Emotion regulation and psychopathology in children and adolescents ( PDFDrive )

48 84 Research Domain Criteria (RDoC) and Emotion Regulation Table 5.1  Left-​most column: bridge principles that can be derived from the three-s​ ystems view. Examples of emotion regulation and dysregulation in neighboring columns. “→” symbolizes “is” or “which means that”, “¬” symbolizes negation. Emotion Bridge Principle Emotion Regulation Examples Emotion Dysregulation Examples Physiology, behavior, or self-​ Regulated breathing, on-​ Maladaptive breathing, saccadic target gaze, clear speech, eye movement not supportive reported experience is (loosely) and reported confidence in of task performance, tremors coordinated → the context of a job interview in voice, and reported desire to reflects a lack of an avoidance leave the room in the context of a motivated action set; → motivation that is functionally a job interview reflects avoidance a motivated action set occurred → appropriate. motivation that is not functionally appropriate. an emotion occurred Stimulus propositions → Changing networked response Changing networked response neurally encoded propositions to be adaptive, propositions to be maladaptive, i.e., “an interview is not e.g., “an interview is something information¬→ something to run away from.” that will make my heart race and is emotion; something I will stammer and want to run away from.” Meaning propositions → neurally encoded information¬→ emotion; Response propositions → neurally encoded information → action → emotion a motivated action set can be The set of avoidance actions The set of avoidance actions can be changed → can be reduced to only heightened or feature an additional hand sweating, reducing response of sweating hands, emotion can be changed self-​reported feelings of increasing self-​reported feelings of anxiousness. anxiousness. (i.e. regulated) prompt actions rather than as action dispositions and observable actions. In Gross’s view, “emo- tion regulation requires the activation of a goal to up-​or down-r​egulate either the magnitude or duration of the emotional response” (Gross, Sheppes, & Urry, 2011, as cited in Gross, 2013, p. 359). Here, goal activation holds the logical status of an unobservable psychological construct that serves as the target of regulation, instead of observable psychophysiological action (or action preparation) that is to be changed through regulatory behavior typical of the Bradley-​Lang models. Gross’s view of emotion, which combines four major views of mentalized phenomena contributing to emo- tion (basic, appraisal, psychological constructionism, and social constructionism), emphasizes the commonalities among the four views, that 1) emotions elicit loosely coordinated changes in feel- ing states, physiology, and behavior (a problematic triad that mixes inferred and observed phe- nomena), 2) emotions unfold over time, and 3) emotions are context-d​ ependent (Gross, 2015a). Gross’s initial conceptualization, a major contribution to this area of research, was the delineation of emotion regulation as behavior classified along a time-​unfolding emotion-​generation process, dubbed the process model (Gross, 1998; Kalisch, Wiech, Herrmann, & Dolan, 2006; Webb, Miles, & Sheeran, 2012). The process model demarcates emotion generation as one that begins with a situation, followed by the attendance to a stimulus, then to a cognition, and ends in an emotional response that provides input and changes the situation (beginning the cycle over again). This model provided a way to classify differing emotion regulatory behaviors by the time at which they were

58 Diverse perspectives of emotion 85 elicited in the emotion-g​ eneration cycle. Specifically, emotions can be regulated by selecting one- self into or out of a situation, known as situation selection strategies (e.g., when one chooses to leave a noisy room while studying), changing the situation in some way, known as situation modi- fication strategies (e.g., telling others to “stop all the commotion”), shifting one’s attention away from an emotional stimulus, known as attentional allocation or attentional redeployment strate- gies (e.g., putting on headphones or distracting oneself), changing one’s interpretations towards an emotional stimulus to reduce the emotional impact, known as cognitive change or reappraisal strategies (e.g., interpreting the midnight noise of studying as an integral part of a memorable university experience), and changing one’s behaviors, known as response modulation (e.g., biting one’s lip to avoid expressing contempt at the noisemakers). Further, emotion-r​ egulatory behaviors can be directed at the self, known as intrinsic emotion regulation, or directed at others, known as extrinsic emotion regulation. In what are now classic studies, Gross demonstrated that regulatory strategies that occur early in such an emotion-g​ eneration process are more effective at downregulating indices of negative emotion than are response-​modulation strategies, a dichotomization he termed antecedent-​ focused versus response-​focused emotion regulation (Gross & Levenson, 1993). Critically, he also defined successful emotion regulation by relating the outcome to the individual’s goals. He pos- ited that regulation is successful if the resulting emotion meets the regulator’s goals, regardless of social norms or long-​term adaptive value (Gross, 1998; Gross & Thompson, 2007; Thompson & Calkins, 1996). Gross was able to demonstrate that instructed cognitive reappraisal, an unob- servable process, causes robust reductions in observable indicators of emotion (those featured in the three-​systems model) relative to conditions where participants were instructed to emote as normal or to use response-f​ocused expressive suppression (e.g., the resistance of expressing visible emotion on the face; Gross & Levenson, 1993). Controlled comparisons have shown that an instruction to change one’s interpretation reduces physiological responding and self-r​ eported negative affect and alters facial behavior toward an emotional stimulus. At the same time, it was found that expressive suppression had no effect on psychophysiological or self-r​eported indica- tors of negative emotional responding and some studies even showed prolongation of respond- ing. Researchers then concluded that these strategies were maladaptive because it was presumed that the individual’s goal was to reduce negative emotional responding. Following this reasoning, empirical links have been found indicating negative predictive effects on important indices of cognitive performance such as memory (Richards & Gross, 1999, 2000), social function (Butler et  al., 2003; Gross & John, 2003), mental health (Gross & Muñoz, 1995), and physical health (DeSteno, Gross, & Kubzansky, 2013). Later work sought to validate this understanding of emo- tion regulation neurobiologically, to demonstrate both its temporality and to identify the top-​ down sources of cortical control (Goldin, McRae, Ramel, & Gross, 2008; Ochsner & Gross, 2005; Thiruchselvam, Blechert, Sheppes, Rydstrom, & Gross, 2011). Findings generally indicate that regions such as prefrontal cortex, orbital frontal cortex, and cingulate are active in paradigms of negative emotion downregulation via instructed cognitive control and that cognitive reappraisal activates these areas earlier than do expressive suppression strategies. The process model view has since been extended by borrowing concepts from cybernetic control (Carver & Scheier, 1982; Wiener, 1961). This updated view, dubbed the extended process model (EPM; Gross, 2015a), achieved several things. Conceptually, it separated emotion generation from emotion regulation, it defined emotion and emotion regulation in terms of valuations, it posited and defined three explicit stages of the emotion regulation process (identification, selection, and implementation), and it proposed two ways in which emotions may be dysregulated at each step of the process (regulatory failure and misregulation). By using concepts from cybernetics, the processes of both emotion generation and emotion regulation could be defined strictly through a

68 86 Research Domain Criteria (RDoC) and Emotion Regulation goal-​instantiated information-​to-​action feedback loop. First, the information from the situational context of the world (W; World) is perceived in a sensory array (P; Perception). Next, a discrepancy calculation is made between the percept and the goal state. If this discrepancy is large enough that it crosses some threshold, this information will be evaluated in the form of a “good for me/​bad for me” proposition (V; Valuation). This valuation will generate allostatic emotional actions, both mental and physical, in an effort to reduce this discrepancy. Information is finally fed back to pro- cess the need for continued emotive action or the termination of emotive action (A; Action) if the goal state(s) is met. Taken together, these stages are called the World, Perception, Valuation, Action (WPVA) cycle (Gross, 2015a). The conceptual separation between emotion generation and emo- tion regulation here is one of first-​order (a control system on a passive percept) vs. second-​order cybernetics (a control system imposed on the control system that is emotion; Von Foerster, 2003). In other words, emotion generation involves a calculated valuation of percepts made relative to goal states, and these valuations can be generated in a multitude of ways. Indeed, various models of emotion explain the generation of valuations in different ways, for example as an “affect program” from the basic view, an appraisal, or as a result of a psychological or social construction. Emotion regulation, on the other hand, is a valuation of emotions themselves. In summary, emotion regula- tion begins with the process of evaluating a valuation (Gross, 2014). Emotion regulation involving an evaluation of a valuation is described not as one but as three sequential WPVA cycles (see Figure 5.1). Specifically, these are 1) the emotion identification cycle, 2) the emotion regulation strategy selection cycle, and finally 3) the emotion regulation strategy implementation cycle (Gross, 2014, 2015a, 2015b). These cycles and their components imply a host of ways emotion regulation can go wrong. Gross posits two classes of such dysregulation. The first class is emotion-r​ egulation failure, which refers to the lack of appropriate emotion regu- lation when it would serve one’s goals. The second class is emotion misregulation, the enacting of regulatory behavior that is counterproductive to one’s goals (Gross, 2015a, 2015b). We further observe that emotion-​regulation failure or emotion misregulation can occur at either perception or valuation stages in each cycle. For example, in the emotion identification cycle, perception fail- ure is a failure to detect a counterproductive emotional display (e.g., Michael impulsively screams in a fit of rage at a cashier while trying to return an item, leading him to be kicked out of the store without receiving a refund), whereas valuation failure is a failure to understand that one’s emo- tional display is counterproductive to one’s goals (e.g., Meghan decides to scream at a cashier, not understanding that this behavior will not make the cashier more likely to help her). Misregulation can be exemplified in the emotion identification cycle as well, where perception misregulation might involve thinking that one has or will have panic symptoms (ostensibly and ironically to W Emotion Generation A PV Emotion Regulation WP VA WP VA WP VA Identification Selection Implementation Figure 5.1  The extended process model of emotion generation and regulation Reproduced from James J. Gross, The Extended Process Model of Emotion Regulation: Elaborations, Applications, and Future Directions, Psychological Inquiry, 26 (1), pp. 130–​137, doi.org/1​ 0.1080/1​ 047840X.2015.989751, Copyright © 2015 Routledge, with permission.

