(Oxford Library of Psychology) Theodore P. Beauchaine, Sheila E. Crowell - The Oxford Handbook of Emotion Dysregulation-Oxford University Press (2020)
(Oxford Library of Psychology) Theodore P. Beauchaine, Sheila E. Crowell - The Oxford Handbook of Emotion Dysregulation-Oxford University Press (2020)
(Oxford Library of Psychology) Theodore P. Beauchaine, Sheila E. Crowell - The Oxford Handbook of Emotion Dysregulation-Oxford University Press (2020)
Area Editors:
Clinical Psychology
David H. Barlow
Cognitive Neuroscience
Kevin N. Ochsner and Stephen M. Kosslyn
Cognitive Psychology
Daniel Reisberg
Counseling Psychology
Elizabeth M. Altmaier and Jo-Ida C. Hansen
Developmental Psychology
Philip David Zelazo
Health Psychology
Howard S. Friedman
History of Psychology
David B. Baker
Neuropsychology
Kenneth M. Adams
Organizational Psychology
Steve W. J. Kozlowski
1
2020
1
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C O N T R I B U TO R S
Contributors ix
Table of Contents xiii
Chapters 1–486
Index 487
v
A B O U T T H E E D I TO R S
Sheila E. Crowell earned her PhD in child clinical psychology from the
University of Washington. She completed her clinical internship at Seattle
Children’s Hospital through the University of Washington Psychology Internship
Program. Dr. Crowell has expertise in emotion dysregulation across the lifespan,
including infants, children, adolescents, and adults. Her work on emotion dys-
regulation extends across a number of diverse clinical populations, such as depres-
sion, substance use disorders, trauma, personality disorders, and self-injury.
Dr. Crowell is also a licensed clinical psychologists with expertise in Dialectical
Behavior Therapy (DBT), an evidence-based treatment for diagnoses character-
ized by emotion dysregulation. Dr. Crowell has served on study sections for the
National Institutes of Health and as a reviewer or editorial board member for
several journals. She has received funding for her research from the National
Institutes of Mental Health and the American Foundation for Suicide Prevention.
A primary goal of Dr. Crowell’s research is to prevent suicide and the development
of psychopathology through enhanced identification of those at risk and early in-
tervention.
vii
Margaret A. Fields-Olivieri Hooria Jazaieri, PhD
Department of Psychology Kellogg School of Management
The Pennsylvania State University Northwestern University
Courtney N. Forbes, MEd Parisa R. Kaliush, BA
Department of Psychology Department of Psychology
The University of Toledo The University of Utah
Brett Froeliger, PhD Niranjan S. Karnik, MD, PhD
Department of Neuroscience Department of Psychiatry
Medical University of South Carolina Rush Medical College
Eric L. Garland, PhD, LCSW Erin A. Kaufman, BA
Center on Mindfulness and Integrative Health Department of Psychology
Intervention Development (C-MIIND) The University of Utah
The University of Utah Christiane Kehoe, PhD
Kim L. Gratz, PhD Department of Psychiatry
Department of Psychology The University of Melbourne
The University of Toledo Patricia K. Kerig, PhD
James J. Gross, PhD Department of Psychology
Department of Psychology The University of Utah
Stanford University Mona Khaled, MA
Hunter Hahn, MA Department of Psychology
Department of Psychology University of Southern California
The Ohio State University Joseph C. Leshin, BS
Nathaniel Haines, BA Department of Psychology & Neuroscience
The Center for Cognitive and The University of North Carolina
Brain Sciences at Chapel Hill
The Ohio State University Kristen A. Lindquist, PhD
Greg Hajcak, PhD Department of Psychology & Neuroscience
Department of Psychology The University of North Carolina at
Florida State University Chapel Hill
Lauren A. Haliczer, MA Christina Gamache Martin, PhD
Department of Psychological and Department of Psychology
Brain Sciences University of Oregon
University of Massachusetts Amherst Whitney I. Mattson, PhD
Sophie Havighurst, PhD Brain Development and Social
Department of Psychiatry Cognition Lab
The University of Melbourne Nationwide Children’s Hospital
Sage E. Hawn, BA Kateri McRae, PhD
Virginia Institute for Psychiatric and Department of Psychology
Behavioral Genetics University of Denver
Virginia Commonwealth University Michele A. Morningstar, PhD
Nora H. Hope, PhD, RPsych Brain Development and Social
Department of Psychology Cognition Lab
Simon Fraser University Nationwide Children’s Hospital
Sarah A. Horvath, MA Eric E. Nelson, PhD
Department of Psychology Center for Biobehavioral Health
Ohio University Nationwide Children’s Hospital
Camelia E. Hostinar, PhD Emily Neuhaus, PhD
Department of Psychology Department of Psychology
University of California, Davis University of Washington
x Contributors
Jacqueline O’Brien, MS Ross A. Thompson, PhD
Department of Psychology Department of Psychology
University of Oregon University of California, Davis
Cassie Overstreet, MA Matthew T. Tull, PhD
Department of Psychology Department of Psychology
Virginia Commonwealth University The University of Toledo
Ruchika Shaurya Prakash, PhD Andero Uusberg, PhD
Department of Psychology Department of Psychology
The Ohio State University University of Tartu
Sarah E. Racine, PhD Helen Uusberg, PhD
Department of Psychology Department of Psychology
McGill University University of Tartu
K. Ashana Ramsook, MA Robert D. Vlisides-Henry, BA
Department of Psychology Department of Psychology
The Pennsylvania State University The University of Utah
Lance M. Rappaport, PhD Gemma T. Wallace, BA
Virginia Institute for Psychiatric and Department of Psychiatry
Behavioral Genetics University of Utah School
Virginia Commonwealth University of Medicine
Julia R. Richmond, MA Sara F. Waters, PhD
Department of Psychology Department of Human Development
The University of Toledo Washington State University,
Darby Saxbe, PhD Vancouver
Department of Psychology Linnie E. Wheeless, JD
University of Southern California Department of Psychology
Heather T. Schatten, PhD The University of Toledo
Department of Psychiatry and Patrick Whitmoyer, MA
Human Behavior Department of Psychology
Brown University The Ohio State University
Tiffany M. Shader, MA Dominika A. Winiarski, PhD
Department of Psychology Department of Psychology
The Ohio State University Rush University
Brittany C. Speed, MA Maureen Zalewski, PhD
Department of Psychology Department of Psychology
Stony Brook University University of Oregon
Sarah A. Stoycos, MA Paree Zarolia, PhD
Department of Psychology Department of Psychology
University of Southern California The University of Denver
Contributors xi
TA B L E O F C O N T E N T S
xiii
16. Epigenetic Foundations of Emotion Dysregulation 221
Mindy Brown, Elisabeth Conradt, and Sheila E. Crowell
17. Emotion Dysregulation and Externalizing Spectrum Disorders 237
Tiffany M. Shader and Theodore P. Beauchaine
18. Emotion Dysregulation and Internalizing Spectrum Disorders 249
Camelia E. Hostinar and Dante Cicchetti
19. Emotion Dysregulation and Childhood Trauma 265
Patricia K. Kerig
20. Emotion Dysregulation in Autism Spectrum Disorder 283
Emily Neuhaus
21. Emotion Dysregulation and Psychosis Spectrum Disorders 299
Gemma T. Wallace and Anna R. Docherty
22. Emotion Dysregulation in Addiction 313
Eric L. Garland, Spencer Bell, Rachel M. Atchley, and Brett Froeliger
23. Emotion Dysregulation and Eating Disorders 327
Sarah E. Racine and Sarah A. Horvath
24. Emotion Dysregulation and Self-Inflicted Injury 345
Erin A. Kaufman and Sheila E. Crowell
25. Emotion Dysregulation and Borderline Personality Disorder 361
Katherine L. Dixon-Gordon, Lauren A. Haliczer, and Lindsey C. Conkey
26. Behavioral Assessment of Emotion Dysregulation 377
Molly Adrian and Michele Berk
27. Self-Report Assessment of Emotion Dysregulation 395
Kim L. Gratz, Courtney N. Forbes, Linnie E. Wheeless,
Julia R. Richmond, and Matthew T. Tull
28. Assessment of Emotion Dysregulation Using Ecological Momentary
Assessment 411
Heather T. Schatten, Kenneth J. D. Allen, and Michael F. Armey
29. Treating Emotion Dysregulation in Externalizing Disorders 427
Dominika A. Winiarski, April L. Brown, Niranjan S. Karnik,
and Patricia A. Brennan
30. Treating Emotion Dysregulation in Internalizing Disorders 443
Christiane Kehoe and Sophie Havighurst
31. Dialectical Behavior Therapy and Treatment of Emotion
Dysregulation 463
Alexander L. Chapman and Nora H. Hope
32. Future Directions in Research and Treatment of Emotion
Dysregulation 477
Theodore P. Beauchaine, Hunter Hahn, and Sheila E. Crowell
Index 487
Abstract
Work on this chapter was supported by grant DE025980 from the National
Institutes of Health, and by the National Institutes of Health Science of
Behavior Change (SoBC) Common Fund.
1
circumscribed attention, it is of considerable inter- One common use of the term functionalism as-
est to developmentalists, psychopathologists, and sumes evolutionary selection of at least some human
other invested parties (e.g., Beauchaine, 2015; emotions. Such accounts presume that broad classes
Bradley et al., 2011; Gratz, Rosenthal, Tull, Lejuez, of emotion evolved to motivate adaptive, survival-
& Gunderson, 2006; Linehan, 1993). In this volume, related functions including approach, avoidance,
we place primary emphasis on emotion dysregulation and social affiliation (e.g., Keltner & Gross, 1999).
and how it compromises adaptive human func- According to evolutionary functionalist perspectives,
tioning through its effects on initiating, maintain- emotions that subserve these functions are preserved
ing, and modulating diverse human behaviors (cf. across species and experienced by all mammals, in-
Campos, Mumme, Kermoian, & Campos, 1994; cluding humans, because they were selected in our
Thompson, 1990). Given our objective of convey- environments of adaptation (e.g., Panksepp, 2011,
ing contemporary perspectives on emotion dysregu- 2016). For example, approach emotions (e.g., want-
lation, both emotion and emotion regulation must ing, enthusiasm) elicit consummatory behaviors
be discussed. However, they are not primary foci (e.g., foraging, food seeking); avoidance emotions
given widespread coverage in other sources. Interested (e.g., anxiety, fear) elicit precaution (e.g., passive
readers are referred to excellent recent reviews (Aldao avoidance, suppression of approach); and affiliative
et al., 2010; Barrett, 2017a; Braunstein, Gross, & emotions (e.g., compassion, affection) elicit proso-
Ochsner, 2017; Gross, 2014; Gross & Barrett, 2011). cial behaviors (e.g., group cohesion, pair bonding).
Without emotions motivating approach, avoidance,
Variants of Functionalism and affiliative behaviors, likelihood of survival in
When defining emotion dysregulation, one must our environments of adaptation would presumably
first consider what emotions are, and the day-to-day have been lower. Evolutionary functionalist perspec-
functions they serve and do not serve in both their tives have a long history in animal, human, and
ordinary and extreme forms. From this perspective, comparative research on emotion and suggest that
affect dysregulation cannot be defined by overt ex- emotion and motivation are inextricable facets of
pressions of emotion without first specifying the human function, despite being separated in the his-
contexts in which such expressions occur, then tory of behavioral science (see, e.g., Beauchaine &
evaluating whether the emotion expressed and the Zisner, 2017; Gray & McNaughton, 2000; Panksepp,
intensity of its expression are context appropriate, 2011; Porges, 1997).
inappropriate, or neutral vis-à-vis social and cultural An important corollary of this perspective is
norms. For example, intense expressions of anger that humans sometimes behave at the behest of
toward others may be fully functional if the safety of their emotions. Such is especially likely when
one’s offspring is threatened, but similarly intense environmental contingencies are extreme and pull
displays of anger interfere with adaptive behavior in strongly for survival-relevant actions (e.g., in situ-
most social and cultural contexts. Although often ations of food deprivation, threats to physical
not considered, it is also important to note that in safety to oneself or one’s kin). Strong emotional
some situations expressions of anger are afunctional. reactions to these situations motivate urgent be-
Even moderately intense solitary displays of anger, havioral responses that override ongoing activities
for example, such as those elicited by frustration (see, e.g., Corr, 2004). Notably, however, evolu-
while driving, may serve no function or dysfunction tionary functionalist accounts do not imply that
whatsoever. Thus, whether particular displays of all or even most emotional reactions are survival
emotion are functional, dysfunctional, or afunc- relevant. In fact, evolutionary theorists have long
tional, and whether they are regulated, dysregu- recognized that (1) over any extended period of
lated, or unregulated, depends in large part on time individual differences in emotional and be-
eliciting contextual events, and match or mismatch havioral response tendencies confer probabilistic
between context and expressive intensity (e.g., Aldao, rather than deterministic effects on adaptive fit-
2013). Furthermore, given two common uses of ness, and (2) some behavioral response tendencies
the term functionalism that partly but do not fully are coincidental byproducts of evolution—not
overlap (see immediately below), classifying emo- direct outcomes of adaptive selection (Beauchaine,
tions as functional or dysfunctional, regulated or 1999; Buss, Haselton, Shackelford, Bleske, &
dysregulated, is not as straightforward as it might Wakefield, 1998; Gould, 1991). In the latter case,
first appear (e.g., Barrett, 2017b). such response tendencies have no bearing on
Abstract
Emotions, when viewed from the affective neuroscience perspective, arise from organized patterns of
brain activity, which function to generate adaptive behavioral responses. Behavior that emerges from
emotional brain engagement can almost always be characterized as motivated. Thus, emotion and
motivation are highly interdependent concepts, particularly when it comes to behavioral expression.
However, emotions do not always generate behavior, and behavioral outcomes of emotional
engagement—that is, motivated behavior—are not always adaptive. The intersection and dissociation
of emotion and motivation are reviewed in this chapter from an affective neuroscience perspective
that is heavily influenced by the work of Jaak Panksepp.
13
more from the standpoint of biological utility than tions and motivated behaviors evolved because they
experiential or constructivist perspectives (LeDoux, serve useful biological purposes. However, evolved
2012; Barrett, 2016). Core aspects of emotion can biological utility is not always adaptive across
be found in fundamental brain response patterns modern-day contexts, or for all individuals. Next,
(Hamann, 2012; Panksepp & Biven, 2012). In both we briefly discuss methodological approaches and
human and animal studies, emotional states such as current controversies, and close with important
desire and pleasure are associated consistently with challenges for future research in this area.
activity in mesolimbic brain regions, particularly
the ventral striatum and ventral prefrontal cortex Terms and Concepts
(Kuhn & Gallinat, 2012; Berridge & Kringelbach, Much of the terminology used herein refers to
2015). Recent neuroimaging research demonstrates common concepts in psychology and biology. Terms
that the distinctiveness of different emotional cate- such as motivation and emotion refer to “states”
gories is not as clear as once assumed (Hamann, that are generally understood but difficult to clearly
2012; Lindquist, Wager, Kober, Bliss-Moreau, & define. Though some general aspects of these con-
Barrett, 2012). However, we believe that on balance, cepts are shared in the field, important differences
evidence supports core neural constituents for spe- in conceptualization can lead to misunderstandings
cific emotions. Specifically, these emotions are dis- among researchers. Therefore, we offer some level of
tinguishable at the neurobiological systems level definitional detail and provide examples for key
(which include both anatomical and neurochemical concepts in the following sections.
components) and are shared across individuals and
species (Berridge & Kringelbach, 2013; Panksepp, Motivated Behavior
Lane, Solms, & Smith, 2017). However, we also Motivated behaviors are focused and goal-directed.
agree with perspectives put forth in traditional cog- Importantly, however, not all “goal directed” behav-
nitive neuroscience that the interaction between ior can be conceptualized as motivated behavior.
older brain regions and higher neocortical struc- Motivated behavior tends to be focused and highly
tures can generate complexities that are uniquely prioritized in terms of neuronal resources (Bradley
human (Panksepp et al., 2017). Additionally, we et al., 2003). Such behaviors typically involve move-
agree that emotional distinctions are not likely to ments that are rapid, are direct, and contain an ele-
emerge at the level of individual structures but ment of urgency (Beatty, Cranley, Carnaby, &
rather in interactions of several regions across inte- Janelle, 2016). For example, walking across the
grated circuits (Hamann, 2012). street is a behavior that is clearly goal oriented, but
In this chapter, we consider the confluence of it does not necessarily meet our definition. In con-
emotion and motivated behavior from a neurosci- trast, if this behavior was done rapidly to escape the
entific and biological perspective. Our overriding cold or to retrieve one’s crying toddler, it would be
framework is that, from the standpoint of behav- considered motivated. Given that motivated behav-
ioral expression, behaviors that arise from emotion ior contains an element of urgency, it may be per-
are motivated behavior (Beauchaine & Zisner, formed in favor of other potential behavioral lures
2017). Behavior that emerges from emotional ex- or influences (such as cross-traffic or encounters
perience is energized, directed, and focused by the with friends) in the environment.
emotional brain systems engaged: for instance,
withdrawal from threat is a behavior motivated by Emotion
fear, the compulsive search for sex or drugs is be- Emotion is a difficult and often contentious con-
havior motivated by pleasure, and prolonged cept to define clearly. Although terms such as fear
crying after losing a loved one is motivated by grief and anger are commonly used in the scientific lit-
and sadness. Thus, motivated behavior and emo- erature and offer convenient shorthand, interpreta-
tion are tightly coupled. However, they are not tions of such terms vary. Several theories have been
synonymous. There are important ways in which proposed to explain the experience of emotion
emotion can be dissociated from motivated behav- itself, referencing biological influences on physio-
ior, and some of these differences may be particu- logical arousal (Scherer, 2009), cognitive labeling
larly important for psychological health and psy- and contextual interpretation (Schacter & Singer,
chopathology. 1962; Reisenzein, 1983; Scherer, 2009; LeDoux,
We begin by defining key terms and concepts, 2014; Barrett, 2016), and social learning processes
then outline our theoretical perspective that emo- (Fogel et al., 1992), among others (Barrett, 2016).
Abstract
This chapter provides an overview and novel theoretical synthesis of the literature on how and
why emotions regulate social behaviors. It outlines how theorists in this domain have long disagreed
on how to conceptualize the role of evolution and innateness in terms of functions of emotions.
Parsing theoretical and empirical traditions by level of domain specificity, the chapter argues for
a domain-relevant approach to emotion, which is more congruent with current understanding of
neurodevelopment and gene–environment interactions. It examines emotion as emergent information
about the motivational landscape and offers an alternative metaphorical approach to thinking about
evolution as it relates to socioemotional life based on river formation and change.
