building emotion regulation and interpersonal skills in the aftermath of abuse; these include Dialectical Behavior Therapy (Robins, Schmidt, & Linehan, 2004), Seeking Safety (Najavits, 2002), Trauma Adaptive Recovery Group Education and Therapy, (Ford & Russo, 2006), and Skills Training in Affect and Interpersonal Regulation (STAIR)/P╉ rolonged Exposure (Cloitre et al., 2002). STAIR is a cognitive–âb•‰ ehavioral treatment that targets the development of emotion management and interpersonal skills. Each session focuses on a different deficit understood within the context of the experience of child abuse:  1)  labelling and identifying emotions, 2)  managing emotions, 3)  distress tolerance, 4) acceptance of emotions and enhanced experiencing of positive emotions, 5) identification of

913 Conclusion 319 trauma based interpersonal schemas and their enactment in day-t╉o-d╉ ay life, 6) identification of conflict between trauma-âg•‰ enerated feelings and current interpersonal goals, 7) role plays related to issues of power and control, and 8)  role plays highlighting the presence and expression of emotion, related to developing flexibility in interpersonal situations involving power differentials. This program was found to be valuable for the emotional development of women with a history of child abuse, who showed significant reductions in negative mood regulation, anger expression and interpersonal skills deficits, when compared to those on the wait-âl•‰ist (Cloitre et al., 2002). However, an unmet need remains for the more extensive use of emotion regulation skills train- ing in the context of child abuse and neglect (Hernandez, Nesman, Mowery, Acevedo-âP•‰ olakovich, & Callejas, 2009). In particular, policies and programs that focus on parenting behaviors are likely to be beneficial. A large body of research suggests caregiver behavior can have a positive influ- ence on children’s emotional development. Morris et al. (2011) examined specific parenting prac- tices associated with children’s emotion management, assessing whether particular practices were linked to successful emotion management. Findings indicated that certain practices were more effective at improving children’s emotion regulation. Specifically, redirecting attention away from, and cognitively reframing emotions with the child, were the most effective strategies used by mothers to help children manage the expression of negative emotions, and were associated with less expressed anger and sadness. Further parenting practices which have been linked to improved emotion regulation skills include directing positive emotion and behaviors toward children, help- ing children to label and discuss emotions, soothing children’s reactions through appropriate physical contact and encouraging activities such as reading or drawing to reduce arousal (Calkins & Hill, 2007; Eisenberg et al., 2001). Such practices should therefore be utilized in interventions targeted at abusive caregivers. Furthermore, school-b╉ ased interventions that focus on promoting social emotional compe- tence among children have been shown to be effective in fostering emotion regulation develop- ment. For example, the Promoting Alternative Thinking Strategies (PATHS) curriculum has been successful in reducing internalising problems among primary school students by teaching them to identify, understand, and discuss their emotions (Greenberg, Kusche, Cook, & Quamma, 1995). In the PATHS program improvements were seen in the range of emotion related vocabulary, flu- ency in discussing emotional experiences, efficacy beliefs regarding the management of emotions, and the developmental understanding of emotions. Such training could potentially be applied to equip abused children with the emotional skills they fail to develop in abusive homes. Conclusion Through processes of caregiver socialisation and neurobiological changes, child abuse and neglect can lead to a range of emotional problems during childhood, which can endure into adulthood. These emotion regulation deficits are manifested throughout development in a variety of ways, including difficulties in identifying, understanding, expressing and regulating emotions and hypervigilance. Although the altered emotion regulation strategies developed by abused and neglected children do have certain adaptive qualities, which allows the child to avoid further emotional or physical harm by quickly removing themselves from conflict, evidence indicates that such strategies also lead to a range of maladaptive consequences. Via mechanisms of emotion reg- ulation, abuse can lead to internalising and externalising problems, and interpersonal problems, including peer rejection. The presence of such psychological, behavioral and social problems can result in the maintenance of abuse. The extensive range of evidence, which indicates how critical emotion regulation problems are in the relationship between child abuse and negative outcomes, has led to a range of interventions

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