78 The takeaway 87 avoid feeling panic) and valuation misregulation might involve a valuation that one’s heart rate represents anxious feelings (a “bad-âf•‰or-m╉ e” valuation) in a social evaluative situation, leading to greater attention to one’s heart rate, which serves to further increase one’s anxiety. As the example illustrates, the distinctions between perception and valuation, as well as regulation failure and misregulation, will likely have mechanistic and conceptual overlap, as each will implicate the other. Nonetheless, it is a useful nuance that fosters the construction of hypotheses regarding the specific mechanistic implementations of emotion regulation. Ochsner and Gross have worked to elaborate the neural implementations of emotion regulation from the EPM viewpoint (Ochsner & Gross, 2014). This research has demonstrated that regions including dorsal medial prefrontal cortex, rostral medial prefrontal cortex, ventral medial pre- frontal cortex, ventral striatum, amygdala, and insula provide neural implementation of various valuation systems. Regions such as dorsal anterior cingulate, dorsal posterior medial prefrontal cortex, dorsolateral prefrontal cortex, ventrolateral prefrontal cortex, and inferior parietal lobe implement various regulatory control systems (Ochsner & Gross, 2014). Acknowledging the mul- tifaceted nature of valuation itself, they propose that valuation can range from stimulus-g╉ enerated core valuations (e.g., amygdala-âi•‰mplemented threat or ventral striatum-âi•‰mplemented reward), context-d╉ erived valuations (e.g., ventral medial prefrontal cortex-i╉mplemented contextual under- standing) and conceptual valuation (e.g., dorso-âm•‰ edial prefrontal cortex-i╉mplemented concep- tual/âc•‰ ategorical understanding). The insula notably plays a role in all valuation processes in that it is posited to account for interoceptive awareness when calculating values in a way that resembles the James-âL•‰ ange view (Ochsner & Gross, 2014). Summarily, in the EPM view, emotions and emotion regulation are conceptually separate and maintain their logical status as unobserved hypothetical constructs. The valuation component of the EPM incorporates private data. Therefore, this viewpoint does not lend itself to the construc- tion of bridge principles between emotion or emotion regulation and empirical indices. Brain regions important for emotion regulation are conceptualized as either control areas or valua- tion areas. The valuation areas can themselves be sorted into regions central to core evaluation (important for emotion generation) or central to contextual evaluation (important for appraisal and meaning creation). Both psychological and neuroanatomical conceptualizations of emotion regulation based on the EPM imply a taxonomy of dysregulation and possible sources of dys- regulation in the brain (see section “Scientific Advancement of Emotion Regulation with RDoC-╉ Consistent Thinking” below). The takeaway The Bradley and Lang view, supported by a wealth of empirical data, allows for a bridging between the hypothetical construct of emotion (or specific, more granular concepts demonstrating clear relationships with emotion) and hallmark psychophysiological observables (e.g., hemodynamic and electromagnetic neuroimaging, skin conductance, heart rate). It also readily complements research in other areas of psychology such as motivation, attention, learning, and memory. While this view allows for private data such as subjective awareness, it does not describe a role for them, which some other theorists believe should be in a comprehensive theory of emotion and psycho- pathology. The Gross and Ochsner EPM offers an elaborated, multiple-âp•‰ rocess model that includes a taxonomy of emotion dysregulation, testable across multiple implementing neurobiological mechanisms, yet remains highly speculative. They do not equate emotion with its indicators, but they make many assumptions about private data that cannot yet be tested given limitations in the articulation of the model to date. The EPM appears to assume a parity between unobservables and observables (e.g., valuation causes mental and physical action) in a way that the Bradley and Lang

8 88 Research Domain Criteria (RDoC) and Emotion Regulation view does not. Arguably, the virtue of each of the two views is its weakness: Bradley and Lang are more circumspect, so data and construct map well over but cover more limited terrain, whereas Gross and Ochsner reach further conceptually and further from observable phenomena. The research domain criteria It is possible to study emotion without terms such as joy, fear, or sadness, or any other classifica- tion of discrete emotion. As reviewed by Tracy and Randles (2011), contemporary theories of dis- crete emotions vary in the criteria used to define emotion. This results in lists that can vary from four—âh•‰ appiness, sadness, fear, and anger (Ekman & Cordaro (2011); Izard (2011), happiness is labelled enjoyment by Levenson (2011), and PLAY by Panksepp and Watt (2011)), while sadness and anger are respectively labelled PANIC/âG•‰ RIEF and RAGE by Panksepp and Watt (2011)—t╉o as many as 11 emotions (along with the aforementioned ones, disgust (Ekman & Cordaro, 2011; Izard, 2011; Levenson, 2011), interest (Izard, 2011; Levenson, 2011) or SEEKING (Panksepp & Watt, 2011), contempt (Ekman & Cordaro, 2011; Izard, 2011), love (Levenson, 2011) or LUST (Panksepp & Watt, 2011), CARE (Panksepp & Watt, 2011), relief (Levenson, 2011), and surprise (Ekman & Cordaro, 2011)). Both the Bradley-L╉ ang view and the Gross-âO•‰ chsner EPM comple- ment discrete emotion classification. In the same way, the RDoC presents a complementary dimensional framework for diagnostic categorization (Hyman, 2010). Thus, as with the study of emotion, one need not invoke diagnostic labels of depression, anxiety, or schizophrenia (or any other label) to study psychopathology. The dimensional approach invites investigators from multiple disciplines to study the constructs that underlie mental health and mental illness with a different emphasis than that of the DSM tradition. The metaphorical workspace provided by the RDoC is represented visually as a matrix of rows and columns. The rows represent psychological constructs of interest organized in broad domains of neurobiological organization. (A few are arguably both psychological and biologi- cal; more on such a merger below.) These domains include: Negative Valence Systems, Positive Valence Systems, Cognitive Systems, Social Systems, and Arousal/R╉ egulatory Systems. Within each domain are more specific psychological constructs, selected because they are concepts with a relatively well-âd•‰ eveloped supporting neuroscience literature. A  current list of the constructs and sub-âc•‰ onstructs that have been agreed upon can be found on the RDoC website (http://w‰•â ww. nimh.nih.gov/•r≠esearch-p╉ riorities/r‰•â doc/╉constructs/•r‰â doc-âm•‰ atrix.shtml; (National Institutes of Mental Health, 2016). They represent specified functional dimensions of behavior that can be characterized across units of analysis. The columns represent these units: genes, molecules, cells, brain circuits, physiology, behavior, and self-r╉ eport. A final column includes the paradigms used to elicit the putative constructs of interest. This array of measurable psychological and biologi- cal phenomena is intended to eventually inform interventions (Kozak & Cuthbert, 2016; Miller, Rockstroh, Hamilton, & Yee, 2016; Yee, Javitt, & Miller, 2015). Table 5.2 displays the matrix domains and units, with example targets and citations of research that could reside in each cell. Of course, the vast, multidisciplinary breadth of this work precludes a complete presentation of the extant literature in such a matrix, even within cells, let alone rela- tionships between cells. The matrix is a research framework that represents the consensus of experts attending a series of NIMH workgroups, one for each domain. The goals of these workgroups were to form and clarify formal definitions of each construct within each domain. The matrix is incomplete and is meant to be a work in progress (Cuthbert, 2014). A common misunderstanding is that the matrix is the RDoC, when in fact it just an initial proposal, an exemplar (Miller et al., 2016). Further work is expected to refine the matrix. Researchers are encouraged to evaluate, modify, and further define

Table 5.2  The RDoC Matrix with relevant exemplar literature citations Domains Genes Molecules Cells Units o Circuits Negative Valence Systems e.g. 5-​HTT (Hariri & e.g. Serotonin e.g. GABAergic cells Holmes, 2006) (Krakowski, 2003) (Capogna, 2014) e.g. ante Constructs: cortex-​a e.g. Fear (Hartley & Phelps, (Hung, S 2010) 2012) Positive Valence Systems e.g. DRD2 (Peciña e.g. Dopamine e.g. dopaminergic e.g. nuc et al., 2013) (Salgado-P​ ineda, neurons (Chinta & accum Constructs: Delaveau, Blin, & Andersen, 2005) tegme e.g. Approach Motivation Nieoullon, 2005) (Der-A​ va (Wacker, Mueller, Pizzagalli, Marko Hennig, & Stemmler, 2013) e.g. COMT (Drabant e.g. Glutamate, e.g. Pyramidal e.g. dors Cognitive Systems et al., 2006) GABA (Stan et al., cells (Helmeke, prefront Ovtscharoff, Poeggel, amygdal Constructs: 2014) & Braun, 2001) et al., 20 e.g. Cognitive Control (Ochsner, Silvers, & Buhle, 2012) Systems for Social Processes Constructs: e.g. OXTR (Kim e.g. Oxytocin e.g. Fusiform gyrus e.g. fusif e.g. Social Communication et al., 2011) (Quirin, Kuhl, & neurons (Pizzagalli gyrus— Düsing, 2011) et al., 2002) (Laurent & Powers, 2007) (Faivre, C Lehéric 2012) Arousal and Regulatory Systems Constructs: e.g. Apoe4 e.g. Amyloid e.g. Pineal cells e.g. hyp e.g. Arousal (Cuthbert, (Delano-​Wood plaque deposition (Waider, Araragi, pituitary et al., 2008) (Sturm et al., Gutknecht, & Lesch, gland ax Schupp, Bradley, Birbaumer, 2013) 2011) Powers, & Lang, 2000)

98 of Analysis Physiology Behavior Self -​Report Paradigms s erior cingulate e.g. fear e.g. avoidance e.g. Behavioral e.g. Fear amygdala potentiated startle (Schmader & Lickel, Inhibition Schedule Conditioning Smith, & Taylor, (Lissek et al., 2008) 2006) (Carver & White, (Hermans, Craske, 1994) Mineka, & Lovibond, 2006) cleus e.g. postauricular e.g. approach e.g. Behavioral e.g. Appetitive mbens—​ventral reflex (Benning, (Schmader & Lickel, Activation Conditioning (Shabel Patrick, & Lang, 2006) Schedule (Carver & & Janak, 2009) entum 2004) White, 1994) akian & ou, 2012) solateral e.g. pupillometry e.g. distraction e.g. Emotion e.g. Reappraise/​ tal cortex-​ (Silk et al., 2009) behaviors Regulation Watch—​Negative vs. la (Goldin Questionnaire Neutral (Goldin et al., 008) (Thiruchselvam (Gross & John, 2008) et al., 2011) 2003) form e.g. eye contact e.g. emotion e.g. Affect e.g. Dyadic —a​ mygdala (Adams Jr & Kleck, recognition Valuation Inventory conversation tasks 2005) performance (Tsai, Knutson, & with one member of Charron, Roux, (Szanto et al., 2012) Fung, 2006) the dyad instructed cy, & Kouider, to regulate (Richards, Butler, & Gross, 2003) pothalamic-​ e.g. cortisol (Lam, e.g. sleep (Mauss, e.g. Self-​ e.g. Actigraphy y-​adrenal Dickerson, Zoccola, Troy, & LeBourgeois, Assessment (Baum et al., 2014) xis (Laurent & & Zaldivar, 2009) 2013) Manikin Arousal Scale (Bradley & 2007) Lang, 1994)