Keywords: emotion, social behavior, evolution, domain specific, construction, basic emotions,
attachment, emotion theory, emotion regulation, social baseline theory
Emotions, even though their hallmark is the internal state of the individual—the
viscera, the gut—are above all social phenomena. They are the basis of social
interaction, they are the products of social interaction, their origins, and their currency.
—Zajonc (1998, pp. 619–620)
27
related to nature and nurture, arguing that these phenomenon and developed a domain-general view
processes behave more like the development of river of emotion. That is, the brain does not produce
systems than the en vogue computer processing emotions via domain-specific neurobiological mecha-
metaphor can capture. This heuristic view of social- nisms, but rather via domain-general core systems
emotional development predicts specific types of (Barrett, 2014). The first is core affect, which is com-
hypotheses linking emotion and social behavior posed of both valence (determination of whether
through developmental processes. Finally, we argue something is positive or negative as it relates to the
that humans are adapted to a primarily social eco- organism) and some degree of peripheral nervous
logical niche that drives organization of neural sys- system arousal (Lindquist, 2013). The second ingre-
tems in a manner that is domain relevant. dient, conceptualization, is a process by which
In this chapter, we start with a discussion of the bodily sensations (core affect) and cues from outside
theoretical divisions regarding the domain specific- of the body are made meaningful, transforming
ity of emotion processes. Indeed, emotional influ- ambiguous core affect into a disambiguated discrete
ences on social behavior can only be understood by emotion.
taking a particular theoretical perspective. Because Critically, this view of emotion argues that each
of disagreements about most basic elements of what instance of an emotion may be highly variable, but
defines an emotion, the theoretical convictions of that through degeneracy the brain categorizes the
any given theorist are critical in interpreting evi- context and physiological state of the organism as a
dence and decoding relations between emotion and specific emotion (Barrett, 2017). Degeneracy refers
social behavior. to the fact that many different neurons will feed
into one, suggesting that many different patterns of
Theoretical Perspectives on the Nature and activity can result in the same categorization. Thus,
Mechanisms of Emotion and Its Functions many possible patterns across perceptual, motor,
Quarrels among emotion theorists emerged long and cognitive systems might produce any given
ago in philosophical debates between seminal phi- emotion. Conceptualization also functions primarily
losophers such as Plato and Aristotle (see Scherer, to assist allostasis (stability through change) or the
2000). The greatest dividing feature of these ap- maintenance of homeostatic systems through the
proaches is currently the degree of domain specific- procurement of resources, such as food from the en-
ity of emotions. Domain-specific mechanisms of vironment, and functions in a predictive rather than
emotion are most strongly associated with basic reactive manner.
emotion theories, which argue for natural kind We contend that Barrett’s (2017) view of emo-
types of emotion (c.f. Barrett, 2006). Domain- tion is likely more correct on several fronts than
specific approaches assert that mental mechanisms, most current emotion theories. Yet, there are some
often conceptualized as mental modules (see Fodor, potential problems with this view of emotion, rais-
1983), act to guide responses to recurring adaptive ing important questions. Is everything domain gen-
problems in human evolutionary history (Cosmides eral, and are there gradients of domain generality
& Tooby, 1994). These mechanisms are frequently and specificity? We all agree that certain outcomes
thought to act independently and automatically are necessary for survival, growth, and reproduc-
with the appropriate sensory or motivational input, tion, but where do they fit in the domain-general
leading to preprogrammed or prepared behavioral model of emotion? Behaviorists made a mistake
repertoires. For example, I may feel jealousy because decades ago when they assumed all learning was
I perceive a threat to my relationship from an inter- simply a function of our most basic needs (e.g.,
loper, and that emotional state produces behavioral food, water, etc.). Harlow (1958) disproved this po-
tendencies such as mate guarding or intrasexual sition, showing that infant monkeys preferred a soft
competition (Arnocky, Ribout, Mirza, & Knack, stimulus to a food stimulus. Given that we need
2014). Thus, emotion in such models predicts clear, various resources—hence the need for allostasis—
stereotyped elements within the emotion–social be- and that those resources are rewarding and preferred
havior relationship. Despite the heuristic benefits, it in a noncontingent manner, how does an entirely
is now widely believed that theories arguing for domain-general system self-organize in such an
domain-specific mechanisms in most areas of psy- adaptive manner? Furthermore, how does sexual
chology are largely untenable. behavior develop given that it is not a physiological
Lisa Feldman Barrett (2017) has taken early need? If the conceptual separation of the brain and
ideas about emotion as a psychologically constructed body is a mistake (c.f., Barrett, 2017), then how
emotion is widely recognized by emotion research- but are not clearly definable only from the external
ers, it is clearly the case that arousal of the sympa- world. In a sense, emotional episodes can be thought
thetic nervous system can occur before an emotion. of as having mobilizing and perceptual features that
If this is true, it creates a conundrum for defining dynamically and recursively feed back to each other.
emotion. Arousal typically occurs in response to a Emotion as a concept is better characterized as the
change in the motivational landscape. It frequently perceptual part of the cycle and motivation as the
entails the detection of something surprising or mobilization part of the cycle.
of motivational relevance such as an opportunity In addition, we argue that many human emo-
or risk, which leads to the body’s preparation for tions will be social in nature. As information, those
action. If this is not an emotion, then more compo- emotions feed into our ability to form opinions and
nents are needed for emotion to occur. judgments or to decide on actions, and ultimately
We think a separation between the mobilization are critical in determining many of our social behav-
and perceptual phases of emotions clarifies this dis- iors. Many of those emotions are domain relevant
tinction. If we consider the mobilization element as because they tap into flexible behavioral systems
more closely related to changes in the motivational that act as adaptive basins for human behavior.
landscape and emotion as part of the perception of Those basins include attachment behavior—including
that change, then it might be better to clarify that separation distress and felt security—and sexual be-
motivation is more associated with the mobilization havior, for which lust and passionate love may pro-
phase and emotion is more associated with the per- vide information about our goals, whether we can
ceptual phase. Further, this definition comports achieve them, and, if so, how.
well with the idea that emotion serves as informa-
tion. Notably, we are not arguing that this separa- Future Directions
tion is always clear in practice, or that one can truly We recommend several directions for future re-
separate these two constructs. Both constructs are search. First, researchers should pay close attention
conceptual ideas that have correlations with reality to developmental processes. Any understanding of
Abstract
Emotion dysregulation often implies that high levels of (frequently negative) emotion are simply not
regulated by cognition. However, emotion dysregulation can refer to positive feedback loops that
are created and maintained both by a lack of effective cognitive processes that regulate emotion,
and by strong effects of emotion on cognition. This chapter first discusses the effect of cognition on
emotion, with an emphasis on the effects of attention and cognitive control (e.g., emotion regulation)
processes upon emotions. Then, it discusses the effect of emotion on cognition, with an emphasis on
attention, memory, decision making, and cognitive control. Finally, it examines the implications of both
types of emotion–cognition interactions by discussing the positive-feedback cycles that can produce
dysregulated emotion.
Keywords: cognition, emotion, cognitive control, emotion regulation, decision making, memory,
attention
39
How Cognition Affects Emotion et al., 2003; Habel et al., 2007; Winston, O’Doherty,
There is a large literature focused on the effects of & Dolan, 2003), and some scholars argue that con-
cognition on emotion. Specifically, one prolific re- scious awareness is not required, much less focused
search tradition defines emotion regulation as a va- attention (Jessen & Grossmann, 2015; Morris &
riety of processes by which someone can influence Dolan, 2001; Whalen et al., 2004; but see Pessoa,
his or her own emotional trajectory in terms of the 2005).
onset, offset, magnitude, duration, or quality of an Another set of studies explores a closely related
emotional response (Gross, 2015; Gross & question: whether restricting attentional resources
Thompson, 2007). This research was born of the affects the magnitude of brain and bodily emotional
coping literature, but in its current instantiation, it responses. These studies examine restricted atten-
largely references the process model of emotion tion by presenting emotional and nonemotional
regulation, which outlines five points during emo- stimuli together, with instructions to respond to
tion generation in which regulation processes might nonemotional stimuli, or by presenting a dual task
occur (Gross, 1998b). These include situation selec- along with emotional stimuli. These researchers find
tion (avoidance or engagement with situations that that emotional responding diminishes as concur-
have potential to cause unwanted emotion), situa- rent attentional demands increase (Pessoa, Padmala,
tion modification (utilizing agency to change prop- & Morland, 2005; Silvert et al., 2007). In other
erties of situations that may cause unwanted emo- words, emotional responses to stimuli can be di-
tion), attentional modification (directing attention minished significantly under more impoverished at-
toward and away from aspects of situations that tentional conditions (Habel et al., 2007). So, while
may cause unwanted emotion), cognitive change complete attention does not seem to be required for
(changing the cognitions, evaluations, and apprais- the production of brain and/or bodily emotional
als that lead to emotion), and expressive suppression responses, these responses do decrease when atten-
(directly influencing emotional responses, including tional resources are more limited.
bodily responses and facial expressions of emotion). Examining distraction as an explicit emotion
Attentional modification and cognitive change are regulation strategy is one way that emotion re-
most relevant to this review because they refer to searchers have examined influences of attention on
well-specified cognitive processes. It is possible to use emotion (Gross, 1998b; Salovey, Mayer, Goldman,
attentional modulation and cognitive change to either Turvey, & Palfai, 1995). In an everyday context, dis-
diminish or enhance emotional responding. traction from a negative event, such as a breakup of
a romantic relationship, might involve a purpose-
How Attention Influences Emotion fully overstuffed social calendar; an increased focus
How attention can diminish emotion on other priorities, such as work; or engagement
Most theories of emotion imply that some atten- with unrelated narratives, such as those in books or
tional resources must be devoted to an emotional films. In a laboratory context, distraction from neg-
event to elicit a response (Gross, 1998b). If emotion ative stimuli can be implemented either broadly,
is a downstream consequence of attention, it follows with an instruction such as “think of something else
naturally that changes in attention can have strong so that you do not feel as negative,” or quite specifi-
effects on subsequent emotion. More recently, re- cally, by giving the participant a secondary task to
searchers have examined whether emotional stimuli complete while processing emotional stimuli. Both
require focused attention (or even conscious aware- types of distraction are effective, in that when im-
ness; Jessen & Grossmann, 2015; Pessoa, 2005) to plemented, they reduce self-reported negative emo-
be processed preferentially in the brain compared to tion (Joorman, Siemer, & Gotlib, 2007; Sheppes &
neutral stimuli (Anderson, Christoff, Panitz, De Meiran, 2008), along with other brain and bodily
Rosa, & Gabrieli, 2003). These studies use labora- emotional responses (Kanske, Heissler, Schönfelder,
tory manipulations that severely limit or prevent Bongers, & Wessa, 2011; McRae et al., 2010; Shafir,
conscious processing of emotional stimuli, and ex- Schwartz, Blechert, & Sheppes, 2015). One benefit
amine whether a stimulus still elicits an emotional of distraction is that it can be used even when there
(> neutral) brain and/or bodily response. Using is limited time for emotion regulation (Sheppes &
amygdala activation and physiological responses as Gross, 2011; Sheppes & Meiran, 2008). In addition,
indices of emotion, there is considerable evidence it can be used to effectively reduce emotional re-
that directed attention is not necessary for the brain sponding even in response to relatively intense emo-
and body to respond to certain stimuli (Anderson tional stimuli. However, there is some evidence that
Abstract
Recent conceptualizations of emotion dysregulation define it as a process that unfolds over multiple
time scales and that leads to short- or long-term impairments. This chapter discusses the advantages
of observational methods for measuring emotion dysregulation as a process, focusing on three
patterns and associated evidence of them from observational studies. First, the chapter discusses
context-inappropriate emotion, the absence of an expected emotional reaction or an atypical reaction
for the situational context. Second, it discusses atypical emotion dynamics, specifically emotional
expressions that change abruptly, including but not limited to emotional lability. Third, it discusses
ways in which emotions endure and are difficult to modify, pointing to ineffective strategy use as a
mechanism. It concludes by discussing new directions for observational research, including creative
study design and analytic methods that can capture emotion dysregulation.
53
processes, such as those involved in healthy emo- functional perspective on emotional development
tional functions, deviate from normal and become (K. C. Barrett & Campos, 1987; Campos, Mumme,
dysfunctional. The RDoC matrix comprises five Kermoian, & Campos, 1994), as well as dynamic
domains, including positive, negative, cognitive, systems principles (Fogel et al., 1992; M. D. Lewis
social, and arousal/regulatory systems—which col- & Granic, 2002). According to these perspectives,
lectively capture aspects of emotional functioning emotions are relational, dynamic, and continuous
involving threat, frustration, loss, reward, and affili- psychological processes rather than events. These
ation. Taken together, clinical observations, clinical perspectives inform how we approach the concept
research, and the efforts such as RDoC underscore of emotion regulation and how we distinguish regu-
the need to understand the role of emotion in im- latory patterns that are normal and effective from
paired psychological function. The study of emo- those that are atypical and dysfunctional.
tion dysregulation is one approach to understand- The functionalist perspective views emotions as
ing the nature and development of these problems relational processes. That is, emotions are defined
and ultimately treating or preventing them (e.g., by how we relate to situations, both actual and per-
Beauchaine & Zisner, 2017). ceived, as they bear on our short- and long-term
In this chapter, we discuss how observations of goals for well-being (K. C. Barrett & Campos, 1987;
emotional behavior can be translated into meaning- Campos et al., 1994). In this view, emotions are not
ful research on emotion dysregulation. We offer discrete events; they are not things. Rather, emo-
definitions of emotion, emotion regulation, and tions are continuous, interactive processes through
emotion dysregulation, acknowledging the lack of which we relate to changing environments in ways
consensus, and exploring whether emotion regula- that promote our own well-being, while simultane-
tion can be differentiated from emotion. We then ously preparing us to act to achieve those goals (see
illustrate three clinical patterns of emotion dysregu- Cole, 2016 for further discussion). What we inter-
lation that can be studied using behavioral observa- pret as a discrete emotion—a feeling or an emo-
tions (Cole, Hall, & Hajal, 2017). Next, we review tional expression—is the product of (1) continuous
available evidence for these patterns, discuss limita- appraisal of the significance of ongoing circum-
tions of existing research, and suggest future direc- stances for well-being and (2) continuous changes
tions that can contribute to meaningful observa- in readiness to act in particular ways (e.g., approach
tional research on emotion dysregulation. with force, yield, escape) to regain, preserve, attain,
or maintain our goals (Arnold, 1960; Frijda, 1986).
Theoretical Perspectives and Definitions This informs how we conceptualize emotion dys-
Defining emotion dysregulation offers several chal- regulation.
lenges. For example, there is no consensus regarding Prior to the 1980s, the term “emotion dysregula-
whether humans are biologically prepared to experi- tion” appeared only sporadically in empirical papers
ence and express a core set of universal emotions, in psychology. During a resurgence of scientific in-
whether emotions are constructions of our percep- terest in emotion in the 1980s, the term appeared in
tions and interpretations of physiological arousal, or titles of a special issue of Developmental Psychology
both (see, e.g., Tracy & Randles, 2011). Discrete (Dodge, 1989) and an edited volume (Dodge &
emotion theories posit that emotions such as joy, Garber, 1991). These publications did not define
anger, fear, sadness, and disgust are biologically pre- emotion dysregulation but used the term to imply
pared and observed across cultures and even species dysfunctional patterns of emotion regulation. The
(Ekman, 1992; Izard, 2007; Tomkins, 1962, 1963; emphasis on regulation is important. It acknowl-
Panksepp, 1992, 2017; Sauter, Eisner, Ekman, & edges that emotions are never out of control; what
Scott, 2010; Chapter 2, this volume). In contrast, appears out of control to the average person is a pat-
according to core affect theory, humans’ physiologi- tern of emotion that is problematic by some crite-
cal experiences vary in valence and arousal, and our rion (Cole, Michel, & Teti, 1994). Even sustained or
interpretations of these experiences yield cognitive intense emotion is not inherently dysfunctional;
constructions that we experience as emotion over millennia, the capacity for strong, enduring
(L. F. Barrett, 2011; James, 1884; Russell, 2003; emotions has been conserved because this capacity
Widen & Russell, 2008). enables us to protect and achieve our goals for well-
We see value in understanding both the funda- being, helping us communicate our needs and act
mental function of emotion and different functions on our own behalves (Cole, 2016; Cole, Martin, &
of discrete emotions. To this end, we draw from the Dennis, 2004).
Abstract
This chapter presents an overview of literature relevant to understanding relations between aging
and emotion dysregulation. Although a number of studies suggest that aging leads to shifts in emotion
regulation and emotional well-being, the extent to which aging affects emotion dysregulation is less
clear. To clarify the effects of aging on emotion dysregulation, this chapter begins by examining shifts
in effectiveness of emotion regulation that occur with age, considering pertinent theories, and then
expands on these findings by examining more specifically how context appropriateness of emotions,
consequences of emotions on behavior, duration of emotions, and etiology and presentation of
psychopathology are altered by aging processes. Finally, this chapter concludes by identifying gaps in the
literature and recommendations for future empirical endeavors to advance our current understanding
of effects of aging on emotion dysregulation.
Keywords: aging, emotion dysregulation, strategy use, context, cognitive control, behavior
69
reactivity (i.e., emotion generation and behavioral emotions (Carstensen et al., 1999; Lang & Carstensen,
responsivity to emotion), which leads to reduced 2002), and a critical role of cognitive control in
sensitivity to negative, but not positive, stimuli, successful emotion regulation among older adults
thus explaining age-related shifts in well-being. (Mather & Knight, 2005; Opitz, Lee, Gross, &
However, contrary to this model, there is significant Urry, 2014). However, there is inconsistent evidence
neuroimaging evidence for structural and functional for limited future time perspective as an underlying
preservation of the amygdala with increasing age mechanism of positive emotional function in late
relative to other brain regions (Allen, Bruss, Brown, & adulthood (Charles & Carstensen, 2008; Lang &
Damasio, 2005; Nashiro, Sakaki, & Mather, 2012). Carstensen, 2002). Rather, numerous studies in-
Postmortem studies indicate no volumetric decline dicate that limited future time perspective is asso-
in the amygdala with age (Brabec et al., 2010), and ciated with worse negative emotional outcomes
functional studies suggest preserved amygdala reac- (Allemand, Hill, Ghaemmaghami, & Martin, 2012;
tivity in older adults (Jacques, Dolcos, & Cabeza, Gruhn et al., 2015; E.M. Kessler & Staudinger,
2010; Wright et al., 2008). 2009; Ramsey & Gentzler, 2014). Thus, there may
Thus, there is currently little support for the in fact be an increasing emphasis on emotion regu-
theory that age-related shifts in general emotional lation with advancing age, but shrinking future ho-
reactivity are responsible for age differences in emo- rizons may not mediate effects of age on enhanced
tional well-being. In contrast, emerging evidence well-being.
from behavioral and neuroimaging investigations The selection, optimization, and compensation
suggests that emotion regulation goals and strategies with emotion regulation framework (SOC-ER; Urry
play a critical role in explaining age-related shifts in & Gross, 2010), an application of Baltes and Baltes’s
emotional well-being (for a review see Nashiro et al., (1990) selection, optimization, and compensation
2012). As a result, emotion regulation—referring theory (SOC), offers a different explanation for how
here to volitional (explicit) and avolitional (implicit) age-related shifts in emotion regulation lead to
processes involved in modulation of initial emotional enhanced well-being. The SOC-ER framework sug-
responses (Cole et al., 2017; Gross, 1998, 2015)—is gests that older adults use alternative methods of
a dominant topic of study in the aging and well-being emotion regulation that rely more heavily on re-
literature. Several recent theories propose that sources that improve or are relatively preserved with
emotion regulation goals and the manner in which age (e.g., social networking, predicting feelings of
such goals are implemented shift with age, and that arousal) to compensate for losses of other resources
these shifts help to account for shifts in well-being. (e.g., cognitive control). Support for this framework
Socioemotional selectivity theory (SST; Carstensen, comes from findings indicating that in the wake of
Fung, & Charles, 2003), for example, proposes that significant cognitive decline, older adults exhibit
as temporal horizons shrink with increasing age, greater preference for and are more effective at
emotion regulation goals become more salient. As a implementing emotion regulation strategies that
result, older adults are more motivated to allocate rely less on cognitive control processes than young
greater resources to emotion regulation and use adults (Allard & Kensinger, 2014b; Isaacowitz,
more effective strategies to regulate, leading to en- Toner, Goren, & Wilson, 2008; Scheibe, Sheppes,
hanced emotional well-being. The cognitive control & Staudinger, 2015). Combining aspects of the SST
hypothesis subsumed within SST accounts for age- and SOC frameworks, strength and vulnerability
related cognitive decline, positing that older adults integration theory (SAVI; Charles & Piazza, 2009)
still require cognitive control for successful emotion specifies several age-related strengths and weak-
regulation and thus older adults with preserved nesses that appear to account for instances in which
cognitive control should exhibit greater emotional age confers affective benefits. Strengths identified
well-being than those with lower cognitive control include increased motivation to regulate emotions
capacities (Mather & Carstensen, 2005). and shrinking perception of time left with age,
Consistent with predictions from SST, there is whereas weaknesses include ability to regulate emo-
reliable evidence supporting age-related shifts in tions in response to prolonged stressors that elicit
strategies used to regulate emotions (for a review see high levels of arousal. SAVI extends upon tenets of
Mather, 2016), age-related decreases in future time SST and SOC by proposing that daily contexts in
perspective (Carstensen, Isaacowitz, & Charles, 1999; which emotions are experienced and regulated are
Gruhn, Sharifan, & Chu, 2016; Lang & Carstensen, integral to developing a complete understanding of
2002), age-related increases in motivation to regulate age-related shifts in emotional well-being. Together,
Abstract
Emotion generation, regulation, and dysregulation are complex constructs that are challenging to
define and measure. This chapter reviews prevailing definitions and theories of these constructs
and examines the literature across multiple levels of analysis. It adopts a developmental perspective,
which guides interpretation of the literature and helps clarify discrepant points of view. The extent
to which emotion generation and regulation are separable represents a significant controversy in the
field. When viewed as cognitive constructs, it is virtually impossible to disentangle emotion generation
and regulation. However, at the biological level, there are important differences in neural structures
involved in bottom-up emotion generation processes versus those associated with top-down regulation
of emotions. From a developmental perspective, emotions and emotion dysregulation emerge early
in life, whereas emotion regulation strategies develop more gradually as a function of maturation
and socialization. Future research should continue to reconcile different perspectives on emotion
generation, regulation, and dysregulation.
85
examine epigenetic effects as mechanisms of early to inform the literature today—many scholars still
temperament (Conradt, Adkins, Crowell, Monk, & view emotional processes as emerging from interac-
Kobor, 2018). Epigenetics, defined by alterations to tions between physiology and cognitions (see, e.g.,
gene expression rather than gene structure, repre- Gross, 2015). Importantly, however, Schachter and
sent one type of Gene × Environment interaction Singer’s conceptualization does not account fully for
that contribute to early emerging individual differ- individual differences in emotion generation and
ences in emotional processes (see Chapter 16, this expression early in life, that is, prior to developing
volume). By birth, postnatal environments begin to cognitive schemas needed to label and categorize
shape emotional expression through Temperament × emotional reactions.
Caregiving interactions, which lay a foundation More recently, distinctions between emotion
for emotion regulation and dysregulation. Thus, generation and regulation have become a source of
emotion generation, regulation, and dysregulation ongoing debate in the field. According to one per-
are developmental processes that result from com- spective, emotion generation is affected by apprais-
plex transactions across multiple levels of analysis als, or the extent to which an emotional stimulus
beginning at conception. (1) captures a person’s attention and (2) is given mean-
In this chapter, we review emotion and related ing (Gross, 2015). In other words, for an emotion to
constructs from a developmental perspective. This emerge, a person must attend to and appraise a
helps clarify discrepant empirical findings and theo- stimulus in some manner, even if that process occurs
ries that emerge when researchers investigate emo- automatically and outside of conscious awareness.
tional processes cross-sectionally or within relatively This “situation–attention–appraisal–response” per-
narrow developmental windows (e.g., adolescence). spective has been articulated in many foundational
Indeed, when environments are constrained, such theoretical papers (Gross, 1998, 2015; Gross &
as in early development, there are fewer influences Feldman Barrett, 2011; McRae, Misra, Prasad, Pereira,
on emotional processes and, consequently, biologi- & Gross, 2011; Gross, Sheppes, & Urry, 2011;
cal predispositions take precedence. Over time, so- Ochsner et al., 2009; see Chapter 10, this volume).
cialization, family and peer dynamics, cultural fac- This perspective offers an advantage of identifying
tors, exposure to interventions, and many other distinct and separable elements of the emotion
forces interact to affect emotion-related processes. generation process, each of which could be amena-
Consistent with the developmental psychopathol- ble to regulation.
ogy perspective (Beauchaine, Constantino, & In an alternate theoretical perspective, Panksepp
Hayden, 2018; Cicchetti, 1984, 1993), taking a lifes- and colleagues define emotion generation as a bio-
pan approach helps elucidate continuities and dis- logically driven process that emerges from coordi-
continuities in risk/resilience trajectories and poten- nated interactions between subcortical and neocor-
tial points for intervention. tical regions (Panksepp, 1982, 1998; Panksepp &
Watt, 2011; see Chapter 2, this volume). According
Terms and Concepts to this theory, primary emotions originate within
Emotion Generation subcortical structures, which have been preserved
For the past half century of psychological research, evolutionarily across species (see also Beauchaine,
scholars have typically conceptualized emotions as a 2015a). These primary emotions are not shaped by
multilevel process, emerging from rapid feedback environmental inputs, prior learning, or appraisals.
between physiological and cognitive systems. For Rather, their principal function is to stimulate mo-
example, Schachter and Singer (1962) described tivated behaviors, such as those that allow an organ-
emotion generation in two steps: First, physiologi- ism to acquire new skills, maintain homeostasis,
cal arousal occurs; then, a person evaluates whether survive, and reproduce (Panksepp & Watt, 2011).
that arousal is consistent with observable stimuli. If Consequently, neural structures involved in primary
a person perceives a match, he or she can label that emotion generation are essentially indistinguishable
experience in terms of readily available cognitions from circuits involved in movement, approach-
(e.g., my heart is racing and I am about to receive a or avoidance-related motivation, and reward
shock; therefore, I am anxious). However, if there is (Beauchaine et al., 2017). Across development,
dissonance between arousal and perception, the primary emotions become associated with specific
person may need to search for alternate explana- contexts, stimuli, or patterns of stimuli. This leads to
tions to describe an experience appropriately (e.g., secondary emotion processes, which are characterized
too much caffeine). This two-step model continues by learned associations between primary emotions
Abstract
99
marital interaction documents) but are most readily between infants and caregivers, and the psychological
observed in the early years when young children are significance of such ties. Bowlby argued that humans
so dependent on others for managing their feelings. have been motivated to develop these attachments
Viewed in this light, emotion dysregulation may throughout evolution because of the importance of
not be solely a problem of individual adjustment, infant–caregiver proximity for protection, nurtur-
but may also reflect relational problems. Indeed, ance, and social learning. As attachment researchers
this view is at the cornerstone of the field of infant/ have learned more about early psychological devel-
early childhood mental health, which regards early opment, however, many have concluded that early
problems of psychological functioning as inherently attachments serve broader functions, including sup-
relational. It is captured in Winnicott’s famous line, porting emotion regulation that derives from an
“There is no such thing as a baby. . . you are describ- infant’s trust in an adult who responds sensitively,
ing a baby and someone” (Winnicott, 1957, p. 137). buffers stress, provides relief from distress, and
In this chapter we consider the development of manages environmental demands (Brumariu, 2015;
emotion dysregulation in developing relationships. Cassidy, 1994). Viewed from this perspective, secure
Our focus is primarily on the early years because attachments promote the growth of constructive
this is a formative period for growth of emotion forms of emotion self-regulation in several ways, in-
regulation and thus also a period of vulnerability to cluding the parent’s acceptance of the child’s feelings,
social influences that can promote emotion dysreg- willingness to communicate openly about them,
ulation. For this reason, developmental study of and coaching emotion regulation skills (Thompson,
early emotion regulation is also the study of risk for 2015). From these influences, children develop a
emotion dysregulation (see Garber & Dodge, 1991). greater understanding of emotion and its manage-
Yet some developmental processes that contribute ment, and develop a broader understanding of the
to emotion dysregulation are very different from role of emotions in the context of close relationships.
those that lead to skills in emotion management. The benefits of secure attachments are especially
We organize the chapter in this manner. In the noteworthy when contrasted with the kinds of emo-
section that follows, two central theoretical per- tion dysregulation apparent in insecure parent–child
spectives are considered: attachment theory and attachments, whether insecurity is manifested in
functionalist emotions theory. The section closes with resistant, avoidant, or disorganized responses. When
reflection on some unresolved theoretical issues. insecure-resistant infants are observed with their
The next section focuses on central findings and mothers, they exhibit self-evident signs of emotion
conclusions from the research literature, with par- dysregulation. For example, when stressed by a brief
ticular attention to interactions among social and separation, they have difficulty soothing even after
biological influences on developing emotion dys- the mother’s return and instead show continued and
regulation in relationships. The chapter concludes sometimes angry distress throughout reunion. By
with some ideas about future directions for this field contrast, insecure-avoidant infants are more placid
of research. during separations from their mothers, but their
behavior is belied by physiological indications of
Theoretical Perspectives on the strong arousal, suggesting that they minimize ex-
Development of Emotion Dysregulation pressions of distress to a caregiver who has been
Attachment theory and functionalist emotions theory relatively insensitive to these signals in the past
are two perspectives that frame current thinking (Spangler & Grossmann, 1993). Disorganized in-
about the development of emotion dysregulation in fants show the most atypical patterns of attachment
the context of developing relationships. The first fo- behavior including indications of disorientation,
cuses on the nature of early relationships and their inconsistent responses to their mothers (e.g., ap-
role in the development of self-regulation and emo- proach combined with avoidance), fearful behavior,
tion dysregulation. The second contributes a com- and/or inconsolability during reunion episodes.
plementary focus on the nature of emotion and its Attachment researchers believe that this indicates
management in the context of an individual’s trans- that disorganized infants lack a constructive strategy
actions with the social world. for engaging their mothers after separation because
their mothers are not reliable sources of safety and
Attachment Theory emotion management.
Attachment theory was formulated by Bowlby Considerable research conducted with infants,
(1969) to explain the development of emotional ties children, and adolescents confirms the advantages
Abstract
Caregivers play a foundational role in the development of children’s emotion dysregulation. Yet,
because there are a multitude of ways in which parent behavior can intersect with children’s emotions,
the development of emotion dysregulation is complex. This chapter specifically examines the role of
operant reinforcement, where the way in which caregivers respond contingently to their children’s
expression of emotion influences child emotion dysregulation. It reviews (1) the central theoretical
models that explicate the process by which parental responses to children’s emotions reinforce
emotion dysregulation, (2) current evidence supporting these theories, and (3) interventions designed
to reduce emotion dysregulation through operant reinforcement processes. It emphasizes that, in
addition to unidirectional effects, operant reinforcement from a parent interacts with traits inherent
to the child, and parents and children mutually influence one another in ways that highlight the
transactional, dynamic processes underlying the development of emotion dysregulation. Limitations
and future directions are discussed.
115
increasing the likelihood that the child will use and behavioral measures. Specific methods often
similar strategies in the future) or negatively rein- vary based on the developmental period assessed
forced (e.g., a child whines to avoid eating broccoli (Adrian, Zeman, & Vetis, 2011). For example, mea-
and then throws it on the floor; the parent then re- suring behavioral responses through observational
moves the broccoli, increasing the likelihood that methods is more common in young children,
the child will use similarly dysregulated strategies in whereas assessing subjective experience through
the future). self-report is more prevalent in older children and
The development of emotion dysregulation is adolescents. Researchers often measure facial,
complex because emotions and efforts to regulate bodily, or vocal cues associated with discrete emo-
emotions are multifaceted. In addition, there are a tions using laboratory tasks designed to elicit nega-
multitude of ways in which parent behavior inter- tive emotions. Then the corresponding emotional
sects with child emotions. The pairing of children’s expressions and any behavioral attempts to manage
emotions and regulatory efforts with positive and those emotions are coded (i.e., problem solving, dis-
negative reinforcement by parents can lay the foun- traction, disruptive behavior) so that attempts are
dation for emotion dysregulation during childhood. made to disentangle expression of negative emo-
Improved understanding of the mechanistic pro- tions from regulatory efforts. In contrast, internal
cesses that shape emotion dysregulation has also led experiences of emotion dysregulation are measured
to novel interventions that target children’s emo- via self-report and through physiological measures.
tional expression, promote effective regulation, and, More recently, self-report methodologies have been
importantly, intervene with parents to support ef- enhanced by the use of ecological momentary as-
fective responses to their child’s emotions (e.g., sessment (EMA), particularly with adolescents
Havighurst, Wilson, Harley, Prior, & Kehoe, 2010). (Shiffman, Stone, & Hufford, 2008), in which sam-
This chapter reviews theory, current evidence, pling occurs at various instances throughout the day
and interventions that target the development of to more accurately assess the dynamic nature of
emotion dysregulation in children. Specifically, we emotions. The most common physiological index of
will address the following questions: (1) What are emotion dysregulation is respiratory sinus arrhyth-
the central theoretical models linking parental mia (RSA). RSA, also known as vagal tone or heart
responses to children’s emotions with emotion dys- rate variability, is a measure of parasympathetic
regulation? (2) What is the current evidence sup- nervous system influence on cardiac activity. Higher
porting these theories? (3) How do interventions resting RSA has been linked consistently with emo-
targeting operant reinforcement processes provide tional stability, whereas lower resting RSA has been
additional evidence of mechanistic processes under- linked consistently with emotional lability and dys-
lying emotion dysregulation? (4) What are the limi- regulation (e.g., Beauchaine, Gatzke-Kopp, &
tations of the current literature and key next ques- Mead, 2007). Small decreases in RSA in response to
tions? Although beyond the focus of this chapter, it a stimulus or stressor (i.e., vagal withdrawal) have
is important to recognize that operant reinforce- been linked to effective emotion regulation (Calkins,
ment, in terms of positive and negative reinforce- Graziano, Berdan, Keane, & Degnan, 2008),
ment patterns, continues to develop within peer whereas larger decreases appear to mark significant
and romantic relationships and may replicate and dysregulation (e.g., Crowell et al., 2005).
maintain problematic patterns of emotion dysregu- While these measurement tools offer ways to
lation across the lifespan (see Dishion & Snyder, assess emotion dysregulation, they must be embed-
2016). The current chapter focuses on how operant ded within specific study designs to accurately in-
reinforcement in caregiver–child relationships shapes vestigate operant reinforcement of emotion dysreg-
child emotion dysregulation. ulation. Specifically, a parent’s response must follow
a child’s expression of emotion or regulatory strat-
Terms and Measurement Issues egy. Alternatively, reciprocal models that examine
Measurement tools are reviewed briefly because the dynamic reinforcement patterns between parent
definition of a construct is informed by the way in and child must measure transactional influences of
which it is measured (Larsen & Prizmic-Larsen, parents and children on each other across time.
2006). Emotion dysregulation is inherently multi- Interaction models examine how parenting affects
faceted because emotions entail full-system re- children’s emotion dysregulation in the context of
sponses. Therefore, measurement is accomplished another variable, such as child sex, trait characteris-
using a range of methods, including observational tics, or genetic predispositions. The dominant
Abstract
This chapter examines cognitive processes that underlie the development of emotion dysregulation.
It first introduces and defines key terms including emotion, emotion regulation, and emotion
dysregulation. It then introduces the authors’ theoretical perspective, the extended process model of
emotion regulation, which considers emotion generation and emotion regulation as valuation systems,
and describes core regulation processes, including regulation strategies. Next, using the extended
process model of emotion regulation as the guiding framework, the chapter discusses how emotion
dysregulation may occur during the identification, selection, implementation, and monitoring stages.
The chapter concludes by considering unresolved controversies and suggests several exciting avenues
for future research across basic and applied domains.
Keywords: cognitive processes, emotion, emotion regulation, emotion dysregulation, process model
127
This full-body response is typically referred to as either increasing or decreasing their magnitude,
“emotional reactivity.” The notion that emotions duration, or type. Second, regulation of emotions
arise and unfold over time is at the heart of most can occur through conscious and intentional pro-
contemporary conceptions of emotions, and there cesses or without conscious awareness and explicit
are commonly said to be four key steps in the intention (Gross & Thompson, 2007). Third, emo-
emotion-generative process: a situation that draws tion regulation processes cannot be deemed categor-
one’s attention, an evaluation or appraisal of the ically “good” or “bad,” as understanding the specific
situation, and a multisystem whole-body response context is necessary to evaluate whether emotion
(Gross & Thompson, 2007). regulation is adaptive or maladaptive in light of
Although emotions are often categorized into one’s goal(s).
binary groups (e.g., “good” vs. “bad,” “positive” vs.