09 90 Research Domain Criteria (RDoC) and Emotion Regulation constructs, as well as consider new constructs as warranted. Indeed, NIMH leadership advocates development of “hybrid” psychological-​biological constructs (Kozak & Cuthbert, 2016). Perceived gaps or paucities in certain cells could represent potential avenues of valuable research (Cuthbert & Insel, 2013; National Institutes of Mental Health, 2014). The RDoC matrix represents three efforts toward validity. The first is to provide descriptive validity by answering questions about how largely psychological constructs are implemented bio- logically (mechanistic). This is represented in the columns of genes, molecules, cells, and brain circuitry and will involve research in genetics, endocrinology, immunology, neuroscience, etc. The second is to increase our ability to validly explain neurobiological functions through a pre- liminary consensus on the questions pertaining to why a biological system works the way it does or for what reason a neurobiological structure is as it is. This consensus is represented by the rows of domains and constructs, which will involve the efforts of psychology working in tandem with neuroscience and other disciplines. The third effort addresses predictive validity by providing sci- entific evidence that may answer what might happen should changes in a certain unit of analysis occur. In the clinical care of mental illness, such answers may be most important for quality of life, indexed most prominently in the columns of physiology, overt behavior, and self-r​ eport. This research will involve a cross-​fertilization of research from the fields of psychology, epidemiology, and sociology. As it pertains to emotion, emotion regulation, and emotion dysregulation, the RDoC matrix comfortably accommodates the concepts presented by Bradley and Lang. Arousal exists as a con- struct within the Arousal and Regulatory Systems domain, and motivational valence is repre- sented in two domains (Negative Valence System and Positive Valence Systems). Related concepts of attention and perception reside in the Cognitive Systems domain. The three systems of prepa- ratory psychophysiology, overt behaviors related to approach and avoidance, and self-r​eport are represented in the physiology, behavior, and self-r​eport columns respectively. The matrix also accommodates the concepts of Gross’s process model: • Situation selection and modification belongs in Positive Valence System Domain > Approach Motivation > Action Selection/​Preferential Decision Making. • Attentional deployment belongs in Cognitive Systems > Attention and Perception. • Cognitive appraisal/r​ eappraisal belongs in Cognitive Systems > Perception, Language, and Cognitive Control. • Response modulation/​suppression belongs in Cognitive Systems > Cognitive Control > Response Selection; Inhibition/​Suppression. It is abundantly clear that even these concepts can be, and perhaps need to be, unpacked. Cognitive reappraisal, for example, involves perception, language, and cognitive control (see McRae, Ciesielski, & Gross, 2012, for such an analysis of cognitive reappraisal). One of the characteristics that differentiates the RDoC from the DSM is that the RDoC constructs are selected to be firmly grounded in research on neuroscience phenomena (e.g., Infantolino, Crocker, Heller, Yee, & Miller, in press). To date, hemodynamic neuroimaging studies focused on emotion-​regulation strategies such as those developed by Gross (1998) have primarily focused on fear conditioning (e.g., Milad, Rosenbaum, & Simon, 2014; Phelps, Delgado, Nearing, & LeDoux, 2004) and cognitive reappraisal (Banks, Eddy, Angstadt, Nathan, & Phan, 2007; Ochsner & Gross, 2008; Ochsner et al., 2012), although some work has examined emotional suppression (Goldin et  al., 2008). Fear conditioning paradigms commonly include phases of fear habituation, fear acquisition, fear extinction, and fear extinction recall. These components of fear learning involve both unique and shared neural circuitry. Subdivisions and subnuclei of the amygdala, as well as the dorsal anterior cingulate, are considered central to fear acquisition (Milad et al., 2014). The

19 The takeaway 91 basolateral complex of the amygdala, hippocampus, and infralimbic region of the medial prefron- tal cortex are thought to interact during fear extinction (Milad & Quirk, 2012). In terms of cogni- tive reappraisal paradigms, a meta-a​ nalysis of 48 hemodynamic neuroimaging studies revealed involvement of cognitive control regions, including dorsomedial prefrontal cortex, dorsolateral prefrontal cortex, ventrolateral prefontal cortex, and posterior parietal lobe, as well as bilateral amygdala (Buhle et al., 2014). Interestingly, this meta-a​ nalysis did not find evidence of differential ventromedial prefrontal cortex activation during cognitive reappraisal, a region that had been thought to be important for this process in previous studies (e.g. Diekhof, Geier, Falkai, & Gruber, 2011). Functional connectivity analyses using EEG, MEG, fMRI, PET, and optical imaging meth- ods also provide valuable information regarding the relationships between brain regions during emotion-r​egulation paradigms. Functional connectivity is assessed by examining the coactiva- tion of neural regions; regions are said to be functionally connected if their activity increases or decreases in tandem. These analyses have demonstrated significant positive correlations of ven- tromedial prefrontal cortex and hippocampus with amygdala during fear extinction recall (Milad et al., 2007), and dorsolateral, dorsal medial, anterior cingulate, and orbital cortices correlate with amygdala during cognitive reappraisal (Banks et al., 2007). For an investigation to be aligned with the RDoC framework, it should assess specific psychopathology-​related constructs (whether basic or clinical), preferably across multiple units of analysis. For an investigation to make progress pertinent to the RDoC aim of constructing and clarifying conceptual granulanda, the “anchor” unit of interest might be brain circuitry (Insel et al., 2010; Insel & Cuthbert, 2015). This focus on brain circuits, rather than brain regions in iso- lation, reflects an important shift in neuroscience toward viewing the brain more often as a highly interconnected and dynamic organ. The matrix is not yet structured to foreground the effects of the environment (e.g., parenting, culture), development (e.g., stages, such as infancy, childhood, adolescence, adulthood, and old age, relevant biological processes, such as puberty and senescence), and learning history. These could be conceived as dimensions orthogonal to the matrix, thus related to all of its cells, and often must be taken into consideration when making a determination about what is healthy versus abnormal (National Institutes of Mental Health, 2012). One could imagine a two-​dimensional matrix for each cultural context and for each stage of development, both powerful forces that shape one’s learning history. For example, developmentally, outward exuberance may not be dys- regulatory for children too young to understand contexts where such displays are inappropriate (e.g., a three-​year-o​ ld laughing at a solemn funeral). Culturally speaking, exuberance may not necessarily be a positively construed experience (Tsai et al., 2006) or even functional for the indi- vidual (Tsai, Sun, Wang, & Lau, 2016) if one’s culture imposes limits upon positive emotional dis- plays (Matsumoto, 1990). Therefore, one of the RDoC-​relevant goals will be to reliably and validly identify for whom, where, and at what stage to predict the development of emotion dysregulation difficulties across the lifespan to help guide intervention and prevention. Problematic functional configurations in the Negative Valence System might be labeled anxi- ety, whereas problematic configurations in the Positive Valence System domain might be labeled depression, and so on. The RDoC matrix itself presents no obstacle to this kind of categorical classification. Indeed, complementation would be preferred, as it would be unwise to disregard decades of DSM-​based clinical research. However, the bulk of the research used to support diag- nostic classification systems is limited to one unit of analysis: self (or clinician) report. As emo- tion scientists know well, self-r​eports are ultimately unsatisfactory due to their dependence on cultural norms and individual differences in disclosure (Bradley & Lang, 2006). Some would even consider them flawed hypotheses about one’s own functioning (Kozak & Miller, 1982; Miller & Kozak, 1993). By encouraging study and integration of multiple units of analysis, the RDoC

29 92 Research Domain Criteria (RDoC) and Emotion Regulation framework overcomes limitations inherent to sole reliance on self-âr•‰eport without dismissing them. Furthermore, even though the RDoC can complement existing nosology, it offers starting points for scientific advancement by highlighting heterogeneity within these existing categories (e.g., anhedonia within the broader category of depression). RDoC investigators can choose to advance the field in several ways. They may take an empiri- cally expansive approach, such as clarifying emotion concepts by taking into account more units of analysis from the RDoC framework. They may take a conceptually granular approach. This might involve subdividing existing constructs and subconstructs into components that more closely match the resolution of the anchoring unit of analysis, introducing new theoretical concepts, or investigating endophenotypes that result in smaller causal chains (more on this in “Scientific Advancement of Emotion Regulation with RDoC-C╉ onsistent Thinking” below). They can choose to advance the field by developing bridge principles, such as by ascertaining cutoffs or a profile of multiple units of analysis that is sensitive to dysfunction. They can develop robust laboratory paradigms that reliably elicit constructs of interest. Scientific progress is guided and sometimes constrained by the availability of experimental paradigms and stimuli, and these paradigms often need to be as natural as possible to reflect naturalistic and ecologically valid elicitation of emotion, and its regulation, and dysregulation. The RDoC matrix provides space for intellectual flexibility. Instead of appealing to unob- servable constructs derived from folk theories of psychology that are latent and hypotheti- cal in nature (Bentler, 1980)  (e.g., stress), we can examine observable principal components (Jolliffe, 2002) (e.g., HPA-âa•‰ xis release of corticotropin releasing hormone) from multiple units of analysis. These principal components may even serve as a bridge to laymen’s folk concepts. To be sure, the RDoC is not yet that bridge, and RDoC users must avoid the unhelpful concept reification that came to characterize traditional classification systems. Metaphorically speak- ing, the clarification of constructs in each row reinforces the constitution of the bridge toward a well mapped understanding of psychological function and biological function. Developing rows representing more fine-g╉ rained constructs will tell us where to take the next step. Both clarification and development will be primary tasks for the discipline of psychology at large, with input from investigators in the areas of emotion generation, regulation, and dysregulation, broadly conceived. Scientific advancement with RDoC-consistent thinking Empirical advancement: Genetic, molecular, and cellular units of analyses Since its introduction in 2008, the RDoC has spurred a great deal of research on emotion regula- tion along multiple units of analysis. There has been substantial growth in the literature contain- ing the words “emotion,” “emotion regulation,” and “emotion dysregulation” in combination with keywords at each unit of analysis. RDoQ displays a cross-ât•‰ abulated index and visual literature map (see Table 5.3 and Figures 5.2a, 5.2b, 5.2c) of PubMed articles of combined search terms, which, although crude, can provide some preliminary insight in future areas of growth in the study of emotion regulation (RDoQ, 2016; http://‰â•datamining.cs.ucla.edu/r•â‰ doq/‰â•). Given the relative citation numbers, it is clear that connections between genes, molecules, cells, and emotion warrant far more study. Studying genes as they relate to emotion dysregulation using the RDoC approach may be particularly fruitful. For example, the serotonin transporter gene (5HTTLPR) has been identified as a candidate gene for populations diagnosed with DSM-I╉V Major Depressive Disorder, but this has not been replicated in genome-âw•‰ ide association studies,

39 Table 5.3  Cross-​tabulation of new publications containing the keywords “Emotion,” “Emotion Regulation,” and “Emotion Dysregulation” with important keywords pertaining to each unit of analysis for the years 1976, 1995, 2000, 2008, 2010, and 2015. 1976 Genes Molecules Cells Circuits Physiology Behaviors Self-R​ eports Paradigms Emotion Genes 5 26 45 142 6 Emotion Genes 14 7 4 Regulation Genes Molecules Cells Circuits Physiology Behaviors Self-​Reports Paradigms Emotion Dysregulation Genes 2 33 45 106 1619 98 1995 Genes 4 8 13 49 4 733 Emotion 215 1 41 Emotion 15 Molecules Cells Circuits Physiology Behaviors Self-R​ eports Paradigms Regulation 3 102 46 117 2380 186 Emotion Dysregulation 12 8 15 83 8 2000 3 1 82 Emotion Molecules Cells Circuits Physiology Behaviors Self-R​ eports Paradigms 75 5 490 60 153 4861 564 Emotion 16 81 8 19 265 44 Regulation 15 2 29 4 Emotion Dysregulation Molecules Cells Circuits Physiology Behaviors Self-​Reports Paradigms 115 5 660 78 187 5853 706 2008 28 112 9 21 354 65 Emotion 24 1 3 46 9 Emotion Molecules Cells Circuits Physiology Behaviors Self-​Reports Paradigms Regulation 240 440 1326 1212 59 252 2808 19848 10124 141 Emotion 80 Dysregulation 408 2413 911 2010 2 7 52 66 375 175 21 Emotion Emotion Regulation Emotion Dysregulation 2015 Emotion Emotion Regulation Emotion Dysregulation Data from RDoQ search retrieved February 25, 2016 (http://d​ atamining.cs.ucla.edu/r​ doq/)​ .

(a) 14000 7000 \"Emotion\" 0 1979 1982 1985 1988 1991 1994 1976 30 300 300 150 + ”Genes” 150 + ”Cells” 15 1994 0 2012 0 1994 2012 1976 + ”Molecules” 1976 1994 30 300 300 150 150 + ”Circuits” 15 0 2012 0 1994 2012 1976 1976

49 Since RDoC 1997 2000 2003 2006 2009 2012 2015 00 300 50 + ”Psychophysiology” 150 + ”Self-Report” 1994 0 1994 2012 0 2012 1976 + ”Behavior” 1976 + ”Paradigms” 2012 1994 00 300 50 150 0 1994 2012 0 1976 1976

(b) 2000 1000 \"Emotion Regulation\" 0 1979 1982 1985 1988 1991 1994 1976 2 2000 2000 1000 + ”Genes” 1000 + ”Cells” 1 1994 1994 0 2012 0 2012 1976 1976 2 2000 2000 1000 + ”Molecules” 1000 + ”Circuits” 1 1994 2012 0 1994 2012 0 1976 1976 Figure 5.2  (Continued)

59 Since RDoC 1997 2000 2003 2006 2009 2012 2015 2000 2000 1000 + ”Physiology” 1000 + ”Self-Report” 1994 1994 0 2012 0 2012 1976 1976 + ”Paradigms” 2012 1994 2000 2000 1000 + ”Behavior” 1000 0 1994 1976 2012 0 1976

(c) 300 150 \"Emotion Dysregulation\" 0 1979 1982 1985 1988 1991 1994 19 1976 300 300 300 150 + ”Genes” 150 + ”Cells” 150 1994 1994 0 2012 0 2012 0 1976 1976 19 300 300 300 150 + ”Molecules” 150 + ”Circuits” 150 0 1994 2012 0 1994 2012 0 1976 1976 19 Figure 5.2 New publications per year containing the keywords (a) “Emotion,” (b with words pertaining to each unit of analysis, curated by the NIH-f​ unded UCLA R the RDoC initiative was implemented. Note that year-b​ y-y​ ear numbers and figures © Michael Sun, 2016.

69 Since RDoC 997 2000 2003 2006 2009 2012 2015 300 + ”Psychophysiology” 150 + ”Self-Report” 1994 1994 976 2012 0 2012 1976 300 + ”Behavior” 150 + ”Paradigms” 976 1994 2012 0 1994 2012 1976 b) “Emotion Regulation,” and (c) “Emotion Dysregulation” in combination RDoQ Tool as a predefined term set. Shaded area represents the years that s do not represent cumulative publications.

79 Scientific advancement with RDoC-consistent thinking 97 likely in part due to the heterogeneity inherent in this diagnosis (Bosker et  al., 2011). Results of candidate-g​ ene research and genome-w​ ide association studies may converge should the field move toward defining emotion regulatory phenotypes from the RDoC perspective. For example, research that selects individuals based on their scores on measures of positive valence may reveal new genetic relationships as they relate to specifically defined constructs of dysregulation, such as failure in reward learning. Future study of molecular and cellular units of analysis in the context of the RDoC, not only diagnostic categories, will also surely build upon existing research. The role of dopamine receptors in reward processing is one example of existing research that fits within the RDoC framework because this process is not unique to a specific diagnostic category (e.g., Peciña et al., 2013; Pizzagalli et al., 2008; Vrieze et al., 2013). The RDoC is well positioned to foster and benefit from research on potential endophenotypes, which bridge gene and disease expression (such as major depression). Research on endophenotypes pursues narrower relationships and shorter, intermediate causal chains (Miller & Rockstroh, 2013; Miller et al., 2016) and can readily accommodate specific roles for emotion dysregulation in mental illness. Endophenotypes can be used to parse the genetics of emotion dysregulation into smaller, more tractable components. It is presumed that such components would have simpler genetic architectures than a disorder itself (Goldstein & Klein, 2014). In investigations that seek to clarify psychopathology, the emphasis on microbiological or behavioral units of analysis need not and should not distract from considerations of clinical practice and understanding. A vision for the future of clinical research must be complemented with an understanding of present needs in the field. We recommend that researchers embark- ing on RDoC-​congruent investigations of emotion dysregulation consider questions of applica- tion, whether that be in patient conceptualization or clinical decision making. Clinical science has traditionally focused on impaired function and subjective distress (Antony et al., 1994), and replacing this with a reductionistic focus on a “gene/m​ olecule/​cell/​circuit for psychopathology” impoverishes rather than enriches the phenomenological understanding of psychiatric disorders (Miller, 2010). Research on hybrid psychology-b​ iology concepts with diverse degrees of granular- ity may improve assessment in such a way that prediction of dysfunction and disease course could be made earlier. Furthermore, empirical understanding at multiple levels can provide better cut points and more finely tuned bridge principles that can help delineate function from dysfunction, including healthy regulation from dysregulation. Holistic assessment of an individual can result in precision clinical care on a personal level (Insel & Cuthbert, 2015). Finally, new treatments may be developed through a combined use of pharmacology, behavior, and mediating technological devices (Craske, Meuret, Ritz, Treanor, & Dour, in press; Cuthbert, 2014). How has RDoC-​inspired thinking already advanced clinical understanding and clinical prac- tice? One example comes from the study of fear-​based disorders. From an observational stand- point both in the laboratory and in clinical practice (the same standpoint that brought us the DSM), it was surmised that repeated exposure to conditional fear stimuli reduced fearful respond- ing (Foa & Kozak, 1986). The extinction learning laboratory paradigm and its clinical analogue, exposure therapy, were birthed from this observation, and the latter is regularly employed for individuals with anxiety disorders (in which excessive fear responding is a central dysregulated mechanism). It was believed that reduced fearful responding evidenced the erasure of fearful associations between conditional and unconditional stimuli, and efforts were made to ensure that a reduction in fear responding was observed in-s​ession (van Minnen & Hagenaars, 2002). However, efforts to understand emotional learning and memory across multiple disciplines led investigators to conclude that the reduced response was actually due to the formation of new, non-t​hreat-​associated memories of the conditional stimulus, contrary to the widely held view of exposure therapy. These new inhibitory memories need to be consolidated over time (typically

89 98 Research Domain Criteria (RDoC) and Emotion Regulation over 24 hours). Evidence of short-t╉erm reduction in fearful responding (e.g., habituation) during exposure therapy sessions is no longer viewed as essential to clinical progress. Indeed, it has been found that short-ât•‰erm extinction does not predict long-t╉erm extinction learning (e.g., Brown, LeBeau, Chat, & Craske, in press; Peters, Dieppa-âP•‰ erea, Melendez, & Quirk, 2010). These findings have prompted a revised Emotional Processing Theory (Rauch & Foa, 2006). This new theory has the effect of clarifying how fear regulation occurs in nature (inhibitory learning as opposed to habituation), as well as increasing therapeutic efficiency by saving a great deal of clinician and cli- ent effort. Although these advances predate the RDoC proper, it is this type of empirical advance- ment that the RDoC seeks to systematically reproduce more broadly for emotion regulation. Conceptual advancement: Hybrid matrices Researchers coming from other perspectives of emotion, emotion regulation, or emotion dys- regulation may find the transition to the RDoC approach challenging. Indeed, as illustrated in Table 5.4, concepts from the EPM perspective may be difficult to place cleanly within the RDoC matrix. It should be acknowledged that functional conceptualization can be evaluated on dimen- sions according to the degree of heuristic value (likely a subjective evaluation), as well as its dis- tance from a reliably observable unit of analysis (an objective one). These concerns are addressed by the EPM through the invocation of a single valuation unit: The WPVA cycle, which scales flex- ibly and accommodates real-l╉ife biological information-âp•‰ rocessing such as DNA (e.g., Santini, Bath, Turberfield, & Tyrrell, 2012)  or neural systems implementing memory (e.g. Hampson, Hedberg, & Deadwyler, 2000). They are also apparent in the RDoC’s matrix organization and inclusion of granular subconstructs within constructs. Table 5.5 is an example of designing an RDoC-t╉ype matrix to accommodate a Gross-âO•‰ chsner perspective on emotion generation, regulation and dysregulation. With such a strategy, more granular concepts than those already included in the RDoC matrix can eventually be imported when sufficient evidence accumulates. The example hybrid-âm•‰ atrix provided would, like the RDoC, be an imperfect framework subject to revision. For example, the construct of extrinsic regulation may very well be subsumed under intrinsic regulation, as the motivation to extrinsically regulate could arise as a way of regulating one’s intrinsic emotions (e.g., a mother shushing her baby as it cries in public, serving to regulate the mother’s own anxiety and embarrassment, as well as the child’s). For the sake of organizational and visual clarity, intrinsic and extrinsic regulation are presented separately. Many of the subcon- structs, such as those involving valuation, may be mediated by the same mechanism. Indeed, most of these constructs have yet to be well-âd•‰ efined neurally. The hybrid framework serves as an illus- tration for how evolving conceptualizations that are independent of the RDoC may give rise to alternative concepts, spurring more research to validate or reject these notions. Having multiple imperfect frameworks may be valuable to pit strong hypotheses against each other. Core dysregu- latory constructs, such as invoked depressogenic schemas in major depressive disorder targeted by Cognitive Behavioral Therapy, might be more analogous to the construct of [cognitive] genera- tive action (Beck, 1976). The hypergeneration followed by a slow return to baseline in borderline personality disorder conceptualized using Dialectical Behavioral Therapy (Linehan, 1993) may be more analogous to generative action (for the hypergeneration) and intrinsic emotion regulatory stopping action (for the slow return to baseline). The experiential avoidance explanation respon- sible for psychopathology transdiagnostically in Acceptance and Commitment Therapy (Hayes, Strosahl, & Wilson, 1999) may be more analogous to the action of misregulated emotion identi- fication. These associations appear to have better associability than what may be offered from the