“negative”), they are actually highly heterogeneous Emotion Dysregulation
in nature (Gross, Sheppes, & Urry, 2011). Any given We define emotion dysregulation as “a state in
emotion can sometimes be mild and hardly detect- which despite an individual’s best efforts, regulatory
able, while at other times it may be extraordinarily attempts are not achieving the individual’s emotion
intense and demanding of one’s attention. In one related goal(s) and the individual is unable to make
context, an emotion can be useful and adaptive, and necessary corrections to achieve the emotion related
in another context that very same emotion may be goal(s)” (Jazaieri et al., 2013, p. 587). Similar defini-
unhelpful and maladaptive. Emotions can be cogni- tions have been used by others, defining emotion
tively simple and at other times require a high level dysregulation as “the inability even when one’s best
of processing. They can be brief and fleeting and at efforts are applied, to change in a desired way emo-
other times more prolonged. tions cues, experiences, actions, verbal responses,
and/or nonverbal expressions under normative con-
Emotion Regulation ditions” (Neacsiu, Bohus, & Linehan, 2014, p. 493).
At times emotions are useful and adaptive—for ex- Beauchaine (2015) has similarly proposed that
ample, experiencing happiness while on vacation or emotion dysregulation is a “pattern of emotional
experiencing sadness when separated from someone experiences and/or expression that interferes with
you care for. However, at other times, emotions can appropriate goal-directed behavior” (p. 876).
be unhelpful and/or maladaptive (e.g., the specific It has been suggested that characteristics of emo-
emotion type, intensity, duration, and/or frequency tion dysregulation may include
are not well matched to the situation; Gross &
an excess of aversive emotional experiences, an
Jazaieri, 2014). During such times, people often at-
inability to regulate intense physiological arousal,
tempt to influence the specific emotion, its timing,
problems turning attention away from stimuli,
or how it is (or in some cases is not) experienced
cognitive distortions and failures in information
and/or expressed (Gross, 1998). This characterizes
processing, insufficient control of impulsive behaviors
emotion regulation, which involves the activation of
related to strong emotions, difficulties organizing and
a goal to regulate an emotion followed by recruit-
coordinating activities to achieve non-mood-
ment of strategies and tactics to achieve this goal.
dependent goals when emotionally aroused, and a
Sometimes the motivation for an individual to
tendency to “freeze” or dissociate under very high
engage in emotion regulation is driven by wanting
stress.
to simply feel better in a hedonic sense. For exam-
(Neacsiu et al., 2014, pp. 493–494)
ple, one may choose to downregulate anger because
the physical sensations are uncomfortable for the Others have suggested that emotion dysregula-
individual. At other times, the motivation to regu- tion is characterized by deficits in four specific areas:
late a particular emotion is driven by some other (1) (lack of ) awareness, understanding, and accept-
goal and altering the trajectory of an emotion ing of emotions; (2) (in)ability to engage in goal-
simply serves a means to an end. For example, one directed behaviors and inhibit impulsive behaviors
may choose to upregulate anger to garner attention when experiencing negative emotions; (3) (in)flexi-
from others and influence their behavior in a way ble use of situationally appropriate strategies to
that is consistent with one’s goals. modulate the intensity and/or duration of emo-
The scope of emotion regulation spans several tional response rather than to eliminate emotions
key dimensions. First, emotion regulation refers to entirely; and (4) (un)willingness to experience
changing both negative and positive emotions by negative emotions as part of pursuing meaningful
(a) (b)
V
Attentional Cognitive
Deployment Change
V
Valuation P A
Response
P A Modulation
Perception Action a
V
Situation P A
W Selection &
World Modification
W
Figure 10.1 Emotion generation and emotion regulation as a two-level control system. Panel a. Emotion generation. A feedback
process attends to and appraises goal-relevant aspects of a situation to enact changes in multiple response systems. Black arrows
represent points at which emotion regulation can have an impact on emotion generation. Panel b. Emotion regulation. Another
feedback process compares the current emotion to the desired emotion and launches regulation strategies to minimize discrepancies.
The inset shows how panel a can be embedded in panel b for a full representation of emotion generation and emotion regulation.
Selection
V
P
Implementation
V
P
P A
W W W
Monitoring
Figure 10.2 Stages of emotion regulation. According to the extended process model, emotion regulation is initiated when a goal is
activated to change the ongoing emotion at the identification stage. Next, a broad regulation strategy is chosen at the selection
stage. The strategy is then enacted as a specific tactic suitable for the given situation at the implementation stage. This cycle can go
through multiple iterations, which are collectively viewed as a monitoring stage where the system maintains, switches, or stops one or
more aspects of the ongoing emotion regulation episode.
valuation (V), and action (A). Perception involves tactics that fit the situation (e.g., pause and take a
detecting the emotion (e.g., anxiety), valuation in- sip of cold water during the job interview). Getting
cludes determining whether the emotion is helpful from a general strategy to situation-specific tactics
or unhelpful for ongoing goal pursuits, and finally starts with the perceptual substep of the implemen-
the action substep involves activation of the goal to tation stage. At this point, a person is able to assess
regulate the emotion. Importantly, there are many available tactics and relevant situational constraints
points within the identification stage and each sub- and affordances. Then at the valuation substep a
step for emotion dysregulation to occur. person evaluates these tactics and the most promis-
Once a person identifies a regulatory goal, this ing ones are selected for implementation. The action
activates the selection stage. This stage involves a substep is the point at which an emotion regulation
valuation of available emotion regulation strategies strategy directly affects emotion generation. Thus,
from five broad families (situation selection, situa- implementation of an emotion regulation strategy
tion modification, attentional deployment, cogni- results in regulation of the first-level emotion-
tive change, and response modulation). By evaluat- generative valuation system. As in the prior stages,
ing candidate strategies with respect to situational there are many points at which emotion dysregula-
demands and available resources, the selection stage tion may occur.
results in an initial emotion regulation strategy pref- Each stage or loop continues to guide a person’s
erence. At the perception substep of the selection actions until his or her goal state is achieved or
stage, a person perceives the available regulation abandoned. This gives rise to the broader monitoring
strategies. Each strategy is evaluated during the val- stage, in which a person engages in ongoing evalua-
uation substep based on how effective the strategy is tion of whether to (1) keep implementing the cur-
expected to be in minimizing the gap between the rent emotion regulation behavior (“maintaining”);
current emotion and one’s goal in light of contex- (2) switch to a new emotion regulation goal, strat-
tual factors (e.g., cognitive and physiological re- egy, or tactic (“switching”); or (3) stop regulating
sources). After this valuation, the action substep altogether (“stopping”). As long as the action out-
activates the goal to use a particular strategy (e.g., puts of the three emotion regulation stages (identi-
response modulation). Here too, there are many fication, selection, and implementation) continue
points at which emotion dysregulation may occur. to minimize discrepancies between one’s emotion
At this point, the activated strategy is still a and current goal, the system will continue to engage
somewhat abstract representation of the individual’s in regulation. However, if the initially selected
desired end state. Thus, activation of the implemen- action substep does not produce expected results
tation stage allows a person to translate a general (e.g., anxiety is increasing or sufficient progress is
strategy (e.g., response modulation) into specific not being made), a person may consciously or
Abstract
Emotion regulation and dysregulation often unfold within interpersonal contexts. Parent–child
relationships provide early scaffolding of emotion regulation processes. Parents attune to, and
influence, their children’s emotions, through pathways such as physical touch, infant cry, facial
expressions, and stress physiology. Interpersonal emotion regulation and dysregulation processes
continue to evolve within other close relationship contexts such as romantic couple relationships in
adulthood. Partners shape each other’s emotion regulation through stress contagion and physiological
interconnection, and through interactions that can be conflictual or supportive. This chapter reviews
the theoretical foundations and the existing literature describing how emotion regulation and
dysregulation take place within interpersonal relationships.
141
interpersonal emotional regulation and dysregula- language help facilitate the child’s socioemotional
tion has focused on dyads. We begin by describing development, even when the baby is too young to
interpersonal emotion transmission processes understand language (Rimé, 2009), and encourages
within parent–child dyads, including modalities bonding between infant and caregiver (Rilling,
such as touch, cry, facial expressions, and physiol- 2013). Over time, a baby learns that emitting cer-
ogy. We then move to the literature on adult couples tain emotional cues to others will elicit helping be-
and describe research on couple conflict and couple havior and facilitate getting their needs met. The
support. Finally, we conclude with recommenda- baby will also learn that certain others, especially
tions for further research. caregivers, are safe foundations, thereby creating an
enduring attachment. A healthy child learns that he
What Is Interpersonal Emotion Regulation or she can take risks, explore his or her environ-
and Dysregulation? ment, and return swiftly to his or her safe caregiver
Emotion regulation refers to the process of altering to return to a baseline emotional state.
one’s own or another’s emotional states, typically to Vital to this interpersonal process of emotion
reach a desired outcome (Gross & John, 2003; regulation is the caregiver’s ability to interpret the
Ochsner & Gross, 2005; Zaki & Williams, 2013). child’s emotional cues, respond appropriately, and
For example, two adults in a relationship might hug use affiliation rather than avoidance when an infant
and console each other when one partner is upset exhibits distress (Bowlby, 1969; Shaver & Klinnert,
about a troubling interaction at work. A parent may 1982; Dykas & Cassidy, 2011; Rilling & Young,
attempt to calm a crying infant by picking the baby 2014). The adult must be able to accurately process
up and rocking him or her back and forth. A pair of emotional cues and regulate his or her own emo-
athletes may hype each other up for competition. tions while also attending to the child’s needs
All of these are arguably adaptive interpersonal pro- (Rilling & Young, 2014; Rutherford, Wallace,
cesses that facilitate emotion regulation during chal- Laurent, & Mayes, 2015). A caregiver who struggles
lenging experiences. However, what happens when with emotion dysregulation or who has a history of
interpersonal dyadic processes are characterized by disrupted attachment relationships may struggle
emotion dysregulation? Perhaps adults in a relation- to scaffold his or her infant’s emotion regulation
ship direct their stress at each other through arguing (Dykas & Cassidy, 2011; Shah, Fonagy, & Strathearn,
instead of consoling; a parent yells at the child to 2010). Attachment researchers hypothesize that in-
stop crying instead of using touch to comfort; or dividual differences in caregiver responses to distress
athletes deflate each other’s confidence and readi- may act as a mechanism underlying transmission
ness to compete. Each interpersonal process has the of attachment patterns from caregiver to child.
potential to facilitate or hinder adaptive emotion Caregivers may be over- or underresponsive to their
regulation. Here, we review processes of interper- child’s distress, leading to intrusive or indifferent re-
sonal regulation and attunement within specific sponses instead of healthy reciprocity and syn-
types of social relationships, beginning with the chrony (Dykas & Cassidy, 2011; Feldman, 2012a).
parent–child relationship context. Interpersonal emotion regulation may begin to
occur during the transition to parenthood and early
The Role of Affiliative Bonds in Emotion postpartum period via biobehavioral feedback loops
Regulation: The Parent–Child Relationship between caregivers and infant (Feldman, Gordon,
Newborn babies are reliant upon caregivers for Schneiderman, Weisman, & Zagoory-Sharon,
physical, social, and emotional needs. Newborns 2010; Rutherford et al., 2015). Research has linked
have yet to develop language abilities and thus use mothers’ prenatal emotion dysregulation to the
emotional expression to elicit support for getting child’s behavioral functioning at three years old
their needs met. For example, a hungry baby may (Oberlander et al., 2010). Specifically, mothers who
cry to signal that he or she is hungry. A responsive were struggling with depression and taking antide-
caregiver can then meet the child’s needs by trying pressant medication during their third trimester
to decipher and respond to the newborn’s emotional were more likely to have children with internalizing
signal. With the crying baby, the caregiver may problems in early childhood. Furthermore, mothers
speak to the baby in soothing tones or pick the baby with depression in the third trimester who were also
up, providing physical contact intended to help the depressed three years postpartum had children with
baby. This use of physical contact, attention, and higher rates of externalizing symptoms (Oberlander
Abstract
Over the past two decades, emotion dysregulation—defined as the inability to dampen strong
emotional responses in the service of goal-directed behavior—has emerged as a consistent,
transdiagnostic vulnerability to psychopathology. Although specific forms of dysregulated emotion vary
across disorders (e.g., exuberance, anger, and related approach emotions in externalizing disorders;
anxiety, panic, and related avoidance emotions in internalizing disorders), deficits in dampening
emotional responses help define many psychiatric conditions. Peripherally, emotion dysregulation is
often marked by low tonic (resting) parasympathetic nervous system (PNS) activity, as indexed by
respiratory sinus arrhythmia (RSA). In fact, hundreds of studies conducted to date have found low RSA
across diverse forms of psychopathology (e.g., anxiety disorders, autism spectrum disorder, conduct
disorder, depression, panic disorder, psychotic disorders). Associations between psychopathology
and RSA reactivity to laboratory tasks are less consistent. However, wide variability in tasks and
psychophysiological methods may explain some of these inconsistencies. This chapter provides an
updated summary of this literature, ending with discussion of methodological issues.
153
hormonal assays, and neuroimaging made objective 2007; McLaughlin, Rith-Najarian, Dirks, &
assessment of emotion possible, producing a rich Sheridan, 2015) among children, adolescents, and
literature in which emotional states are quantified adults. We focus specifically on literature in which
and studied systematically (e.g., Cicchetti & RSA—measured at rest or in response to emotional
Rogosch, 2012; Crowell et al., 2017; Hajcak, challenge—is used to evaluate emotion dysregula-
MacNamara, Foti, Ferri, & Keil, 2013; Lapate et al., tion among those with various forms of psychopa-
2017). As a result, research on emotion regulation thology. We note that this literature is extensive and
and dysregulation has flourished in the 21st century cannot be reviewed comprehensively in a single
(Adrian, Zeman, & Veits, 2011). chapter. In fact, in a recent meta-analysis on RSA
As articulated by authors throughout this reactivity in psychopathology, an initial literature
volume, emotion regulation (ER) comprises bio- search yielded over 4,000 articles (Beauchaine et al.,
logical, cognitive, social, and behavioral processes 2018). Our goal here is to summarize major find-
that shape and modulate one’s experience and ex- ings. After doing so, we outline key methodological
pression of emotions in the service of adaptive, goal- issues critical to research assessing RSA, before dis-
oriented behaviors (see Thompson, 1990, 1994). cussing future directions for research on RSA as a
However, despite the importance of ER for adaptive biomarker of emotion dysregulation.
human function, quantifying emotion regulatory
processes becomes problematic if we attempt to do Respiratory Sinus Arrhythmia and Emotion
so by inferring emotion regulation from the absence Dysregulation
of maladaptive behaviors and emotional reactions RSA refers to cyclic, respiratory-linked variation in
(see Cole, Martin, & Dennis, 2004; Ramsook, heart beats, as quantified in the R-R interval time
Cole, & Fields-Olivieri, this volume). In contrast, series (see Figure 12.1; Berntson et al., 1997; Zisner
emotion dysregulation—defined as experiences and & Beauchaine, 2016). RSA can be indexed in several
expressions of emotion that interfere with adaptive, ways (see Shader et al., 2018), all of which capture
goal-directed behavior (see Beauchaine & Gatzke- high-frequency heart rate variability (HF-HRV).
Kopp, 2012)—is often easier to quantify through Given appropriate stimulus conditions and quanti-
direct observation (e.g., Beauchaine, 2015b; Cole fication, HF-HRV indexes parasympathetic-linked
et al., 2013). Strong emotional reactions can be ob- inhibitory influence on cardiac activity and reactiv-
served and measured in laboratory settings via be- ity (Beauchaine, 2001; Berntson et al., 1997;
havior observation and physiological reactivity, and Grossman, Karemaker, & Wieling, 1991; Ritz,
depending on context, self-reports. Most contem- 2009). Full explanation of RSA quantification is
porary research uses multiple measures, including beyond the scope of this chapter; interested readers
behavioral, psychophysiological, and/or neural, to are referred to recent, comprehensive reviews
examine correlates and mechanisms of emotion dys- (Laborde, Mosley, & Thayer, 2017; Shader et al.,
regulation, particularly emotional reactions that are 2018; Zisner & Beauchaine, 2016).
experienced too intensely and/or too enduringly to
be adaptive (Beauchaine, 2015b; Beauchaine & Foundational Theoretical Models
Bell; Brown, Conradt, & Crowell; Jazaieri, Uusberg, Although a few studies appeared before the 1990s,
Uusberg, & Gross; Leshin & Lindquist; Martin, research on RSA as a peripheral biomarker of emo-
Zalewski, Binion, & O’Brien; Speed & Hajcak; tion regulation and dysregulation began in earnest
Rappaport, Hawn, Overstreet, & Amstadter; following a foundational paper by Porges, Doussard-
Stoycos, Corner, Khaled, & Saxbe; Thompson & Roosevelt, and Maiti (1994), who linked RSA spe-
Waters, this volume). cifically to emotion regulatory processes. This paper
In this chapter, we summarize current litera- was soon followed by Porges’s (1995) elaborate theo-
ture on respiratory sinus arrhythmia (RSA) as a retical model in which he presented a phylogenetic
peripheral, physiological biomarker of emotion reg- account of brainstem development that distin-
ulation and dysregulation. RSA has been quantified guished between a reptilian “vegetative” branch and
in literally thousands of studies designed to evaluate a mammalian “smart” branch of the vagus nerve.
emotional processes and their relations to typical According to Porges, the vegetative vagus, shared by
and atypical development (see, e.g., Shader et al., both reptiles and mammals, is mediated by the
2018), vulnerability to adversity (e.g., El-Sheikh, dorsal motor nucleus (DMNX) and produces heart
Harger, & Whitson, 2001), and existing psychopa- rate slowing (bradycardia) during orienting re-
thology (e.g., Beauchaine, Gatzke-Kopp, & Mead, sponses. In contrast, the smart vagus evolved in
R R R R R R
T T T T T
P P P P P P
Q Q Q Q Q
Q
S S S S S S
Figure 12.1 Time series of heart beats collected from a standard electrocardiogram (ECG). QRS complexes, P-waves, and T-waves
are marked. Respiratory sinus arrhythmia indexes periodic lengthening and shortening of R-R intervals across successive breathing
cycles.
mammals, is mediated by the nucleus ambiguus in each case, deficient top-down inhibition of the
(NA), and provides for rapid mobilization responses subcortex by one or more functional subdivisions of
in contexts of environmental challenge. Porges con- the PFC is observed. This suggestion is supported
tended that moment-to-moment vagal modulation by neuroimaging findings of altered functional con-
of cardiac activity is a precondition for evolution of nectivity between (1) specific subcortical (striatum)
complex social behaviors among mammals, since and cortical structures (e.g., dorsolateral PFC, ante-
fight/flight (F/F) reactions need to be inhibited to rior cingulate) implicated in externalizing disorders
engage effectively with friendly conspecifics. In a and (2) specific subcortical (amygdala) and cortical
series of papers, Porges invoked the “vagal brake” structures (e.g., ventrolateral PFC, ventromedial
metaphor to describe inhibitory functions on car- PFC) implicated in internalizing disorders (for
diac output of the PNS, especially during social in- recent reviews, see Beauchaine, 2015b; Beauchaine
teractions (e.g., Porges, 1995, 2007). & Zisner, 2017; Heatherton, 2011; Tone, Garn, &
Although Porges’s (1995, 2007) phylogenetic ac- Pine, 2016).
count of PNS function has been debated (e.g., Thayer and Lane (2000) introduced neurovis-
Grossman & Taylor, 2007), polyvagal theory ush- ceral integration theory (NIT), which specifies a
ered in a new generation of research on physiological neural network through which PFC function regu-
markers of ER and emotion dysregulation (see lates RSA. According to NIT, a central autonomic
Appelhans & Luecken, 2006; Beauchaine, 2001; network—including the ventromedial PFC and an-
Beauchaine & Zisner, 2017). Porges’s perspective terior cingulate cortex—provides top-down regula-
provided researchers with a mechanistic theory from tion of cardiac function via the vagus nerve. Since
which to launch studies linking RSA to emotion reg- 2000, Thayer and colleagues (e.g., Thayer, Hansen,
ulatory processes across development, including as- Saus-Rose, & Johnsen, 2009) have elaborated and
sociations between RSA and psychopathology. extended NIT in a series of pharmacologic blockade
and neuroimaging studies. These studies demon-
Contemporary Theoretical Models strate associations between resting RSA and perfor-
Since publication of Porges’s (1995, 2007) theory, mance on executive function tasks that recruit the
considerable elaboration on likely neural substrates PFC, including sustained attention and continuous
of RSA has emerged. Much of this research links performance tasks (see Beauchaine & Thayer, 2015).