Table 5.4  A rough mapping between Gross-O​ chsner emotion regulatory concepts and Domains Acute Threat Potential Harm Responses Sustained Threat Negative Valence Responses Responses Systems Emotion generation to Emotion generation to acute threat potential threat Emotion regulatory Positive Valence maintenance, stop, an Systems Approach Initial responsiveness to switch to sustained th Motivation reward attainment Sustained/L​ onger-​te Trait emotion Emotion generation to reward responsiveness to generation toward acquisition reward attainment rewards Emotion regulatory maintenance, stop, sw to sustained reward Cognitive Systems Attention Perception Declarative Memory Internal perception in all Stored representations Systems for Social External sensory-​ WPVA cycles, appraisal and influence perception Processes array level perception reappraisal in all WPVA Perception and cycles, attentional Social Communication Understanding of th redeployment Self Social emotion genera Affiliation and Extrinsic emotion Attachment regulation Sleep and Wakefuln Arousal and Social emotion Social emotion generation, Regulatory generation, Extrinsic Extrinsic emotion regulation emotion regulation Systems Circadian Rhythms Arousal Magnitude of action in all WPVA cycles Note: Default Mode Network was a considered construct within the Arousal and Regulatory Systems but putatively serves an important role in the goal engagement required for emotion regulation, which is no

9 d the RDoC constructs. Loss Emotion generation to loss Constructs Frustrative Non-​Reward Habit nd Emotion generation to hreat frustration, Non-r​ eward Valuation erm Reward Learning witch Reward-​Valuation Emotion generation and Working Memory y regulation traits, effortfulness and s that Language automaticity of emotion Holding Appraisal and Reappraisal generation and emotion regulation representations he of perception and Perception and Cognitive Control referent for valuation Understanding of Others processing Emotion Regulation Selection, Situation Selection, Situation Modification, Reappraisal, Suppression ation, Social emotion generation, Extrinsic emotion regulation ness Consider: Default Mode Network Goal engagement necessary for emotion regulation t was determined to not yet be ready for inclusion due to a lack of sufficient evidence. Nonetheless, it ot adequately captured by other constructs.

Table 5.5  An example of a hybrid EPM-​RDoC view of emotion regulation to exemplify R Rows—D​ omain: Emotion Constructs Sub-C​ onstructs Generation Initial Initial Valuation Generative Action—​ Init Perception Cognition and Behavior Ext Per Regulation Intrinsic Regulation em Identification Perception of Valuation of own Intrinsic Action –​ Kno own emotive emotive states Cognition and of u states Behavior to Identify Sel own emotion Mo Att Selection Intrinsic Intrinsic Valuation of Selective Action on Co Implementation Perception Situation Selection, the emotive self and of Situation Situation Modification, Mo Selection, Attentional Allocation, Situation Cognitive Reappraisal, Modification, and Response Attentional Modulation Allocation, Cognitive Contextual valuation Implemented Co Reappraisal, of emotion regulatory regulatory action on of i and Response appropriateness the self in context sele Modulation Contextual knowhow of implementing a selected strategy

01 RDoC-​type thinking. tial Perception Initial Valuation Generative Columns—​ Action—​Cognition Units of Analysis trinsic Regulation and Behavior rception of other’s Genes motive states Valuation of other’s Extrinsic Action –​ emotive states Cognition and Molecules owhow (Perception) Behavior to Identify using Situation Valuation of other’s emotion Circuits lection, Situation using Situation odification, Selection, Situation Selective Action on Cells tentional Allocation, Modification, the emotive other ognitive Reappraisal, Attentional Allocation, d Response Cognitive Reappraisal, odulation on others and Response Modulation on others ontextual knowhow Contextual valuation Implemented Physiology implementing a of implementation regulatory action ected strategy on others in context

Maintenance Perceiving one’s Valuation of Action to Maintain Per Stopping online intrinsic maintaining one’s emotion self-​ ext Switching regulation as online intrinsic regulatory behavior one one to maintain regulation Action to Stop Per Perceiving one’s Valuation of stopping emotion self-​ ext online intrinsic one’s online intrinsic regulatory behavior one regulation as regulation one to stop Valuation of switching Action to Switch to Per Perceiving one’s one’s online intrinsic another emotion self-​ ext online intrinsic regulation regulatory behavior one regulation as one to switch

10 rceiving one’s online Valuation of Action to Maintain Behavior trinsic regulation as maintaining one’s extrinsic regulation Self-​Report e to maintain extrinsic regulation Paradigms rceiving one’s online Valuation of stopping Action to Stop the trinsic regulation as one’s extrinsic extrinsic regulation e to stop regulation rceiving one’s online Valuation of switching Action to Switch trinsic regulation as one’s extrinsic to another extrinsic e to switch regulation regulatory behavior

201 102 Research Domain Criteria (RDoC) and Emotion Regulation current RDoC framework. Time will tell which functionalism serves as a better explanation across units of analysis and in their associations with one another. It might be argued that emotion regulation, given its centrality in psychopathology, deserves its own domain in the RDoC matrix. Indeed, this discussion did occur in the Cognitive Systems domain workgroup (National Institute of Mental Health, 2011). As it is viewed currently, research relevant to emotion regulation is scattered across the matrix. Research on maladaptively up-╉ regulated fear and anxiety falls primarily within the Negative Valence Systems domain, whereas the lack of generated reward valuation in anhedonia and adaptive habit formation involves the Positive Valence System domain. Top-âd•‰ own regulatory strategies involve the Cognitive Systems domain, and their adaptive and maladaptive use in social contexts involves the Social Systems domain. Finally goal engagement, a critical referent in emotion regulation, involves the Arousal and Regulatory Systems domain. This distribution across the matrix of constructs related to emotion regulation may fuel more confusion than seems necessary. It should be noted that, as improvements in conceptual clarity accrue, we are likely to see a blurring of boundaries between traditional psychological concepts such as cognition and emotion (Miller, 2010). One may wish to adopt a hybrid conceptualization for this reason. Whether one decides to adopt the current RDoC matrix or a hybrid matrix yet to be drafted, it should be noted that “the usefulness of any approach will ultimately rest upon the degree to which it promotes an empirical understanding of the emotions and their role in behavior” (Panksepp, 1982, p. 421). Summary and conclusion The primary aim of this chapter was to explicate the RDoC framework and its development, and to describe its relevance to the study of emotions and their regulation and dysregulation. The tension between classical nosology and the development of the RDoC parallels historic disputes between views of discrete and dimensional emotions. Both the Bradley-âL•‰ ang view and the Gross-âO•‰ chsner EPM view are dimensional accounts of emotion that complement discrete emotion views. The RDoC matrix accommodates each of these theories while complementing the clinically useful categorical views of psychological disorders represented in the DSM. The tension between the RDoC and traditional classification systems mimics the tension in emotion science between discrete and dimensional theory. Just as most emotion researchers uti- lize both discrete and dimensional conceptualizations (Ekman, 2016) clinical research can and indeed must move forward with discrete and dimensional conceptualizations of psychopathology. As emotion researchers have long known, many of these dimensions lie in units of analysis out- side of the traditional tools in psychology. Instead of rejecting this reality, a wiser policy will be to embrace it for the sake of advancing the understanding of emotion regulation and increasing the precision of clinical care. The RDoC is a promising platform for all of these aims. Acknowledgements We would like to thank Richard LeBeau, Anna S. Lau and members of the Anxiety and Depression Research Center (ADRC) as well as the Culture Attention Emotion Science and Research (CAESAR) lab for their helpful comments during the preparation of this chapter. Michael Sun gratefully acknowledges the generous financial support of the Graduate Research Mentorship award (with Michelle Craske) from the UCLA Graduate Division as well as a training fellowship with the National Institute of Mental Health (NIMH) of the National Institutes of Health (NIH) under award number T32-M╉ H015750.

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Part II Emotion Regulation and Child and Adolescent Psychopathology

21

31 Chapter 6 Emotion Regulation and Attention Deficit Hyperactivity Disorder Blossom Fernandes, Roseann Tan-âM•‰ ansukhani, & Cecilia A. Essau Diagnostic criteria Attention Deficit Hyperactivity Disorder (ADHD) is considered one of the most pervasive disor- ders of childhood (Castellanos & Tannock, 2002). ADHD frequently persists into adolescence and adulthood and is consistently associated with a range of negative outcomes. The term ADHD was first coined as part of the restructure and enhancement of the Diagnostic and Statistical Manual of Mental Disorders (DSM) by the American Psychiatric Association (American Psychiatric Association, 1980); prior to this, children with ADHD were diagnosed with brain dysfunction or brain damage with hyperkinesia (Barkley, 1990). The diagnostic criteria for ADHD has undergone several changes, but most notably, the DSM-╉ IV (American Psychiatric Association, 2000)  has classified behavioural symptoms comprising three major subtypes:  Inattention (I), hyperactivity-âi•‰mpulsivity (HI), and Combined. Children presenting with the inattentive subtype have difficulty with tasks that require sustained mental effort, are more disorganized and are easily distracted and forgetful when compared to peers of a similar age (Sergeant, Oosterlaan, & van der Meere, 1999). Children with the HI subtype were characterized as more fidgety, restless and “squirmy” when compared to typically developing chil- dren. The combined subtype is the most commonly diagnosed sub-ât•‰ype and involves six or more symptoms of each of the inattention and hyperactivity subtypes (APA, 2000). Research has shown children with ADHD, as compared to other children, also have difficulty inhibiting on-âg•‰oing behavior (Oosterlaan, Logan, & Sergeant, 1998) and difficulty inhibiting immediate gratification (Douglas & Parry, 1983). As with attention problems, these difficulties lead to serious problems in home and school functioning. The fifth revision of the DSM (DSM-â5•‰ ; American Psychiatric Association, 2013) characterized ADHD as a neurodevelopmental disorder consisting of a pattern of inattention and/o╉ r hyperac- tivity-i╉mpulsivity that affects every day functioning. It further specifies the severity of ADHD as mild (involving minor impairments with few, if any, symptoms in excess of the six required for diagnosis), moderate (impairment between mild and severe), and severe (marked impairment and with several symptoms in excess of those necessary for a diagnosis). The DSM-5╉ suggests that these symptoms should have persisted for at least six months, directly impacting social and aca- demic/o╉ ccupational activities and be present before the age of 12 years. Additionally, the DSM-5╉ allows for diagnosis in adolescents and adults, including types of behaviour and examples of how the disorder could manifest itself in different age groups. The symptoms are expected to persist for at least five months in individual above the age of 17, unlike six months for children and adoles- cents; moreover, those aged 17 and older need to exhibit only five of the requisite symptoms, not the six required for younger children.