RSA to prefrontal cortex (PFC) function, with Thus, understanding associations between RSA and
brainstem nuclei outlined by Porges serving as the psychopathology may help elucidate transdiagnos-
final common pathway of efferent neural traffic tic neural underpinnings of psychopathology and
from the PFC to the heart (e.g., Thayer & Lane, treatment response. RSA is of course easier to meas-
2000). According to this perspective, low RSA and ure than central nervous system function in diverse
emotion dysregulation—both of which are ob- contexts, and with clinical and developmental sam-
served in many forms of psychopathology—emerge ples who have difficulty participating in neuroimag-
from insufficient top-down cortical (PFC) modula- ing studies.
tion of subcortically generated affective responding Although further validation of NIT is needed,
(see Beauchaine, 2015a, 2015b). Although emo- support for the hypothesis that RSA activity and
tional predispositions differ across subtypes of psy- reactivity fall at least in part under prefrontal con-
chopathology (e.g., anxiety, fear, panic, anger, etc.), trol has emerged. For example, in a recent review
0.02
PSD (s2/Hz)
0.01
0.15Hz 0.33Hz
0
0 0.1 0.2 0.3 0.4 0.5
Frequency (Hz)
Figure 12.2 Spectral density plot of heart rate variability collected from a typical 4-year-old. Given normal respiration rates in this
age range, respiratory sinus arrhythmia (RSA), which indexes parasympathetic nervous system (PNS)-linked cardiac activity—is
captured by the frequency band spanning 0.33 and 0.50 Hz. Above 0.50 Hz, there is no appreciable spectral power. Below 0.33 Hz,
spectral power is not respiratory related, and therefore not PNS linked. Note that when an adult respiratory frequency of 0.15 Hz is
used, excess noise is added to the RSA estimate, as indicated by the double-headed arrow (see text for details). Frequency (Hz) is
plotted along the x-axis, and power spectral density is plotted along the y-axis. Reproduced from Shader et al. (2018) with permission
from Cambridge University Press.
an estimate of RSA. Notably, however, children to and exceeding 10 minutes are often most effective
breathe much faster than adults, so the high- for minimizing physiological arousal (e.g., Jennings,
frequency band must be adjusted to capture RSA Kamarck, Stewart, Eddy, & Johnson, 1992). When
accurately (see Figure 12.1). Since preschoolers re- a resting state is not achieved, baseline RSA is
spire at over twice the rate of adults, this is not a -underestimated, which in turn underestimates
trivial concern (Zisner & Beauchaine, 2016). RSA reactivity to subsequent tasks, since reactivity
To date, many studies have used respiration is quantified as baseline minus task. Such effects
bands appropriate for adults when quantifying RSA are especially important to minimize in psychopa-
among preschoolers, middle schoolers, and adoles- thology research. For example, failure to collect
cents. This results in overestimates of resting RSA true baseline RSA data from participants who
and underestimates of RSA reactivity (Shader et al., arrive at the lab anxious or angry may result in
2018). Although specific implications for our underestimates of both resting RSA and RSA
understanding of RSA–emotion regulation and
reactivity.
RSA–psychopathology relations across develop- In research with children, it is common to use al-
ment are not fully clear, literature-wide biases in ternative baseline conditions in which participants
estimates of RSA and RSA reactivity may exist, es- engage in minimally demanding tasks, such as color
pecially for younger samples. At the very least, this detection (Jennings et al., 1992), or watch quiet, age-
adds measurement error to existing data, which appropriate videos (e.g., Sulik, Eisenberg, Silva,
could explain some null findings. Spinrad, & Kupfer, 2013). These approaches follow
from common assumptions that children with inter-
Measurement Issues nalizing or externalizing disorders cannot tolerate true
Several additional measurement issues should be baselines, or that young children, regardless of their
considered when collecting and interpreting RSA level of functioning, cannot tolerate true baselines.
data. Among these, baseline conditions during Notably, however, even moderate levels of attention
which resting RSA is assessed stand out as particularly allocation alter RSA (see Beauchaine, 2001).
important. As a general rule in psychophysiology Accordingly, true baselines are preferred. Although
research, resting, tonic measures should be collected 10 minutes is long for young children, even pre-
following a movement- and stimulus-free baseline schoolers with ADHD tolerate five-minute base-
condition that is long enough to induce a resting lines well given the novelty of lab visits (e.g., Crowell
but wakeful state (Obrist, 1981). These are often re- et al., 2006).
ferred to as “true” baselines and are designed to Finally, in our recent meta-analysis we
minimize effects of endogenous and exogenous (Beauchaine et al. 2018) found that adherence to
stressors on resting physiological activity. Extensive standards set forth by the Task Force of the European
research indicates that extended quiet baselines up Society of Cardiology and the North American
Conclusion
References
In this chapter, we summarize literature indicating Adrian, M., Zeman, J., & Veits, G. (2011). Methodological
that resting RSA marks emotion regulation capac- implications of the affect revolution: A 35-year review of
ity, and excessive RSA reactivity marks in vivo emo- emotion regulation assessment in children. Journal of
tion dysregulation. We also review socialization Experimental Child Psychology, 110, 171–197.
Åhs, F., Sollers, J. J., Furmark, T., Fredrikson, M., & Thayer, J. F.
mechanisms through which emotion dysregulation
(2009). High-frequency heart rate variability and cortico-
develops and is maintained. Because emotion dys- striatal activity in men and women with social phobia.
regulation is a transdiagnostic feature of many psy- NeuroImage, 47, 815–820.
chiatric disorders, low resting RSA is often observed Aldao, A., Nolen-Hoeksema, S., & Schweizer, S. (2010).
among those with psychopathology. Although the Emotion-regulation strategies across psychopathology:
A meta-analytic review. Clinical Psychology Review, 30,
literature is more mixed regarding RSA reactivity,
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we discuss a number of potential explanations for Alkon, A., Boyce, W. T., Davis, N. V., & Eskenazi, B. (2011).
heterogeneity of findings, including diversity of Developmental changes in autonomic nervous system resting
eliciting tasks, clinical versus nonclinical nature of and reactivity measures in Latino children from 6 to 60
samples, methods used to quantify RSA, and preci- months of age. Journal of Developmental and Behavioral
Pediatrics, 32, 668–677.
sion of measurement.
Appelhans, B. M., & Luecken, L. J. (2006). Heart rate variability
Existing literature demonstrates that RSA is a as an index of regulated emotional responding. Review of
useful measure for assessing emotion regulation and General Psychology, 10, 229–240.
dysregulation, especially when used with data col- Asmundson, G. J., & Stein, M. B. (1994). Vagal attenuation in
lected across other levels of analysis (e.g., self-report, panic disorder: An assessment of parasympathetic nervous
system function and subjective reactivity to respiratory
informant report, behavior observation, dyadic in-
manipulations. Psychosomatic Medicine, 56, 187–193.
teractions). In fact, most contemporary studies of Balzarotti, S., Biassoni, F., Colombo, B., & Ciceri, M. R. (2017).
emotion regulation and dysregulation use multiple Cardiac vagal control as a marker of emotion regulation in
measures (see Beauchaine, 2015b). Although we do healthy adults: A review. Biological Psychology, 130, 54–66.
not recommend inferring emotion dysregulation Baroncelli, L., Braschi, C., Spolidoro, M., Begenisic, T., Sale, A.,
& Maffei, L. (2010). Nurturing brain plasticity: Impact of
solely from RSA, physiological measures provide
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since they are objective. Beauchaine, T. P. (2001). Vagal tone, development, and Gray’s
Given the heterogeneity of findings for RSA motivational theory: Toward an integrated model of
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as a physiological index of emotion regulation and
Beauchaine, T. P. (2012). Physiological markers of emotion and
dysregulation. We assert that such abandonment behavior dysregulation in externalizing psychopathology.
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Abstract
Emotion dysregulation is a common feature of many psychological disorders. To date, however, most
research evaluating emotion regulation has been limited to self-report assessments. Event-related
potentials (ERPs) are well suited to disentangle discrete aspects of emotional processing that are
critical to understanding both healthy and aberrant emotional functioning. This chapter focuses on
a particular ERP component, the late positive potential (LPP), and reviews evidence that the LPP
is modulated by emotional content and is sensitive to various emotion regulation strategies. Next,
studies leveraging the LPP to examine individual differences in emotional processing in the context
of psychopathology are reviewed. Finally, this chapter discusses methodological limitations of past
research and current gaps in our understanding, including suggestions for future research using ERPs
to study emotion dysregulation.
Keywords: event-related potential, late positive potential, emotion, regulation, depression, anxiety,
trauma, substance use
167
Clore, 2002). Thus, it is necessary to use multimethod many other psychophysiological measures (Breiter
assessments that leverage different dependent meas- et al., 1996; Codispoti & De Cesarei, 2007; Codispoti,
ures to more comprehensively assess emotional pro- Ferrari, & Bradley, 2006, 2007), potentiation of
cesses and their regulation. LPPs to emotional relative to neutral stimuli does
Meaningful changes in emotional processing not habituate over repeated presentations (Codispoti
occur rapidly, and electrocortical measures derived et al., 2006; Levinson, Speed & Hajcak, in prepara-
from event-related potentials (ERPs) are an ideal tion). It has been proposed that the LPP indexes
method for studying neural correlates of emotional sustained attention and engagement with emotional
processing (Weinberg, Ferri, & Hajcak, 2013). ERPs content (Hajcak, MacNamara, & Olvet, 2010;
represent near-instantaneous event-locked activity Hajcak & Olvet, 2008; Hajcak et al., 2011; Weinberg
of large and synchronous neural populations— & Hajcak, 2011b).
which is ideal for quantifying rapid changes in A variety of motivationally salient stimuli elicit
brain activity. In fact, ERPs can be used to track LPPs, such as emotional scenes, faces, and words
neural changes in response to emotional stimuli on (Cuthbert et al., 2000; Dillon, Cooper, Grent-‘t-
a millisecond-by-millisecond basis, making it pos- Jong, Woldorff, & LaBar, 2006; Eimer & Holmes,
sible to effectively isolate and quantify core aspects 2007; Schupp, Cuthbert, et al., 2004; Speed,
of emotion reactivity and emotion regulation. Levinson, Gross, Kiosses, & Hajcak, 2017). In
Furthermore, compared to other neuroimaging addition, emotional modulation of LPPs appear to
techniques, ERPs are relatively inexpensive, have be independent of perceptual features of stimuli, in-
few contraindications, and are well tolerated in cluding size (De Cesarei & Codispoti, 2006), and
both young and old populations. other perceptual characteristics (Bradley, Hamby,
Several distinct ERPs are modulated by emotional Low, & Lang, 2007). Previous work indicates that
stimuli, such as the P200 and the P300 (Carretie, emotional modulation of LPPs reflects the emo-
Hinojosa, Martin-Loeches, Mercado, & Tapia, 2004; tional intensity of stimulus content, and is not due
Crowley & Colrain, 2004; Huang & Luo, 2006; merely to stimulus novelty, perceptual differences,
Lifshitz, 1966; Mini, Palomba, Angrilli, & Bravi, or expectation violations. Emotional modulation of
1996; Naumann, Bartussek, Diedrich, & Laufer, the LPP is subject to genetic influence (Weinberg,
1992; Schupp, Junghöfer, Weike, & Hamm, 2004). Venables, Proudfit, & Patrick, 2015), and thus,
Although these ERPs appear to index early attention magnitude differences in LPPs may specify a herita-
to salient information, they are not well suited to ble biomarker of individual differences in emotional
capture changes in emotional responses that result processing. It is important to note that psychometric
from emotion regulation. Accordingly, we focus on evaluations of LPPs to emotional scenes and adjec-
the late positive potential (LPP), which can be used tives indicate good test–retest reliability and internal
to assess both emotional processing as it unfolds over consistency, supporting its appropriateness for the
time and emotion regulatory processes. Although study of individual differences in emotional proc-
the LPP has been used to study individual differences essing (Auerbach, Bondy, et al., 2016; Codispoti
across various psychiatric disorders, we focus on the et al., 2006; Moran, Jendrusina, & Moser, 2013).
most commonly examined disorders, including de- Unlike many more transient ERPs, emotional
pression, anxiety, substance abuse/dependence, and modulation of LPPs is sustained throughout stimu-
posttraumatic stress disorder. lus presentation (i.e., for several seconds; see Hajcak
et al., 2010) and can be observed for as long as 1,000
The Late Positive Potential: From ms after stimulus offset (Hajcak & Olvet, 2008).
Emotional Reactivity to Regulation The time course of LPPs supports the argument that
The LPP is a positive deflection maximal at central- emotional content not only captures but also holds
parietal midline recording sites that begins by 200 attention (Vuilleumier, 2005). Spatially, LPPs appear
ms after stimulus onset (Foti, Hajcak, & Dien, to shift over the course of emotional processing,
2009). As depicted in Figure 13.1, the LPP is poten- beginning with a parietally maximal distribution
tiated by emotional (e.g., pleasant, unpleasant) that progresses to a centrally maximal distribution.
compared to neutral stimuli, and the LPP magnitude This “frontalization” may suggest that earlier
remains potentiated for the duration of stimulus versus later segments of LPPs reflect separable com-
presentation (Cuthbert, Schupp, Bradley, Birbaumer, ponents (Foti et al., 2009; Hajcak et al., 2011;
& Lang, 2000; Hajcak & Olvet, 2008; Hajcak, MacNamara, et al., 2009). Indeed, earlier segments
Weinberg, MacNamara, & Foti, 2011). Unlike of the LPP (300 to 600 ms) appear to represent
Amplitude (µV)
5
10
15 Pleasant
Neutral
Unpleasant
20
Pleasant-Neutral –3 Unpleasant-Neutral
+2
+7
+15
Figure 13.1 Top: Grand averaged event-related potential (ERP) waveforms at electrode site CPz elicited during passive viewing
of pleasant, neutral, and unpleasant pictures. Picture onset occurred at 0 msec. Negative voltage changes are plotted as upward
deflections. Bottom: Voltage maps for pleasant minus neutral and unpleasant minus neutral comparisons at t = 700 msec. The figure is
based on data collected by Hajcak and Nieuwenhuis (2006).
more automatic processing of emotional content, example, studies that use open-ended (i.e., nonspe-
whereas later segments (600 ms and beyond) may cific) instructions to reduce the intensity of negative
represent more deliberative engagement with stimu- emotions show that LPPs to unpleasant pictures are
lus content (Olofsson, Nordin, Sequeira, & Polich, attenuated during regulation relative to control
2008; Weinberg & Hajcak, 2011b; Weinberg, conditions (Krompinger et al., 2008; Moser et al.,
Hilgard, Bartholow, & Hajcak, 2012). Previous re- 2006). In an evaluation of effects of cognitive reap-
search demonstrates that the duration of LPPs can praisal on LPPs, Hajcak and Nieuwenhuis (2006)
be manipulated using instructions that encourage demonstrated that LPP magnitude was substan-
participants to maintain previously viewed stimuli tially reduced when participants were instructed to
in working memory, supporting the argument that reinterpret unpleasant pictures using cognitive re-
more sustained aspects of LPPs index intentional appraisal relative to when participants were in-
engagement with emotional stimuli (Hajcak et al., structed to simply attend to unpleasant picture
2010; Thiruchselvam, Hajcak, & Gross, 2012). content (see Figure 13.2). Furthermore, reduction
Critically, LPPs are sensitive to various emotion in LPP amplitude during reappraisal was correlated
regulation strategies, making them ideal for study- positively with reductions in self-reported emotional
ing individual differences in emotion regulation intensity following reappraisal. Parvaz, MacNamara,
(Foti & Hajcak, 2008; Hajcak & Nieuwenhuis, Goldstein, and Hajcak (2012) found similarly that
2006; Krompinger, Moser, & Simons, 2008; Moser, LPPs in response to unpleasant pictures were re-
Hajcak, Bukay, & Simons, 2006; Thiruchselvam, duced following instructions to use cognitive
Blechert, Sheppes, Rydstrom, & Gross, 2011). For reappraisal compared to unpleasant pictures that
0
Amplitude (µV) +2
10 +7
15
0 500 1,000 1,500 2,000 +15
Time (msec)
Reappraise Attend
Figure 13.2 Left: Grand averaged event-related potential (ERP) waveforms at electrode site CPz associated with unpleasant pictures
during cognitive reappraisal (solid line) and focused attention (dashed line). Picture onset occurred at 0 msec. Negative voltage changes
are plotted as upward deflections. Shaded gray areas represent 100-msec windows in which the reappraise late positive potential (LPP)
differed reliably from the attend LPP. Right: Voltage map for the attend minus reappraise comparison at t = 700 msec. The figure is
based on data collected by Hajcak and Nieuwenhuis (2006).