41 114 Emotion Regulation and Attention Deficit Hyperactivity Disorder Prevalence There is growing consensus that ADHD occurs in approximately 5% of school-âa•‰ ged children, a prevalence rate that is seen across cultures (Esser, Schmidt, & Woerner, 1990; Polanczyk et al. 2007; Polanczyk et al. 2014). However, ADHD prevalence rates diverge widely as a result of age, definition of disorder and assessment method. Distinctions based on definitions (e.g., clinical classifications of ADHD versus scores on a behavior checklist) and more rigorous assessment cri- teria lead to fewer cases of ADHD. For example, a review of 86 studies using the DSM-I╉ V criteria (American Psychiatric Association, 1994) indicated the prevalence of ADHD ranged from 5.9% to 7.1% (Willcutt, 2012). ADHD diagnosis also seems to be influenced by parental practices and beliefs. As reported by Asherson and colleagues (2012), in Asian countries such as Hong Kong and Taiwan parental monitoring of child behavior is considered essential in reducing disruptive behaviors and poor habits, thereby influencing diagnosis and access to treatment. Variations in the prevalence rates of ADHD in different countries has raised a question to whether ADHD is a universal syndrome affecting children worldwide regardless of race and society (Bauermeister et al., 2010; Goetz et al., 2010; Polanczyk et al., 2007) or a cultural construct generally based on a Western conceptualization (Asherson et al., 2012; Faraone et al., 2003; Jacobsen, 2002; Timimi & Taylor, 2003). Gender differences ADHD is observed more often in boys than girls, with a male to female ratio approximating three to one (Skounti, Philalithis, & Galanakis, 2007). Relatedly, girls have been found to have lower levels of inattention, hyperactivity, and oppositional/âd•‰ efiant behaviour compared to boys. Research shows that boys under the age of 13 years tend to be overt and display severe disruptive behaviours in the classroom; whereas, girls appear to exhibit more cognitive and academic prob- lems (Gaub & Carlson, 1997). In addition, females are less likely to be identified in samples due to the manifestation of the disorder, as they are less likely to exhibit disruptive behaviors compared to ADHD males, and are more likely to go unnoticed if they present inattentive behaviours (Gaub & Carlson, 1997). Importantly, a large number of referral for ADHD males who exhibit disruptive behaviours occur in school settings; therefore, females who similarly display disruptive behaviors, may be ignored (Gaub & Carlson, 1997; Gershon & Gershon, 2002). Psychosocial impairment As mentioned previously, children with ADHD often suffer from academic and social impair- ments. Academic deficits, school-r╉elated problems, and peer neglect tend to be most associated with elevated symptoms of inattention; whereas, peer rejection and, to a lesser extent, accidental injury are frequently linked with symptoms of hyperactivity or impulsivity (Willcutt et al., 2012). Compounding the stress for a person with ADHD, family relationships are consistently strained and lead to discord and negative interactions. In addition, attentional problems frequently have a significant impact on rates of mother–c╉ hild rejection; however for fathers, rejection seems to sig- nificantly impact their children’s attention problems (Lifford, Harold, & Thapar, 2008). Moreover, peer relationships are affected by peer rejection, neglect, or teasing of the individual with ADHD. In its severe presentation, ADHD is markedly impairing, due to its deleterious impact on social, familial, and scholastic/o╉ ccupational functioning (Hinshaw & Melnick, 1995; Hoza et al., 2005). Individuals with ADHD have significant difficulty regulating their initial thoughts, behav- iors, and emotions during a given task, thereby impacting their ability to successfully manage tasks and achieve their desired outcomes (Barkley, 2006). A main feature of ADHD is difficulty

51 Comorbidity 115 with behavioral inhibition and self-r╉egulation, with several models supporting this (Cleary & Zimmerman, 2004). One such model primarily conceptualizes ADHD as an issue of behavioral inhibition, which in turn, leads to a flawed concept of time awareness culminating in ineffective time management (Barkley, 2006). This model closely links ADHD and its constructs to executive function—âa•‰ system that underlies the capacity for self-o╉ rganisation and goal-âd•‰ irected actions; thus, impairments in executive functioning result in behavioral disinhibition. Barkley claims that the foundation for the key symptoms of ADHD (i.e., impulsivity, inattention, and hyperactivity) is the result of the initial inability to diminish pre-p╉ otent responses to a given situation. Behavioral inhibition allows individuals to halt an on-âg•‰ oing response or response pattern; thus, creating a delay and permitting self-âd•‰ irected action (Barkley, 2006). These self-âd•‰ irected actions are outlined by core executive function processes, such as planning and working memory (Elliott, 2003); this delay in time and executive functioning during normative functioning is what leads to effectual and appropriate actions in addition to appropriate expression of emotions in relation to a task. In contrast, for individuals with ADHD, difficulties inhibiting behavior and creating this delay indicates they are often unable to prevent immediate responses to situations, such as answering or talking out of turn, moderating emotional responses, controlling movements, or maintaining attention and focusing on tasks with little immediate reward or positive consequence (Travell & Visser, 2006). Emotional impairments in children and adolescents with ADHD involve poor self-âr•‰egulation of emotion, excessive emotional expression, problems with anger and aggression, and greater problems coping with frustration and empathy. Studies show that children with emotional and behavioral difficulties are impulsively emotional and lack the ability to regulate their behavioral responses to emotionally provoking events when compared to children without emotional and behavioral difficulties (Cross, 2011). Comorbidity ADHD is highly comorbid with externalising disorders such as conduct disorder and opposi- tional defiant disorder (ODD) (with comorbidity rates ranging from 43% to 93%) and internalis- ing disorders (with comorbidity rates ranging from 13% to 51%) including anxiety and depression (Jarrett & Ollendick, 2008). Moreover, children with ADHD are highly likely to develop ODD, which involves difficulties with expressions of anger, hostility, frustration, and aggression toward others, especially towards authority figures such as parents, alongside problems such as dis- obedience. Boys with ADHD and comorbid ODD or conduct disorder in particular, have been found to suffer from the impaired regulation of negative emotions (Melnick & Hinshaw, 2000). Concordantly, approximately 45% of children with ADHD may also develop conduct disorder. Furthermore within a subset of those with ADHD and conduct disorder the likelihood of child- hood psychopathy such as callousness, lack of emotion and low empathy for others is increased (Waschbusch, 2002). Importantly, callous unemotional traits have been found to be prevalent in ADHD even after controlling for conduct disorder (Musser et al., 2013). Marsh et al. (2013) compared ten to 17 year olds with and without psychopathic traits on the subjective experiences of emotion during five recent emotionally evocative life events. Their findings revealed that fewer children with psycho- pathic traits reported the subjective experience of fear relative to other emotions. These results suggest that comorbid psychopathy impairs fear learning, physiological responses to threats, and the recognition of fear in others, as these children have difficulties expressing and displaying pro-╉ social emotions and behaviors, which is characterized by lower levels of empathy, a lack of a sense of guilt or remorse, shallow or blunted affect, in conjunction with physiological under arousal

61 116 Emotion Regulation and Attention Deficit Hyperactivity Disorder (Kimonis et al., 2008). These callous unemotional traits are therefore, important when consider- ing emotional arousal and regulation in ADHD. As but one example, Musser et al. (2013) tested ADHD children with age appropriate levels of pro-âs•‰ocial behaviors and those with low levels of pro-âs•‰ ocial behaviors on affect based tasks measuring emotional suppression and arousal. The results from this study showed that children with ADHD and low pro-s╉ ocial behaviours displayed a reduced level of arousal and elevated emotion dysregulation, which highlights the significance of physiological responses in ADHD and emotion regulation. ADHD also has a negative effect on the emotional wellbeing of the affected child or adolescent, including those at risk for major depression (Edbom et al., 2006). Research additionally shows that 75% of children diagnosed with ADHD are likely to have mood disorders and are therefore, at an increased risk of developing depression (Biederman et al. 2008). Furthermore youths with ADHD show greater levels of depressive symptoms, compared to those without ADHD (Lee et al., 2008). A recent study by Seymour et al. (2014) found that emotion regulation mediated symptoms of depression in ADHD youth, such that young people with ADHD and comorbid depression exhibited poor emotion regulation strategies. Seymour et al. argue that this could be as a result of executive function deficits, in particular working memory. Specifically, those with impairments in working memory and inhibition experience and express heightened emotions in response to emotionally laden stimuli when compared to individuals with intact working memory; as work- ing memory affects the ability to effectively appraise emotional stimuli and supress negative and positive emotions. Executive dysfunctions Executive functions are a set of inter-âr•‰elated cognitive processes that allow for effective prob- lem solving, and facilitate goal directed activities; these processes are comprized of inhibition, working memory, attention shifting, planning, initiating tasks, detecting and correcting errors (Willcutt, Doyle, Nigg, Faraone, & Pennington, 2005). Researchers indicate that self-r╉egulatory processes underlie cognitive, behavioral and emotional regulation (Berger, Kofman, Livneh, & Henik, 2007; Posner & Rothbart, 1998). This suggests that executive functions are involved in the self-âr•‰ egulation of emotions in goal directed situations (Zelazo & Cunningham, 2007). Emotion regulation has been found to be consistently linked to inhibitory processes; for exam- ple, a study of typically developing preschool children’s performance on an emotion regulation task (i.e., responses to a disappointing gift) significantly correlated with responses on tasks inves- tigating inhibitory processes (i.e., Simon Says) and suppression or slowing of responses (e.g., not pulling a lever or drawing a line very slowly) (Carlson & Wang, 2007). Moreover, a study measur- ing the performance of young adults during a Stroop task revealed that this measure of inhibitory functions and conflict monitoring was linked with the ability to successfully manage negative responses to unfamiliar and visually unappetizing food (Kieras, Tobin, Graziano, & Rothbart, 2005). Additionally, when asked to divide their attention by remembering an eight-d╉ igit number during a task to challenge executive function processing capacity, individuals were increasingly found to have difficulties modulating their negative responses. This is supported by Walcott and Landau’s (2004) findings, in that emotion regulation was strongly associated with the speed of the inhibition process using tasks such as the Stop Signal Reaction Time Task (SSRT). Hoeksma, Oosterlan, and Schipper (2004) found that in children aged between ten and 13 anger variability over a number of days was strongly associated with outcomes on SSRT, which measures the time needed to stop an inappropriate response. This is a further indication of behav- ioral inhibition, as studies show that deficits in SSRT also reflect impairments in attentional and cognitive processes (Alderson, Rapport, & Kofler, 2007). Rich et al. (2008) showed that children