were viewed normally. This effect appears to be when faces were presented in unattended locations.
independent of methodological differences across Extending these findings, Eimer, Holmes, and
studies, such as how (visual vs. auditory) and when McGlone (2003) found that LPPs are potentiated
(before vs. after picture onset) reappraisal instruc- to faces displaying six basic emotions (angry, dis-
tions are provided (Hajcak & Nieuwenhuis, 2006; gusted, fearful, happy, sad, and surprised) relative to
Parvaz et al., 2012). For instance, one study pro- neutral, but only when faces are the focus of direct
vided auditory reappraisal frames before picture attention (see also Keil, Moratti, Sabatinelli,
viewing (i.e., “preappraisal”) and found that LPPs Bradley, & Lang, 2005). These findings are poten-
were reduced in response to unpleasant pictures tially important, since shifting spatial attention is a
that followed neutral descriptions, compared to relatively common and effective strategy for regulat-
LPPs elicited by unpleasant pictures that fol- ing emotion. For example, when instructed to de-
lowed negative descriptions (Foti & Hajcak, crease emotions to unpleasant images, participants
2008). Replicating and extending these findings, frequently look at unimportant or nonemotional
MacNamara and colleagues (2009) found that areas of pictures—and such changes in gaze account
LPPs were potentiated when neutral pictures were for significant variance in brain activity as assessed
preappraised in negative terms, demonstrating by functional magnetic resonance imaging (fMRI;
that effects of appraisal on LPPs are not specific to van Reekum et al., 2007). Similarly, LPP magnitude
unpleasant pictures. Furthermore, cognitive reap- is reduced when participants’ gaze is directed to
praisal attenuates LPPs when participants view low-arousal aspects of unpleasant pictures com-
words linked to negative autobiographical memo- pared to when their gaze is directed to high-arousal
ries (Speed et al., 2017. This suggests that cognitive parts of pictures (Dunning & Hajcak, 2009;
reappraisal is an effective strategy in reducing LPPs Hajcak, Dunning, & Foti, 2009). Thus, volitional
elicited by idiographic stimuli. Together, these redirection of spatial attention appears to be an ef-
findings illustrate that changing the meaning of an fective strategy for altering LPP magnitude during
emotional stimulus, via reappraisal or preappraisal, processing of visual emotional information. These
can alter amplitudes of LPPs. findings suggest that altering the meaning of or
In addition to cognitive reappraisal, manipulations modifying attention to an emotional stimulus can
of visual attention can effectively modulate LPPs. modify the magnitude of LPPs.
For example, when pictures of neutral or fearful Emotional modulation of LPPs can be observed
faces were presented in attended locations during a in children as young as 5 years (Hajcak & Dennis,
spatial attention task, participants demonstrated a 2009), making it possible to study developmental
potentiated LPP to fearful relative to neutral faces changes in emotional processing over the lifespan.
(Holmes, Vuilleumier, & Eimer, 2003). However, the Evaluations of developmental differences reveal that
effect of emotion expression on LPPs was eliminated younger (18 to 26 years) and older (60 to 77 years)
Abstract
Affective neuroscience, the study of neural mechanisms that give rise to emotional experiences in
humans and animals, has a short but rich history. Almost three decades old, affective neuroscience
has predominantly taken two theoretical approaches to understanding the brain bases of human
emotions, and thus, two stances on the brain bases of emotion dysregulation. One approach, the
traditional approach, argues that specific emotions are hardwired in human biology with specific
neural underpinnings or signatures for said emotions. The second approach, a psychological constructionist
approach, argues that each experienced emotion emerges not from a specific, dedicated anatomical
circuit, but from an interplay of broad networks in the brain that are involved in general operations of
the mind. This chapter provides an overview of these two theoretical approaches with a specific focus
on functional magnetic resonance imaging (fMRI) findings. It concludes with evidence suggesting how
emotion dysregulation may arise and links this work to clinical fMRI investigations of anxiety disorders.
It closes by suggesting future directions affective neuroscience may take to better understand processes
underlying dysregulated emotions.
183
networks that is situation specific and individually localization to subcortical and other structures
different. Taking a constructionist approach, we (unlike EEG, MEG, and fNIRS). Subcortical struc-
discuss evidence of how dysregulation within these tures play a key role in most theories of emotion
networks may result in dysregulation of emotions. (e.g., Damasio et al., 2000; MacLean, 1949;
We begin our chapter by describing terms and Panksepp, 2016; Panksepp & Watt, 2011; cf. Kober
concepts. Next, we outline the two theoretical et al., 2008) and fMRI can image these deep brain
approaches that have guided neuroimaging research structures—often with high spatial resolution
on emotion for the past 25 years: the traditional, (Satpute, Wager, et al., 2013). In contrast, EEG,
anatomically given circuit-based view and the TCE. MEG, and fNIRS offer exceptional temporal reso-
With these theoretical perspectives in mind, we lution and are therefore better suited for answering
discuss what affective neuroscience suggests about questions about “when” activation occurs during
mechanisms underlying human emotion and its the experience of emotion. Temporal dynamics of
dysregulation. We conclude with evidence suggesting neural processing are surely of interest to emotion
how emotion dysregulation may arise, and link this researchers, and more research is needed in this area
work to clinical investigations of anxiety disorders. (see, e.g., Heller & Casey, 2016; Lee, Lindquist, &
Although we recognize there are myriad ways that Nam, 2017; Waugh, Hamilton, & Gotlib, 2010). As
emotion dysregulation affects well-being, behavior, we note later, some recent evidence on network
and psychopathology, we focus specifically on these properties of brain activation using fMRI combines
disorders for illustrative purposes. We close by sug- spatial and temporal domains by examining se-
gesting future directions that affective neuroscience quences of regional brain activation during emotions.
may take to better understand processes underlying Next, we define what we mean by “emotion,” as
dysregulated emotions, conceptually linking the the term is used differently among psychologists/
constructionist approach to other recent attempts neuroscientists, clinicians, and practitioners—and
to identify basic processes that underlie multiple even among affective neuroscientists. We differenti-
disorders (e.g., the Research Domain Criteria [RDoC] ate between what we call “emotions” and “affect.”
approach; Insel, 2014). Whereas “emotions” describe discrete experiences of
specific states, as named with words such as “sadness,”
Terms and Concepts “fear,” and “anger,” (often called “discrete emotions”;
This chapter is about neuroimaging of emotion Keltner, Ekman, Gonzaga, & Beer, 2003), “affect”
dysregulation, but we should first clarify how we is used to describe more general feelings that range
use the terms “neuroimaging,” “emotion,” and in positivity–negativity and activation–deactivation
“dysregulation.” In general, “neuroimaging” refers (see Barrett & Bliss-Moreau, 2009; Barrett, 2016;
to any technology that allows researchers to create Lindquist, 2013; Russell, 2003). We consider affect
images of neural structure or function. In this chap- as constitutive of emotions insofar as affect is a basic
ter, we review the literature on human functional “ingredient” that underlies all emotional experiences
neuroimaging—technologies that generate images of (i.e., all emotions can be described as having
neural processes related to mental states among live, some degree of pleasantness–unpleasantness and
waking human subjects. We focus specifically on activation–deactivation; Barrett & Bliss-Moreau,
functional magnetic resonance imaging (fMRI), 2009; Lindquist, 2013; Lindquist, Wager, Kober,
which assesses changes in blood oxygenation to Bliss-Moreau, & Barrett, 2012; Lindquist, Satpute,
estimate blood flow to specific regions of the brain Wager, Weber, & Barrett, 2016; Russell, 2009).
while humans experience mental states (e.g., fear). Finally, we describe our definition of emotion
Blood flow reflects corresponding changes in activity dysregulation, which is largely but not fully consistent
(both excitation and inhibition) to neural populations with the definition used throughout this volume
in brain tissue (see Logothetis, 2008). Although (i.e., patterns of emotional experience and/or
there are other methods of functional neuroimaging expression that interfere with goal-directed behavior;
(e.g., positron emission tomography [PET], electro- see Beauchaine, 2015b). By some definitions, dys-
encephalography [EEG], magnetoencephalography regulation is the opposite of regulation. Yet regulation
[MEG], functional near-infrared spectroscopy is used differently throughout the emotion and
[fNIRS]), we focus on fMRI for two reasons. First, affective neuroscience literature. In affective neuro-
most recent neuroimaging studies of human emo- science, research on regulation often refers to explicit
tion use fMRI because it does not require injection attempts by an individual to control or change his
of radioactive tracers (like PET) and affords good or her emotions (Gross & Thompson, 2007). There
Abstract
Given the critical role that emotion dysregulation plays in many psychiatric disorders, there is a need
to understand the biological underpinnings of emotion regulation deficits. This chapter opens with a
brief overview of emotion regulation and constructs that fall under its broad umbrella. Next, it provides
a brief primer of behavioral genetic research methods, summarizes existing literature regarding the
heritability of emotional dysregulation, provides an overview of molecular genetic research methods,
and reviews extant molecular genetic literature on emotion regulation. Finally, the chapter reviews the
limitations of existing research and identifies promising areas of future inquiry that may clarify the
underlying structure of emotion dysregulation and identify the role of common genetic loci in associations
between emotion dysregulation and psychopathology.
Affective experiences characterize much of human Wirtz, Svaldi, & Hofmann, 2014; Bylsma, Morris,
life and influence behavior. Memorable events are & Rottenberg, 2008; Mennin, Heimberg, Turk, &
characterized by particularly significant shifts in Fresco, 2002; Tull & Roemer, 2007) and external-
affect (e.g., a wedding, death of a loved one). izing conditions (see Mullin & Hinshaw, 2007;
Moreover, the effects of emotionally charged events Shader et al., 2017). Moreover, emotion regulatory
are felt and expressed after the events (e.g., the hon- deficits clarify points of convergence and distinction
eymoon, loss of a loved one). Notably, altered affective between highly comorbid conditions (e.g., Mennin,
experiences characterize most psychiatric conditions Holaway, Fresco, Moore, & Heimberg, 2007;
(American Psychiatric Association, 2013) and confer Mennin, McLaughlin, & Flanagan, 2009; Rappaport,
risk for clinically relevant behaviors. For example, Moskowitz, & D’Antono, 2014, 2017). Such findings
influential conceptualizations of substance use highlight the importance of understanding influences
(Khantzian, 1985; Wills, Pokhrel, Morehouse, & on emotion regulation, both genetic and environ-
Fenster, 2011), alcohol use (Bolton, Robinson, & mental in nature.
Sareen, 2009), nonsuicidal self-injury (e.g., Klonsky Given the centrality of emotion to psychiatric
& Muehlenkamp, 2007), suicide (Johnston et al., disorders, theories regarding the nature of affective
2017), aggression (Davidson, Putnam, & Larson, experiences and resulting efforts at modulating
2000), and disordered eating behavior (Harrison, them have been a central focus of psychology since
Sullivan, Tchanturia, & Treasure, 2010) emphasize its
inception. As summarized in Gross (1998),
the role of coping with negative affect or augmenting early psychoanalytic theory discussed conscious
positive affect, broadly termed emotion regulation. and unconscious attempts to regulate anxiety or
In fact, emotion regulatory deficits have been asso- general distress conferred by interactions among
ciated with numerous internalizing (e.g., Aldao, the id, ego, and superego (Freud, 1926). As the field
Nolen-Hoeksema, & Schweizer, 2010; Berking, has evolved, so have theories of emotion regulation.
203
In the contemporary adult literature, emotion underpinnings of emotion regulation is important
regulation is often viewed through cognitive and (Beauchaine, 2015b). Although the literature on
behavioral formulations wherein research examines emotion regulation is vast, much remains to be
individual differences in coping behaviors and learned about genetic influences. In this chapter, we
their efficacy (Lazarus, 2000) or cognitive-behavioral use broad definitions of emotion regulation and
approaches to more efficiently downregulate nega- dysregulation, referring to the host of processes—
tive affect (e.g., Linehan, 1993). Child and adolescent conscious, voluntary, or not—through which indi-
researchers often view emotion regulation more viduals influence what emotions they experience,
broadly, defining it as the set processes through when their emotions occur, and how they are ex-
which individuals alter their emotional experience pressed (see, e.g., Cole et al., 2004; Gross, 1998;
and/or expression to achieve goal-directed behaviors Thompson, 1990). Given scant research on the
(e.g., Beauchaine, 2015a; Thompson, 1990). This genetics of emotion regulation, we adopt a broad
definition acknowledges both effortful and auto- interpretation of this definition to select studies for
mated emotion regulation processes (see Cole, review and to provide readers with as complete a
Martin, & Dennis, 2004). basis as possible for understanding this literature.
Gross and colleagues provide an influential Our aims are to (1) provide readers with an overview
framework based on processes of emotional experi- of behavioral and molecular genetic research
ences from an evocative event through attempts to methods, (2) review existing research on genetic
modulate one’s emotional responses (Gross, 1998; and environmental contributions to emotion dys-
Gross & Muñoz, 1995; Gross & Thompson, 2007). regulation, and (3) discuss limitations of the exist-
Their so-called process model of emotion regulation ing literature and propose a framework to guide
describes a sequence of events with potential points future research.
where an individual might intervene to alter his or
her experience (see Figure 4 in Gross, 1998, p. 282). Twin and Family Studies of
For example, one might select or modify a situation Emotion Regulation
to avoid events that evoke negative affect (e.g., in- Overview of Twin and Family Studies
terpersonal conflict) or foster events that evoke Twin and family designs allow researchers to disen-
positive affect (e.g., social interaction with friends). tangle the roles of unique and shared environmental
Additionally, following a positive or negative influences from genetic (i.e., heritable) influences
event, one might attempt to modulate his or her on individual differences (measurable traits), which
physiological-affective response, such as through are referred to as phenotypes. For example, in a sample
shifting attention (e.g., Hakamata et al., 2010) or by of monozygotic twins, dizygotic twins, and/or other
altering his or her cognitive appraisal of the event siblings, between-person variance in emotion regu-
(e.g., Beck, Rush, Shaw, & Emery, 1979). Alternatively, lation can be decomposed into that shared within
one might engage in behavioral strategies to modu- families, which is represented by the correlation
late resulting emotions (e.g., Carver, Scheier, & between twins/siblings/relatives, and residual vari-
Weintraub, 1989). This framework also identifies ance. This phenomenon is, more broadly, referred
possible deficits in successful regulation of emo- to as nonindependence in many other areas of
tional experience. For example, increased reactivity research (see Kenny, Kashy, & Cook, 2006 for
to stress might result from heightened physiological review). To the extent that the trait is heritable, the
sensitivity, impaired attention deployment, or im- correlation between monozygotic twins, who share
paired cognitive reappraisal. Furthermore, difficulties 100% of segregating genes, ought to be larger than
downregulating negative affect may result from im- the correlation between dizygotic twins or siblings,
pairment in initiating emotion regulatory behaviors who share, on average, 50% of segregating genes
or from choosing ineffective regulatory behaviors (Mather, 1949; Mather & Jinks, 1971). Similarly,
(e.g., Berking & Wupperman, 2012; Houben, Van monozygotic twins, dizygotic twins, and siblings
Den Noortgate, & Kuppens, 2015; Kuppens, Allen, share environmental experiences that influence the
& Sheeber, 2010). family (e.g., socioeconomic status, parenting; Jinks
& Fulker, 1970). Therefore, by comparing the corre-
Chapter Aims lation between mono- and dizygotic twins to each
Given the central role that emotion and processes other and to zero, the biometrical model, which is also
involved in emotion regulation play in numerous known as the twin model, can distinguish the pro-
forms of psychopathology, understanding etiologic portion of variance in a phenotype due to heritable
Biometrical Twin and Genetic and environmental contributions to What is the contribution of genetic
Family Models (Single one phenotype are estimated based on known influences (i.e., heritability) to a specific
Phenotype) genetic relatedness (based on gene segregation emotion regulatory deficit (e.g.,
and recombination) and environmental heightened affective intensity)?
relatedness (based on rearing history). What is the contribution, to a specific
emotion regulatory deficit, of
environmental factors within a family?
Biometrical Twin and Known genetic relatedness and/or What is the contribution of common
Family Models environmental relatedness are used to estimate genetic loci to the association of a specific
(Multiple Phenotypes) the magnitude and structure of genetic and emotion regulatory deficit with
environmental contributions to multiple psychopathology?
phenotypes. What is the underlying latent structure of
multiple emotion regulatory deficits based
on common genetic and environmental
influences?
Candidate Gene Genetic information is limited to specific Does this specific genetic allele contribute
Methodology target alleles identified a priori. to a specific emotion regulatory deficit?
Genome-Wide Many alleles across the genome are examined Which genetic alleles contribute to a
Association Study without a priori hypotheses. specific emotion regulatory deficit?
(GWAS)
Polygenic Risk Score Overall genetic liability to a phenotype is What is the aggregate contribution of all
(PRS) estimated by aggregating effects of multiple genetic loci to a specific emotion
genetic loci. regulatory deficit?
What is the overlap in genetic loci
between multiple phenotypes (e.g.,
between a specific emotion regulatory
deficit and psychiatric disorder)?
Linkage Disequilibrium Estimate heritability from the aggregate What is the heritability of a specific
(LD) Score Regression influence of multiple polymorphisms while emotion regulatory deficit?
accounting for LD between multiple
polymorphisms. Estimation is based on
summary statistics rather than raw data.
Univariate Genetic relatedness of participants is What is the contribution of genetic
Genome-Wide estimated based on allelic data across the influences (i.e., heritability) to a specific
Complex Trait genome. Genetic relatedness is used to emotion regulatory deficit (e.g.,
Analysis (GCTA) estimate heritability of a single phenotype. heightened affective intensity)?
Bivariate/Multivariate Similar to univariate GCTA, genetic What is the contribution of common
GCTA relatedness of participants is estimated based genetic loci to the association of a specific
on allelic data across the genome. However, emotion regulatory deficit with
genetic relatedness is used to estimate psychopathology?
heritability of multiple phenotypes and the What is the underlying latent structure of
contribution of common genetic loci to the multiple emotion regulatory deficits based
correlation between phenotypes. on common genetic and environmental
influences?
Molecular Genetic Studies of Emotion 2000), only molecular genetic studies can identify
Regulation specific genetic variants (alleles) that account for
Overview of Molecular Genetics heritable risk. Before reviewing the relevant litera-
Although twin and family studies can determine the ture, we provide a very brief introduction to the rel-
heritability of a phenotype (e.g., Sullivan et al., evant terminology in molecular genetic research.
Abstract
Emotion dysregulation is a pervasive clinical problem that likely emerges from complex Gene ×
Environment interactions across development. Epigenetic processes provide a molecular basis by
which genotype interacts with the environment across the lifespan to produce phenotype.
Epigenetics is defined by molecular processes occurring on and around the genome that regulate
gene activity without changing DNA sequence. This chapter describes how epigenetic mechanisms
are assessed and provides a brief review of current research on epigenetics, emotion dysregulation,
and associated disorders. It then highlights four biological pathways of interest, the serotonin,
dopamine, and norepinephrine systems and the limbic-hypothalamic pituitary adrenal (L-HPA) axis,
and argues that, to advance understanding of the pathophysiology of emotion dysregulation,
biological pathways rather than single genes must be measured. The chapter describes challenges for
the field of epigenetics and how novel methods could be leveraged to overcome those challenges.
221
a wide range of psychiatric conditions for which Histone modification occurs when histone proteins
emotion dysregulation is a central feature. Here we bind to molecules in the cell, which causes the DNA
examine a subset of biological pathways that give to uncoil, creating an open chromatin structure
rise to physiological dysregulation among individu- (Moore, 2015). Transcription factors are proteins
als who exhibit emotion dysregulation. Currently, that translate genetic information gathered from the
there are two common methods for studying epige DNA itself (A, C, T, G) to messenger RNA. This
netic associations with psychological constructs: process is called transcription and is the first step in
candidate epigenetic and epigenome-wide associa- transformation of genes to proteins. Transcription
tion studies. We briefly discuss the merits and limi- factors are critical links for understanding how
tations of these approaches and suggest a more epigenetic processes affect phenotypes. A central hy-
novel pathway-oriented method for analyzing epi pothesis of epigenetic research is that transcription
genetic bases of emotion dysregulation. We focus factor binding sites on a gene, which tend to be in
specifically on the dopamine system, the serotonin areas of the gene where many cytosines and gua-
system, and the limbic-hypothalamic-pituitary- nines cluster together, are critical for uncovering
adrenal (L-HPA) axis—all of which are implicated how environmental events induce (i.e., “regulate,”
in emotion dysregulation. When relevant, we also “activate,” “turn on,” “silence”) gene expression. When
discuss other neurotransmitter systems. DNA uncoils, transcription factors become more
accessible, thereby increasing expression of the gene
Epigenetics (Jones, 2012). Histone modification is unstable and
Epigenetic processes are studied by extracting seems to fluctuate randomly (Wang et al., 2012).
DNA and examining chemical modifications that These modifications are difficult to study in humans
reside “above” (epi) the DNA itself (genetic). because of this instability, so they are not examined
Nuclei of all cells contain chromosomes composed often in human behavioral epigenetic research.
of DNA. DNA sequence is set at conception and, Genomic imprinting is a regulatory mechanism
in the absence of an extreme environmental event that leads to imbalanced expression of one or more
(e.g., radiation exposure), does not change. DNA among about 400 genes (Baran et al., 2015). In this
comprises a sugar and phosphate molecule and case, rather than epigenetics acting as an environ-
four nucleotides: adenine, thymine, cytosine, and mentally induced alteration of gene structure, the
guanine (A, T, C, G). These are arranged in base alteration is inherited. In both cases, molecular in-
pairs (e.g., TA, GC), which form rungs of the formation is telling the DNA information to act
DNA double helix. Single nucleotide polymor- differently depending on the cell type in which it is
phisms (SNPs) are DNA sequence variations that manifest (Greally, 2018). Modification occurs in
occur when nucleotide base pairs differ between either DNA or histones of one parental gamete
members of a species (see Figure 16.1). Active genes (maternal or paternal), which results in the opposite
code for expression of different proteins, which parental gene copy being expressed (Barlow &
affects structural and functional outputs of diverse Bartolomei, 2014). In some cases, the extent of ex-
body systems. These structural and functional pression depends on the gene’s parental origin. For
outputs (e.g., height, mood, personality) make up example, a gene inherited from the mother may be
observable phenotypes. Thus, DNA is an instruction fully expressed, but when the same gene is inherited
manual for our bodies. from the father, it is partly expressed (Flint, 1992).
If extended, DNA from a single human cell Disease severity may therefore vary, depending on
(double helix) would be about three meters long— which parent the gene is inherited from. For exam-
the length of a car. For DNA to fit within each ple, when an individual inherits Huntington’s dis-
nucleus, it is wound tightly around proteins called ease from his or her father, age of onset is much
histones (Carey, 2013). This complex of DNA and earlier than when inherited from his or her mother
histone proteins makes up chromatin (Moore, 2015). (Bird, Caro, & Pilling, 1974; Boehnke, Conneally,
A change in chromatin structure, called chromatin & Lange, 1983; Myers, Madden, Teague, & Falek,
remodeling, forms the basis for a wide range of epi- 1982; Newcombe, Walker, & Harper, 1981). In
genetic mechanisms, the three most common being many genes, chromosomes that come from the
histone modification, genomic imprinting, and DNA mother or the father are indistinguishable. However,
methylation (Lester, Marsit, Conradt, Bromer, & there are cases where epigenetic marks distinguish
Padbury, 2012). chromosomes as coming from a female or a male.
These chromosomes do not function in the same promoter region of a gene, where gene expression
way. For example, the first developmental disorder is controlled. The promoter is a region of DNA
to be recognized as fundamentally epigenetic was that is involved in transcription, and it is marked
Prader-Willi syndrome, which is conferred through by a particular sequence of nucleotides. Cytosine
a missing segment on the 15th paternal chromo- and guanine clusters are called CpG sites (for
some. This area normally produces important small cytosine–phosphate–guanine). Regions on the gene
nuclear RNAs (snRNAs), and without this section, with several clusters of CpG sites are called CpG
these snRNAs are not produced. In typically devel- islands. DNA methylation occurs when a methyl
oping individuals, the corresponding segment on group attaches to a cytosine that is part of this
the maternal chromosome is imprinted and, thus, CpG site. Consequently, addition of this methyl
not expressed. When the paternal gene is not pres- group in the context of a CpG island usually blocks
ent, the maternal gene is unavailable to compensate gene transcription, thereby inhibiting activity of the
for the missing paternal one (Moore, 2015). Histone gene (Charney, 2012). It is important to note that
modification and genomic imprinting are important DNA methylation does not always lead to “gene
epigenetic mechanisms that have been understudied silencing.” When DNA methylation takes place on
in the behavioral epigenetics literature relative to regions other than the promoter, such as the gene
DNA methylation. body, gene expression may be stimulated.
To understand DNA methylation, it is important The assumption that DNA methylation results
to note that nucleotides (A, T, C, G) do not cluster in durable changes to human behavior is tenuous.
randomly on a gene. Rather, C tends to precede G In fact, we do not expect that individual differences
in repetitive patterns that typically occur in the in DNA methylation in one or even 20 CpG sites
Abstract
As described in the literature for many years, a sizable number of children with hyperactive-impulsive
and combined subtypes/presentations of attention-deficit/hyperactivity disorder (ADHD)—especially
males—progress to more serious externalizing syndromes across development. Such outcomes
include oppositional defiant disorder, conduct problems, delinquency, substance use disorders, and in
some cases antisocial personality disorder, incarceration, and recidivism. This chapter summarizes a
developmental model that emphasizes different contributions of trait impulsivity, a highly heritable,
subcortically mediated vulnerability, versus emotion dysregulation, a highly socialized, cortically
mediated vulnerability, to externalizing progression. According to this perspective, trait impulsivity
confers vulnerability to all externalizing disorders, but this vulnerability is unlikely to progress beyond
ADHD in protective environments. In contrast, for children who are reared under conditions of
adversity—including poverty, family violence, deviant peer influences, and neighborhood violence/
criminality—neurodevelopment of prefrontal cortex structure and function is compromised, resulting
in failures to achieve age-expected gains in emotion regulation and other forms of executive control.
For these children, subcortical vulnerabilities to trait impulsivity are amplified by deficient cortical
modulation, which facilitates progression along the externalizing spectrum.
237
for much of the covariation among first-order adulthood for a preponderance of individuals
factors (behavioral syndromes). First-order exter- (Biederman, Petty, Evans, Small, & Faraone, 2010),
nalizing syndromes include constructs such as im- progression to more severe externalizing outcomes
pulsivity, aggression, delinquency, and substance is not foregone. Our ontogenic process perspective on
use, which map closely onto DSM-5 disruptive externalizing progression focuses on relative contri-
behavior and antisocial personality disorders. In butions of different but interconnected neural sys-
contrast, first-order internalizing syndromes include tems to (1) expression of hyperactivity-impulsivity, as
constructs such as anxiety, depression, and with- manifested very early in life by those with ADHD,
drawal, which map closely onto DSM-5 depressive versus (2) emotion dysregulation, as expressed in-
and anxiety disorders. This factor structure is ob- creasingly across development among those with
served in large population-based and twin studies; in ADHD who progress to delinquency and antisocial
child, adolescent, and adult samples; in male, behavior (Beauchaine & McNulty, 2013; Beauchaine
female, and mixed samples; and across self-, parent, et al., 2017; McDonough-Caplan & Beauchaine,
and teacher reports of symptoms (Achenbach & 2018). According to this perspective, subcortical
Edelbrock, 1983, 1991; Caspi et al., 2014; Lahey, vulnerabilities to impulsive behavior are expressed
Van Hulle, Singh, Waldman, & Rathouz, 2011; as ADHD during and even before the preschool
Lahey, Krueger, Rathouz, Waldman, & Zald, 2017; years. This impulsivity may be amplified or molli-
Lahey et al., 2014; Olino, Dougherty, Bufferd, fied by trajectories in cortical neuromaturation that
Carlson, & Klein, 2014; Tackett et al., 2013).1 unfold later in development. In protective environ-
The remarkable consistency of this factor structure ments, developmentally normative cortical neuro-
suggests there may be transdiagnostic etiological maturation results in effective emotion regulation,
influences on what were once seen as distinct
yielding lifelong persistent ADHD (i.e., “regulated”
disorders (see, e.g., McDonough-Caplan, Klein, & impulsivity). In contrast, in high-risk environments,
Beauchaine, 2018). Although elucidating transdiag- compromised cortical neuromaturation results in
nostic influences on internalizing disorder etiology emotion dysregulation and progression to more
is important, we do not consider internalizing dis- severe externalizing behavior across development
orders further in this chapter. Rather, a major goal (i.e., “unregulated” impulsivity). As outlined later, this
of our research is to specify transdiagnostic vulner- interpretation is consistent with several observations
abilities to externalizing spectrum disorders (see concerning vulnerability to delinquency among boys
Beauchaine & Hinshaw, 2016). Ten years ago, the with ADHD who are reared in high-risk environ-
notion of common liability to externalizing disor- ments (e.g., Lynam et al., 2000; Meier, Slutske,
ders enjoyed limited support. In the last decade, Arndt, & Cadoret, 2008) and with increasingly
however, considerable evidence for shared etiology well-characterized effects of environmental adver-
has emerged, including (1) highly overlapping heri- sity on cortical neuromaturation and self-regulation
tabilities, as indicated in behavioral genetics studies (e.g., Hanson et al., 2010; Luby et al., 2013). We
(e.g., Krueger et al., 2002); (2) common molecular begin by discussing trait impulsivity, which mani-
genetic vulnerabilities (e.g., Gizer, Otto, & Ellingson, fests very early in life as ADHD, as a predisposing
2016); (3) overlapping neural correlates in both sub- vulnerability to all externalizing disorders.
cortical brain regions implicated in impulsivity and
cortical brain regions implicated in poor self-control Trait Impulsivity as a Heritable,
and emotion dysregulation (e.g., Beauchaine, Subcortically Derived Vulnerability
Zisner, & Sauder, 2017); and (4) a well-characterized As already noted, trait impulsivity confers vulnera-
developmental trajectory from severe hyperactivity- bility to all externalizing disorders, beginning with
impulsivity (ADHD) very early in life to later ODD, development of ADHD during and even before the
CD, and eventual antisocial behavior, particularly preschool years (see, e.g., Beauchaine & McNulty,
among affected males (see Beauchaine & McNulty, 2013; Beauchaine et al., 2017). Consistent with
2013; Eme, 2015, 2017; Moffitt, 1993, 2006; Robins, the developmental theory of ADHD set forth by
1966).2 Sagvolden, Johansen, Aase, and Russell (2005), we
It is important to note, however, that many define trait impulsivity as a consistent preference for
hyperactive-impulsive children do not traverse
immediate rewards over larger, delayed rewards;
this developmental pathway to later ODD, CD, failures to plan ahead; and poor volitional control
and antisocial behavior. Even though ADHD is over one’s behaviors. Thus, trait impulsive individuals
highly heritable, with symptoms that persist into have difficulty delaying gratification and suppressing
.70
.60
.55
r = –.57
.50
10.0 10.5 11.0 11.5 12.0 12.5 13.0 13.5
Age (years)
Figure 17.1 Associations between age and orbitofrontal cortex (OFC) gray matter density for typically developing boys (triangles)
versus boys with conduct disorder (circles). Age-expected gray matter reductions are not observed in the conduct disorder group.
Adapted with permission from De Brito et al. (2009).
which is highly heritable (e.g., Nikolas & Burt, 2010; working memory deficits (Hanson et al., 2012).
Thapar, Langley, Owen, & O’Donovan, 2007), most Thus, early-life adversity exerts widespread effects
measures of emotion regulation (ER) yield modest on neurodevelopment in cortical brain regions
heritability coefficients, suggesting significant so- that subserve emotion regulation. In fact, adults
cialization (e.g., Goldsmith, Pollak, & Davidson, who were reared in poverty during childhood show
2008). In fact, considerable research indicates reduced ventrolateral and dorsolateral PFC activ-
that ER, self-regulation, and executive functions on ity and fail to inhibit subcortical responses during
which they depend are shaped strongly across devel- effortful regulation of emotion (Kim et al., 2013).
opment by environmental influences, including Thus, effects of childhood poverty and stress extend
parent–child relationship dynamics, among others well into adulthood, with demonstrated effects on
(e.g., Beauchaine, Hinshaw, & Bridge, in press; ER capabilities. Although associated with altered
Beauchaine & Zalewski, 2016; Bell & Calkins, cortical neuromaturation and development of ex-
2000; Bernier, Carlson, & Whipple, 2010; Smith, ternalizing behavior (e.g., Santiago, Wadsworth,
Calkins, & Keane, 2006; Chapters 8 and 18, this & Stump, 2011), poverty of course is not the gen-
volume). Such findings are unsurprising given a erative mechanism through which either behavior
voluminous literature linking environmental en-
dysregulation or cortical brain development are
richment to PFC structure and function across effected (see Luby et al., 2013). Rather, correlated
development among both animals and humans (see adversities such as compromised parenting, neigh-
Baroncelli et al., 2010; Blair, 2016). borhood violence, deviant peer group affiliations,
In contrast to environmental enrichment, envi- and exposure to substances of abuse are likely
ronmental deprivation exerts profound negative mechanisms (Beauchaine, 2015). Perhaps unsur-
effects on PFC neurodevelopment and function, prisingly, these are the very influences associated with
with direct implications for emerging emotion progression from ADHD in early childhood to more
dysregulation and externalizing behavior (see
severe externalizing behaviors across development.
Beauchaine, 2015). Compared with controls,
children who are physically abused exhibit smaller Environmental Influences on
orbitofrontal cortex volumes than controls, which Externalizing Progression
predict both executive function deficits and social An impressively large literature specifies environ-
difficulties with peers (Hanson et al., 2010). mental risk factors that mediate progression of
Furthermore, poverty and associated stress sup- ADHD early in life to ODD, CD, ASPD, and
press cortical brain growth across childhood similar constructs, including aggression and de-
(Hanson et al., 2013). In turn, PFC structure me- linquency in later childhood, adolescence, and
diates links between early childhood stress and adulthood (Beauchaine & McNulty, 2013;
vulnerability
trait (latent)
trait impulsivity dysregulation
subcortical, cortical, highly
highly heritable socialized
(observed)
behavioral
syndrome
Developmental Period
Figure 17.2 A developmental model of progression along the externalizing spectrum for individuals with ADHD-HI/C (middle
panel, left). Early in life, ADHD behaviors derive largely from trait impulsivity, a highly heritable, subcortically mediated vulnerability
(top panel, left). For those who are reared in adverse contexts, myriad accumulating risk factors (bottom panel) mediate progression
along the externalizing spectrum in part by amplifying emotion dysregulation, a highly socialized cortical vulnerability (top panel,
right). According to this perspective, trait impulsivity confers vulnerability to all externalizing disorders across development (solid
arrows) but interacts increasingly with emotion dysregulation (thickening arrows) and related prefrontally mediated deficits in self-
control as externalizing behaviors escalate (see text; Beauchaine & McNulty, 2013; Beauchaine et al., 2017 for further details).
as a result of interactions between their neurobio- established. Indeed, children and adolescents who
logical vulnerabilities and environmental adversity are reared at or below 1.5 times the federal poverty
are far more likely to traverse a developmental level show widespread reductions in gray matter
pathway characterized by emerging oppositionality, volume compared with their peers, particularly in
conduct disturbance, delinquent behavior, problems frontal regions implicated in self-control (Hair,
with substance use, and in some cases criminality, Hanson, Wolfe, & Pollak, 2015). It is our hope
incarceration, and recidivism. This general devel- that specification of mechanisms will lead to more
opmental pathway has been described in the liter- widespread use of prevention and early interven-
ature for many years (Beauchaine & McNulty, tion programs that are known to improve emotion
2013; Moffitt, 1993; Robins, 1966), yet only re- regulation and reduce externalizing progression
cently has the field begun to elucidate complex (e.g., Beauchaine et al., 2013, in press; Webster-
mediating pathways from early-life ADHD to ad- Stratton, Reid, & Beauchaine, 2013). These pro-
olescent and adult externalizing behavior (e.g., grams therefore hold promise toward offsetting
Beauchaine et al., 2017; Eme, 2015, 2017; Moffitt, neurodevelopmental correlates of affect dysregula-
2006; Raine, 2018). In this chapter, we emphasize tion, failures of executive function, and progressive
that such developmental p rogression results from and therefore costly externalizing outcomes (see,
(1) interactions between subcortical vulnerabilities e.g., Beauchaine, Zisner, & Hayden, 2018).
to trait impulsivity and cortical neural vulnerabilities
to emotion dysregulation, (2) interactions between Acknowledgments
Work on this chapter was supported by grant DE025980 from
neurobiological vulnerabilities and environmental the National Institutes of Health, and by the National Institutes
adversities that shape emotion dysregulation, (3) of Health Science of Behavior Change (SoBC) Common Fund.
cumulative effects of c orrelated environmental risk
factors as they accrue across the lifespan, and Notes
therefore (4) complex developmental processes 1. Latent structural models also yield an even higher (third)-
order general liability factor onto which both externalizing
that cannot be understood fully at any single point
and internalizing factors load. This general liability factor is
in time. These processes eventuate in increasingly beyond the scope of this chapter. Interested readers are
poor top-down regulation of behavior and emo- referred elsewhere (e.g., Caspi et al., 2014; Lahey et al., 2011;
tion, which may be impossible to reverse once well Tackett et al., 2013).