71 Executive dysfunctions 117 with severe mood disorder had problems with attentional orienting and initial attentional pro- cessing; moreover, approximately 80% of their participants had comorbid ADHD. This suggests that the underlying processes involved in ADHD are also related to attentional processes and emotion regulation, supporting the view that executive function task difficulties are closely linked to ADHD and emotion regulation (Skirrow, McLoughlin, Kuntsi, & Asherson, 2009). As outlined earlier, children with ADHD consistently display deficits in most areas of executive functions (Barkley, 2006). Research suggests that behavioral disinhibition is an important charac- teristic of ADHD; Nigg (2001) suggests there are two distinct forms of impairments in inhibition that can be applied to ADHD. Firstly, motivational inhibition automatically ceases an on-g​ oing response that is usually caused by fear or anxiety as a result of a novel event. Secondly, execu- tive inhibition involves processing of the deliberate suppression of a response for goal-d​ irected purposes. As proposed by Barkley’s (1997) behavioral disinhibition theory, children with ADHD do not effectively respond to social circumstances, but rather display rules detached from the emotional context of the situation. These children therefore, appear more dysregulated as they fail to consider social cues and rules, thereby appearing more socially dysregulated. According to this theory, the successful regulation of emotions would therefore, depend on successful behavioral inhibition. This is supported by a study investigating behavioral disinhibition and its associations to emotion regulation using a frustration-​inducing task (Walcott & Landau, 2004). In this study, boys with and without ADHD were explicitly given instruction to hide their emotional display in the presence of a peer. Results determined that boys with ADHD failed to succeed on this task, whereas, non-​symptomatic boys were more effective at regulating their emotional displays in response to contextual demands. Importantly, disinhibition scores were higher for boys with ADHD than those without ADHD (Walcott & Landau, 2004). The findings discussed above are generally supported by imaging data investigating executive processes and ADHD, whereby the frontal regions of the brain are associated with inhibitory con- trol and emotional processing (Posner et al., 2011). Thus, children with ADHD are shown to have increased activation in prefrontal regions, relative to healthy controls on an emotional process- ing task; these findings were specific to emotional processing even after controlling for cognitive processes. Essentially, this indicates that normal function in the prefrontal regions are impaired in ADHD, however, they may also mediate or facilitate affective responses i.e., negatively valenced words such as “kill” drew increased attention than neutral words such as “month;” similarly posi- tive words could induce self-r​ eflection to a greater extent than neutral words (Posner et al., 2011). In relation to emotion regulation, Shaw et  al. (2014) proposed a top-d​ own regulatory pro- cess and bottom-u​ p mechanistic theory to explain the processes affecting emotion regulation in ADHD. According to a bottom-​up psychological mechanism, the attention systems identify emo- tionally significant stimuli and exert control—​an aspect that is thought to be impaired in ADHD. In contrast, in healthy individuals, affectively salient stimuli receive appropriate sensory coding and early detection, whilst this effect is significantly reduced in ADHD as a result of heightened emotions (i.e., the over perception of negative stimuli). Concordantly, the accurate identification of emotions in human faces is associated with well-r​ egulated behavior; thus, misperception could be caused as a result of emotion dysregulation. Furthermore, aversion to delayed rewards is an indication of impulsivity; this is mediated in the limbic regions of the brain, which are also respon- sible for emotion processing; thus, it is probable that these brain regions may also be involved in emotion regulation (Musser et al., 2013; Shaw et al., 2014). In relation to top-​down regulatory processes, the importance of the autonomic nervous system is paramount, as it recognizes emotional valence and task demands, particularly when the stimuli are negative rather than positive. This is difficult for those with ADHD because they lack physi- ological indicators of regulation. Thus, the inability to focus on a goal or allocate appropriate levels

81 118 Emotion Regulation and Attention Deficit Hyperactivity Disorder of attention to a task means that individuals with ADHD have difficulties managing emotions or focusing on emotional stimuli. For example, when completing an emotional Stroop task, the per- formance of adolescents with ADHD is severely impaired when compared to healthy counterparts (Posner et al., 2011). Neural mechanisms ADHD is a neurodegenerative disorder with most models highlighting deficits in the frontal lobe networks. In particular the prefrontal cortex (PFC) region has been consistently found to mediate cognitive control processes, including decision-m╉ aking and emotion regulation, in particular the orbitofrontal cortex, dorsomedial prefrontal cortex, anterior cingulate gyrus, dorsolateral pre- frontal cortex and ventrolateral prefrontal cortex (Phillips, Ladouceur & Drevets, 2008). Shaw et al. (2014) claim that for individuals with ADHD, the prefrontal regions, including the ventro- lateral, orbitofrontal and medial prefrontal cortices are impaired. Plessen and colleagues (2009) suggest that deficits in the connections between the amygdala and orbitofrontal cortex may lead to behavioral disinhibition. The orbitofrontal cortex is strongly connected with the amygdala, thala- mus and multiple cortical regions, thus, it is an important region involved in emotion regulation processes. In addition, the amygdala plays a crucial role as it is involved in processing emotion and emotional behavior. The majority of studies have shown amygdala hyperactivation in ADHD, during both the subliminal perception of fearful expressions and while subjects rated their fear of neutral faces (Malisza et al., 2011). These findings are similar to behavioral measures of delay aversion, dur- ing which amygdala hyperactivation was observed for the processing of delayed rewards (Plichta et al., 2009). The anticipation (and receipt) of rewards causes reduced ventral striatum responsive- ness in ADHD, thus contributing to aversion delay. This is supported by dysfunction in a neural network composed of the amygdala, ventral striatum, and orbitofrontal cortex, which mediates emotional stimuli, and is implicated in emotion regulation. Therefore, Shaw et  al. (2014) have argued that emotion dysregulation in ADHD implicates dysfunction in the amygdala, ventral striatum and orbitofrontal cortex. Relatedly, lesion studies have shown that the orbitofrontal region, in particular, is important for the generation of emotional states and emotion regulation (Ochsner & Gross, 2004). Thus, neural theory predicts (Shaw et al., 2014) deficits in these regions are strongly associated with symptoms of both ADHD and emotion dysregulation. Emotion dysregulation One of the earlier models for emotional dysregulation (ED) (Cicchetti, Ackerman, & Izard, 1995) posited that regulating emotion requires certain control mechanisms involving structure or a strategy that will allow for co-o╉ rdination and actions. Cicchetti and colleagues (1995) out- lined four of these aspects: Firstly, control concerns the cause of felt emotion, involving cogni- tive and affective mechanisms. Secondly, control structures mediate the output of this emotional system, whereby earlier mechanisms of cognitive and affective processes are reflected in expres- sion. Thirdly, control structures coordinate expression and inhibit responses based on context. Finally, this control structure deviates for those with externalising and internalising problems, as these individuals tend to suffer from weak or absent control structures. As such, individuals with ADHD are thought to have problems moderating or suppressing the emotional reactions they experience, leading to impulsive and severe emotional reactions toward events when compared to non-A╉ DHD individuals of a similar age. Emotion dysregulation therefore, results from a lack of knowledge concerning affective behavior or difficulty in modulating emotional responses to social situations or environmental demands (Saarni, 1999).

91 Development 119 Impairments in emotional control are closely associated with hyperactive and impulsive symp- toms, and likely arise from the poor inhibitory capacity involved in ADHD (Barkley, Murphy, & Fisher, 2008). Observational studies show that children with ADHD display heightened emo- tional reaction and frustrations compared to their non-A╉ DHD peers; this is further supported by parent reports of increased levels of sadness, anger and guilt. Importantly, these youth have dif- ficulty self-âr•‰ egulating these negative emotions (Berlin, Bohlin, Nyberg, & Janols, 2004; Braaten & Rosen, 2000; Melnick & Hinshaw, 2000). Moreover, as irritability is an aspect of reactive aggres- sion and emotional outbursts, it is considered one of the main outcomes of emotion dysregula- tion in ADHD (Leibenluft, 2011). In fact, a study examining ADHD children with and without irritability found increased rates of ODD and depression/d╉ ysthymia in children with irritable mood and ADHD (Ambrosini, Bennet, & Elia, 2013). A recent meta-âa•‰nalysis by Shaw et  al. (2014) revealed a consistent increase in aggressive behavior in ADHD compared to non-âA•‰ DHD samples. Their results suggest a strong association between aggression and hyperactivity-âi•‰mpulsivity rather than between aggression and inatten- tion. Emotion dysregulation was further reflected in frustration inducing situations in ADHD. In addition, children with ADHD were more likely to express negative affect and have emotional outbursts when compared with non-A╉ DHD participants during challenging tasks. Based on their meta-a╉ nalysis Shaw et al. (2014) described three distinct features of ADHD and emotion dysregu- lation. The first feature suggests that at its core, emotion dysregulation is a main characteristic of ADHD and its symptoms of hyperactivity, impulsivity and inattention, are reflective of defi- cits in executive functions. The second feature considers ADHD and emotion dysregulation as a unique entity, formed as a result of distinct neurocognitive features and the clinical outcomes for those with the combination of ADHD and emotion dysregulation. The third feature refers to the fact that symptoms of ADHD and emotion dysregulation overlap and are underlined by dissociable neurocognitive deficits such as impairments in executive function, which impacts decision-m╉ aking and emotional control. This model is supported by correlations observed for deficits in emotional processes, for example in emotion recognition and frustration tolerance (Banaschewski et al., 2012); however it is important to note that not all those with ADHD display impaired levels of emotion dysregulation Results from longitudinal studies reveal that ADHD symptoms and emotion dysregulation difficulties emerge in early childhood and continue into adulthood (Biederman et al., 2012). Skirrow, McLoughlin, Kuntsi, and Asherson (2009) argue that these symptoms of emotional dysregulation significantly differ from mood instability, as mood instability is used to describe volatile, irritable and changeable mood with a hot temper and low frustration tolerance in the absence of underlying deficits. Emotion dysregulation however, is believed to be an active modification or alteration of on-âg•‰ oing emotional responses. These responses are associated to emotions linked with the environment and therefore, part of emotional patterns. Therefore, those with emotion dysregulation do not usually suffer from mood instability, as mood insta- bility arises from existing processes that lead to deviant emotional responses independent of regulatory processes. Development Research shows a strong association between ADHD and emotion dysregulation (Sjöwall, Roth, Lindqvist, & Thorell, 2012). Stringaris and Goodman’s (2009) study examining 5,326 youth found mood lability (i.e., poorly controlled shifts in emotion) in 38% of children with ADHD. Parent reports of the Child Behaviour Checklist revealed that adolescents with mood and aggres- sion problems also tended to suffer from attention difficulties and were more likely to suffer from

021 120 Emotion Regulation and Attention Deficit Hyperactivity Disorder emotion dysregulation among those likely to have ADHD (Althoff et al., 2006). Shaw et al. (2014) noted that clinic-b╉ ased studies in young people with ADHD conveyed similar levels of emotion dysregulation, ranging between 24% and 50%. Longitudinal research of children with ADHD spanning into adulthood has rarely consid- ered emotion dysregulation, but rather has focused on outcomes from the DSM-I╉ V disruptive and antisocial disorders (Klein et al., 2012). Stringaris, Maughan, and Goodman (2010) con- ducted a longitudinal study of 7,140 children and found that temperamental emotionality in three-ây•‰ ear-o╉ lds predicted co-âm•‰ orbid ADHD with internalising disorders by the age of seven. Another longitudinal study by Sanson, Smart, Prior, and Oberklaid (1993) showed that infants who developed hyperactive symptoms alone did not differ in their temperament from typical infants; whereas, children who developed ADHD and aggressive traits were prominently unco- operative and irritable from infancy. Therefore, a difficult temperament with significant nega- tive emotionality has been linked with later ADHD combined with emotion dysregulation. Nonetheless, environmental factors such as parental criticism and hostility were associated with the development of conduct problems in children with ADHD, and with the development of childhood ADHD in pre-s╉ choolers with behavioral problems. Shaw et al. (2014) claims that poor parental emotion regulation is reflected in high levels of hostility, thereby contributing to the development of emotional dysregulation in children with ADHD. Transition from adolescence to adulthood Transitions during the adolescent years has been associated with numerous issues affecting social interaction and emotional outcomes. Resultantly, low self esteem may manifest due to poor relationships with peers and the inability to effectively participate in social exchanges such as sharing, cooperating, and turn taking. These issues are adversely affected for those with ADHD as a result of delayed self-r╉ egulation (Barkley, 2006). These outcomes are further linked to impairments in self-âe•‰ steem and sociability (Hoy et al., 1978). Research shows that the symp- toms of ADHD are continuously changing during the adolescent years and into adulthood (Wolraich et al., 2006). In particular, hyperactivity becomes less prominent during this age, compared to inattention, which tends to remain persistent during adulthood (Barkley, 2006). Unlike hyperactivity, symptoms of inattention and executive function difficulties greatly affect academic achievement more so than symptoms of hyperactivity and impulsivity. Nonetheless, deficits in certain aspects of executive functioning (e.g., working memory) may prevent ado- lescents from reading, listening and comprehending and therefore, planning, which results in future rewards being less valued (Barkley, 2006). Furthermore, adolescents with ADHD are more likely to display poor delay of gratification and are less likely to persevere with set goals and have poor emotion regulation competencies as a result of deficits in anger and frustration control (Barkley, 2006). Emotional dysregulation is considered to be an important feature of adult ADHD with 34–7╉ 0% of adults in clinical samples of ADHD reporting impaired emotion regulation (Able, Johnston, Adler, & Swindle, 2007). Aggressive behaviors also continue to be persistent, as indicated in a study of 950 adults diagnosed with ADHD. As reported by Able et al. (2007), those with ADHD scored themselves higher in interpersonal conflict and reported negative, conflicted social ties. Somewhat similarly, a longitudinal study investigating the outcomes of ADHD children found higher rates of emotion dysregulation in adults with persistent ADHD when compared with adults with remitted ADHD. This suggests that as symptoms of ADHD improve, so too does emo- tion dysregulation (Shaw et al., 2014).

12 TREATMENT 121 Clinical implications Empirical findings demonstrate physiological and observable behaviors consistent with ED in children with ADHD (Musser et al., 2011; Musser, Galloway-âL•‰ ong, Frick, & Nigg, 2013; Seymour et al., 2012; Walcott & Landau, 2004). These include demoralization, learned helplessness, low self-e╉ steem, fear and anxiety, increased frustration and occupational challenges. Previous stud- ies have found ADHD boys to be socially inflexible, emotionally intense with poor attention and concentration levels (Sanson, Smart, Prior, & Oberklaid, 1993). Using an unsolvable puzzle task to elicit aggression, boys with ADHD who were considered highly aggressive were further found to be more emotionally reactive and less effective at emotion regulation than boys with low lev- els of aggression and without ADHD (Hinshaw & Melnick, 1995). This suggests that aggression rather than ADHD is responsible for this level of emotional response. Additional manifestations of emotion dysregulation involve over-âr•‰eactivity to positive and negative emotions (Martel & Nigg, 2006), lack of emotional control (Erhardt & Hinshaw, 1994; Saunders & Chambers, 1996); and impatience which most likely leads to peer perceptions of youth with ADHD as easily excited, disruptive, or intrusive in their social interactions (Landau & Moore, 1991). Children with inat- tentive presentations of ADHD show emotion dysregulation enhanced by emotional intensity and display heightened emotions (Wheeler, Maedgen & Carlson, 2000). Negative emotionality however is also a characteristic of ODD which includes loss of temper, as the child gets easily angry and resentful (Barkley et al., 2010). Negative emotionality is similar to emotional dysregulation, however it is a risk-f╉actor for ED (Belsky, Friedman, & Hsieh, 2001) and is considered a risk factor for developing ODD in children with ADHD (Martel & Nigg, 2006). Children and adolescents with ADHD are therefore more likely to experience impairments in social relationships, as they exhibit aggressive behaviors and consistent rule breaking unlike typi- cally developing peers (Buhrmester, Whalen, Henker, MacDonald, & Hinshaw, 1992). Treatment Treatments for ADHD involve a broad range of options including behavioral therapy, psycho- therapeutic approaches and pharmacotherapy; the aim of treatment is to treat the disorder as early and as effectively as possible. When considering non-âp•‰ harmacological treatments, studies show that parent and family education is important, along with effective parent training in behavioral management involving teachers to improve classroom behaviors. These treatments indicate that with appropriate behavior modification training and special education placement, outcomes for children with ADHD can be greatly improved (Thompson et al., 2004). In addition, treatment programs have shown that the management of adolescents with ADHD can be effective; these include parent and teacher training in behavioral management, particularly contingency man- agement methods applied in classrooms and similar settings, such as summer camp (Antshel & Barkley, 2008). However, Barkley (2006) argues that interventions for behavioral management in children with ADHD are most effective when inappropriate behaviors are targeted in the child’s natural environment, as it occurs. Subsequently, Barkley suggests it is important to assist the child/âi•‰ndividual in understanding suitable behavior which is contextually expected. Most psychosocial treatment programs involve a multimodal treatment plan part of which includes medication (Jensen et  al., 2001). The Multimodal Treatment Study of Children with ADHD investigated long term outcomes of interventions, including medication and behavior modification in combination and alone. The results showed that medication alone and medica- tion with behavior modification was superior to behavior modification alone or standard com- munity care (MTA Cooperative Group, 1999). Apart from decreasing levels of ADHD symptoms,

21 122 Emotion Regulation and Attention Deficit Hyperactivity Disorder these two intervention strategies improved aggressive behavior, social skills, academic achieve- ment, and parent-âc•‰ hild relationships. Stimulant medications such as methylphenidate have been found to be effective in improving academic outcomes and emotional wellbeing. In addition, a study evaluating the effectiveness of multimodal psychosocial treatment of children with ADHD being treated with methylphenidate reported a consistent pattern of improvement in academic achievement and emotional status, particularly self-e╉ steem and ratings of depression (Hechtman et al., 2004). Non-âs•‰ timulant medications, such as atomoxetine have also been found to reduce core ADHD symptoms, improve social interactions and quality of life in children and adolescents with ADHD (Cheng et al., 2007; Wilens et al., 2006). In relation to psychological intervention, Cognitive Behavioural Therapy (CBT) has been shown to benefit individuals with ADHD by helping them to understand and categorize the emo- tions they experience accurately. Importantly, CBT has been found to help with labeling emotions correctly and coping with intense negative reactions (Mongia & Hechtman, 2012). Moreover, these skills can be developed alongside mindfulness training (Mongia & Hechtman, 2012), which promotes present centered focused awareness of emotions (Farb et al., 2007). Additionally, inter- ventions aiming to treat avoidance behavior and mood disturbances in ADHD may also improve emotion regulation by enhancing motivation and providing individuals with strategies to cope with daily life (Mongia & Hechtman, 2012). Considering emotion dysregulation in ADHD treatment has been challenging, primarily this is due to the fact that studies have measured emotional changes as a secondary outcome (Shaw et al., 2014). However, one of the few studies measuring the attributes of stimulants on emotional expression found improvement in emotional dysregulation, parallel to improve- ments observed in hyperactivity and impulsivity (Mccracken et al., 2003). According to Manos et al.’s (2011) literature review, emotional lability and irritability reduced by 3% in ADHD as a result of medication alone. Stimulants have also been found to improve emotion recogni- tion, whilst concurrently improving performance (Conzelmann et al., 2011). These findings are supported by neural activities, as medicated adolescents have been found to have reduced activity in the prefrontal regions, similar to healthy controls, contrasted by increased reactiv- ity found in ADHD participants not taking medication. ADHD adolescents taking medica- tion were found to have better performance on emotional processing tasks when compared to ADHD adolescents without medication. Shaw et al. (2014) suggest that stimulant treatment of the core symptoms of ADHD also leads towards improvement in emotion dysregulation. Additionally, behaviour modification combined with medication is effective at reducing exter- nalising and internalising symptoms, which are linked with emotion dysregulation (Stringaris & Goodman, 2009). Conclusions ADHD is one of the most commonly occurring psychiatric disorders of childhood (Spencer, Biederman, & Mick, 2007). Moreover, it frequently persists into adolescence and adulthood and is associated with multiple functional impairments. Research has revealed that externalizing behav- ioral problems and social impairment are associated with emotion dysregulation in children with ADHD (Wheeler, Maedgen & Carlson, 2000; Melnick & Hinshaw, 2000; Parker, Majeski, & Collin, 2004). Emotion dysregulation is strongly linked to inhibitory deficit, which may manifest into socially inappropriate behavioral responses to extreme emotional expression and the inability to self-r╉egulate (Barkley, 2006). This then suggests the individual finds it difficult to self-s╉oothe during enhanced emotional experiences, focus on the task at hand, and to organize thoughts to achieve goal driven behavior (Lynn, Carroll, Houghton, & Cobham, 2013). The association

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