Abstract
249
this research with recent discoveries about internal- paradigms capturing independent manifestations
izing disorders from neuroscience, psychophysiol- of emotion and emotion regulation demonstrate
ogy, genetics, and epigenetics? This review aims to that these processes can be studied separately de-
discuss research focusing on these questions and has spite being closely related (Cole et al., 2004). For
three goals. First, we summarize leading theoretical example, in infants, facial expressions of emotion
perspectives on the developmental origins of and and behavioral indicators of emotion regulatory
potential pathways to emotion dysregulation. Second, strategies such as gaze aversion and self-soothing
we review current methods of assessing emotion can be captured independently from one another.
regulation and dysregulation in children and adoles- Second, studies identifying different neural corre-
cents and highlight some of the most recent findings lates for various emotion regulation strategies such
supporting its role as a specific and potentially causal as cognitive reappraisal and emotion suppression
risk factor that precedes the development of inter- elicited in the laboratory (e.g., Goldin, McRae,
nalizing spectrum disorders. Third, we describe recent Ramel, & Gross, 2008) suggest the utility of de-
research attempting to link emotion regulation/ scribing and classifying various forms of emotion
dysregulation with multilevel processes at neural, regulation to allow for closer mapping of complex
psychophysiological, genetic, and epigenetic levels thoughts and behaviors onto their corresponding
of analysis. Finally, we conclude by providing some neural circuitry.
future directions for research and implications for Another compelling rationale for studying
interventions and the promotion of resilience. We emotion regulation is to understand why and when
adopt a developmental psychopathology framework it goes awry, a phenomenon frequently observed in
(Cicchetti, 1984, 2016) throughout this review be- psychopathology. As mentioned earlier, emotion
cause we believe that understanding normal and ab- dysregulation can be defined as a pattern of emotional
normal trajectories of emotional development experience or expression that interferes with goal-
across childhood and adolescence can yield impor- directed behavior (Beauchaine, 2015a; Beauchaine
tant insights into adult endpoints like severe emo- & Gatzke-Kopp, 2012). Leading theories on the
tion dysregulation and clinical levels of symptoma- development of many types of psychopathology
tology. Furthermore, this developmental approach assign important etiological roles to emotion dys-
can inform decisions on when, where, and how to regulation (Aldao et al., 2010; Behar et al., 2009;
intervene before maladaptive emotional patterns Gotlib & Joormann, 2010; Mennin et al., 2002;
become fully consolidated. Before proceeding with Sheppes et al., 2015). These theories also specify
these central aims, we define the primary concepts different types of emotion regulatory failures as
of interest in this review. being involved in different disorders. For example,
the inability to disengage from negative affect is
Defining the Core Concepts more characteristic of depression (Gotlib &
Despite lingering theoretical disagreements on the Joormann, 2010), whereas overuse of avoidance and
ultimate nature of emotions, many scientists agree suppression of emotion are thought to promote
that emotions are processes that motivate and chronic worry and anxiety disorders (Mennin et al.,
organize behavior (Cicchetti et al., 1995) and that 2002). Although these theories have garnered sig-
they reflect an appraisal of a situation’s meaning nificant empirical support in the last two decades,
for individual well-being (Cole, Martin, & Dennis, an ongoing challenge in this area of research is that
2004). An important realization in research from psychopathology can be a result of problems with
the past two decades is that the qualities of our emotion generation, emotion regulation, or both.
emotional experiences (e.g., valence, intensity, du- Thus, it can be difficult to isolate specific effects of
ration) depend on our ability to modify emotional emotion regulation difficulties in the development
responses to accomplish individual goals, which of psychopathology (Cicchetti et al., 1995; Sheppes
has been termed emotion regulation (Thompson, et al., 2015). However, as we discuss later, there is
Lewis, & Calkins, 2008). The challenge of measuring emerging evidence to suggest a unique and additive
emotion and its regulation as separate processes role of emotion dysregulation in explaining variability
has raised a number of questions about the validity in mental health outcomes, over and above the role
of the construct of emotion regulation (Cole et al., of other constructs such as trait negative affectivity
2004). However, two streams of evidence have and exposure to stressful life events.
provided foundational evidence for the validity In this review, we focus specifically on internal-
and utility of the construct. First, experimental izing spectrum disorders, which are psychological
Patricia K. Kerig
Abstract
This chapter describes theoretical models and empirical research devoted to understanding the a ftermath
of childhood trauma exposure and discusses the value of considering posttraumatic stress from an
emotion dysregulation perspective. After describing definitional controversies in the field related to both
trauma and posttraumatic stress, this chapter summarizes research on the effects of chronic, prolonged,
and repeated traumatic experiences in childhood, such as maltreatment, with particular attention to its
potential to compromise development of adaptive emotion regulation capacities. The role of emotion
dysregulation in leading theoretical models of posttraumatic stress is presented, as well as empirical
research testing the hypothesis that emotion dysregulation represents an underlying developmental
mechanism through which childhood trauma affects functioning over the lifespan. Future directions
include a need for clarification in conceptualization and measurement, further developmental processes
to be considered, and opportunities for translational work to inform intervention efforts.
265
Keane, 2014; Kerig, 2017). Since its inaugural in- a child’s perspective, certain events that do not
clusion in the third edition of the Diagnostic and meet Criterion A, including separation from a
Statistical Manual (DSM-III; American Psychiatric caregiver even under conditions when the child is
Association, 1980), the term “trauma” has become physically safe, a caregiver’s emotional unavailabil-
widely used in the research literature but as applied ity, or failure of a caregiver to protect the child
to a range of diverse types of experiences and out- from dangers, can be experienced as traumatic
comes. Moreover, these definitions have shifted (Bowlby, 1973/1998; Kerig, 2017; Pynoos et al.,
with each revision of the DSM, and appear to be 2009). In Bowlby’s (1973/1998) words, for a child,
shifting further in draft criteria for the forthcom- no stressor “is likely to be more frightening than
ing edition of the International Classification of the possibility that an attachment figure will be
Diseases (ICD) manual (Keeley et al., 2016), in absent or, in more general terms, unavailable when
ways that continue to incite controversy. wanted” (p. 234). Overall, appraisals are key, in
that it is whether individuals find events to be
What Is a “Traumatic” Experience? distressing—and, tellingly for emotion dysregulation
In the DSM-5 (American Psychiatric Association, researchers, whether individuals perceive those
2013), there was an intentional narrowing of the events as disorganizing and overwhelming their
definition of trauma in an attempt to avoid “crite- ability to cope—that determines whether experi-
rion creep” (Kilpatrick, Resnick, & Acierno, 2009). ences will result in psychopathology (Bovin &
Nonetheless, a growing body of evidence indicates Marx, 2011; Kerig & Bennett, 2013). In fact, re-
that, especially among children and adolescents, a search involving youth has found that peritrau-
wider range of experiences precipitate posttraumatic matic distress and disorganization—indicators of
stress reactions than those encompassed within dysregulated emotions—are more powerful predic-
DSM criteria, which are specific to life threat or tors of posttraumatic stress than are the objective
sexual violence. Additional experiences that are characteristics of the event itself, including whether
associated with posttraumatic stress symptoms in it meets the criteria specified in DSM Criterion A
youth include some specifically precluded by the (Bennett, Modrowski, Kerig, & Chaplo, 2015; Bui
DSM-5 definition, such as exposure to upsetting et al., 2010; Giannopoulou et al., 2006; Stallard,
events solely through the media (Gil-Rivas, Silver, Velleman, & Baldwin, 1998; Trickey, Siddaway,
Holman, McIntosh, & Poulin, 2007; Lengua, Meiser-Stedman, Serpell, & Field, 2012; Verlinden
Long, Smith, & Meltzoff, 2005) and anticipated, et al., 2013).
nonviolent deaths of loved ones (Kaplow, Howell, At the same time, a growing body of research is
& Layne, 2014). In addition, studies have identified being devoted to the study of the many interrelated
a wide range of childhood adversities that do not cumulative early-life adversities, including poverty,
meet DSM-5 criteria for trauma but which are as- family dysfunction, and chronic life stress, that
sociated with posttraumatic stress symptoms, in- contribute to allostatic load (McEwen, 2017) and
cluding separations from caregivers, incarceration increase the risk of posttraumatic stress disorder
or deportation of family members, bullying victim- (PTSD), as well as other stress-related mental and
ization, teenage pregnancy, romantic breakups, ju- physical health problems (e.g., Anda et al., 2006;
venile incarceration, and racial discrimination (Chou, Myers et al., 2015; Wang, Shelton, & Dwivedi,
Asnaani, & Hofmann, 2012; Copeland, Keeler, 2017; Willard, Long, & Phipps, 2016). As Shalev
Angold, & Costello, 2010; Costello, Erkanli, Fairbank, (2007) has pointed out, although the DSM and
& Angold, 2002; Flores, Tschann, Dimas, Pasch, & ICD criteria were originally intended to be specific
de Groat, 2010; Holman, Garfin, & Silver, 2014; to catastrophic events, such as wars and disasters,
Idsoe, Dyregrov, & Idsoe, 2012; Lansing, Plante, & “events that do not involve extreme stress can be
Beck, 2017; Nielsen, Tangen, Idsoe, Matthiesen, & perceived by some survivors as threatening and by
Magerøy, 2015; Rojas-Flores, Clements, Hwang others as challenging. . . . Indeed, no one has success-
Koo, & London, 2017; Taylor & Weems, 2009). fully distinguished traumatic from stressful events”
Consistent with cognitive and developmental (p. 92). To date, little empirical research is available
psychology, scholarship in the field of traumatic stress to illuminate whether the phenomenology and un-
appears to support views that what is traumatic is in derlying processes involved are equivalent for life
the eyes of the beholder and, moreover, that what is threat–related events that meet DSM-5’s Criterion
traumatic for young people depends on the child’s- A versus other more chronic and pervasive trau-
eye point of view (Kerig, 2017). For example, from matic stressors, and so this is an issue upon which
Kerig 267
epression, and psychosomatic problems following
d Importantly for the present chapter, many of the
child abuse. key neurobiological functions, structures, and neu-
ropsychological connections that are affected by
Biopsychosocial Processes Underlying childhood trauma are implicated directly in emotion
Childhood Trauma and Emotion regulation. Among studies focusing on childhood
Dysregulation maltreatment, these include executive functions in-
The consequences of traumatic stress have been volving inhibitory control and cognitive flexibility,
conceptualized by many scholars as fundamentally as well as the capacities to identify, interpret, and
composing a disorder of dysregulation (Dvir, Ford, modulate emotions, and to tolerate and downregu-
Hill, & Frazier, 2014; Ford, 2005; Frewen & Lanius, late distress (Cross et al., 2017; McLaughlin, Peverill,
2006; Gray, 1988; Horowitz, 2011). As van der Kolk Gold, Alves, & Sheridan, 2015; Pollak, 2008;
(2006) states: “The lack or loss of self-regulation is Shields, Cicchetti, & Ryan, 1994; Shipman, Zeman,
possibly the most far-reaching effect of psychologi- Penza, & Champion, 2000), in which a shift from
cal trauma in both children and adults” (p. 187). prefrontal cortex–governed to amygdala-dominated
Moreover, dysregulation is seen across multiple de- processing is implicated (Ganzel, Kim, Gilmore,
veloping systems in interaction with one another, Tottenham, & Temple, 2013; McLaughlin et al.,
including cognitive, emotional, self, interpersonal, 2015). The diminutions in executive functions re-
and, underlying and integrating all of these, the bio- sulting from unrelenting trauma exposure have direct
logical (Bremner, 2016). implications for emotion dysregulation in that they
Although a comprehensive discussion of the disrupt necessary underlying capacities for managing
neurobiology of the stress response system is beyond emotions.
the scope of the current chapter, a number of recent
Executive function contributes to emotion regulation
well-articulated primers and reviews of the relevant
by controlling the contents of working memory to
research are available (Bremner, 2016; Cross et al.,
prevent excessive attention to negative thoughts or
2017; Ford, 2009; Koss & Gunnar, 2018; Lupien,
stimuli . . ., shifting to new coping strategies when old
McEwen, Gunnar, & Heim, 2009; McCoy, 2013;
ones are no longer effective . . ., and inhibiting
Rasmussen & Shalev, 2014); in addition, a review of
automatic emotional, behavioral, or cognitive
the biological processes underlying resilience in
responses that do not fit the situation or one’s
the face of traumatic stress can be found in Russo,
goals . . ., such as during cognitive reappraisal.
Murrough, Han, Charney, and Nestler (2012). Briefly,
(Cross et al., 2017, p. 115)
repeated exposure to threat, particularly early in
development, activates the LHPA axis and alters Research on biological sequelae of traumatic stress
regulation of glucocorticoids, including cortisol, exposure encompasses multiple systems, including
which can have toxic effects on the developing brain neuropsychological, neurotransmitter, neuroendo-
(Lupien et al., 2009), particularly through inter- crine, physiological, pro- and anti-inflammatory, and
fering with gene expression, protein synthesis, and immune response systems (McEwen, 2017). Recent
communication between the prefrontal cortex and research also yields a complex set of findings in which
hippocampus (Cross et al., 2017). As summarized dysfunctions across these systems are highly variable
by Rasmussen and Shalev (2014), exposure to across individuals and thus no one biological process
chronic stressors such as maltreatment sensitizes can be pinpointed as a source of vulnerability or pro-
neuronal structures in the amygdala to subsequent tection against PTSD. “Instead, these individually
stimulation by other stressors, compromises prefron- variable and often redundant systems appear to in-
tal cortex functioning through dendritic atrophy, teract in complex ways to facilitate or reduce PTSD
and leads to hyperreactivity in the sympathetic risk and recovery, as well as to influence vulnerability
nervous system and a dysregulated response to envi- to a variety of PTSD comorbid . . . conditions”
ronmental challenges. Brain imaging studies of chil- (Rasmussen & Shalev, 2014, p. 276); consequently,
dren exposed to maltreatment and family violence researchers in the field are called upon to take a
show heightened amygdala activation (McCrory dynamic systemic approach that can account for
et al., 2013; McCrory et al., 2011) and reductions in complex interactions and “deep translational rela-
white mater connectivity, particularly within the tionships between individually v ariable component
ventromedial prefrontal cortex, which, in turn, are neurobiological processes in PTSD” (p. 276).
associated with cortisol attenuation and maladapta- Epigenetic mechanisms also may come into play,
tion (Puetz et al., 2017). with studies of infants, children, adolescents, and
Kerig 269
Gnehm, & Vollrath, 2012; Nugent, Ostrowski, Theoretical Models of Emotion
Christopher, & Delahanty, 2007; Ostrowski et al., Dysregulation in Posttraumatic Stress
2011). In turn, parenting support in the aftermath Although, as noted, PTSD is not the only maladap-
of trauma exposure plays an important protective tive outcome associated with exposure to childhood
role, one that has been examined directly in relation trauma, and not all trauma-exposed young people
to its beneficial effects on children’s capacity to develop psychopathology, theoretical models of
manage emotions (Katz et al., 2012; Shipman & PTSD are useful because they highlight emotion
Zeman, 2001). Significantly, from infancy onward, dysregulation as an essential feature of the disorder.
emotion regulation capacities develop in the con- Although the DSM and ICD list disparate symp-
text of attachment relationships (Calkins & Hill, toms associated with the disorder, a variety of theo-
2007; Cassidy, 1994; Sroufe, 1996), and parents’ retical models have been offered in an attempt to
modeling, provision, and socialization of emotion lend central coherence to these lists by placing them
regulation strategies have a profound effect on those in a dysregulation framework.
of their children (Eisenberg et al., 2003; Grolnick
& Farkas, 2002). Particularly in the case of child Phasic Dysregulation Model
maltreatment, however, when a caregiver also is the One of the seeming internal contradictions to the
source of trauma, children are likely to be exposed PTSD diagnosis is its requirement that individuals
to poor models of emotion regulation and to experi- demonstrate simultaneously symptoms that are dia-
ence insecure and disorganized attachments that metrically opposed such as intrusions and avoid-
promote development of maladaptive self-soothing ance, or numbing and arousal. Horowitz’s (2011)
strategies and increase the likelihood of posttrau- seminal work has proposed that these symptoms are
matic stress reactions (Kobak, Cassidy, & Zir, best understood as representing distinct phases in
2004). For example, in an observational study com- the posttraumatic response cycle, which is organized
paring a sample of physically maltreating and non- around efforts to engage, and resultant failures, in
maltreating mothers, Shipman and colleagues (2000) emotion regulation. Given the aversiveness of the
found that maltreating mothers engaged in more traumatic event and the emotions surrounding it,
invalidation of their school-age children’s emotions attempts at affect suppression, such as avoidance,
and exhibited less supportive emotion coaching; in numbing, and denial, may be an adaptation strategy
addition, mothers’ emotion socialization styles ac- that is effective in the short term. However, efforts
counted for associations between maltreatment and at suppressing strong emotions are ultimately drain-
children’s adaptive emotion regulation skills. ing and difficult to maintain over a longer term; as
Even when the parent is not the source of the the individual’s suppressive coping strategies
trauma, parents may themselves be affected by trau- become exhausted, posttraumatic symptoms such as
matic experiences, whether historically due to their intrusions and arousal begin to break through, once
own childhood traumas, contemporaneously when again prompting attempts at emotion suppression.
they and the child are victims of the same event, or
indirectly when parents are distressed by the fact Overmodulation Versus Undermodulation
that harm has come to their child. Effects of trauma Although the term “emotion dysregulation” often is
on parenting should also be viewed in the context of used to refer to an impaired ability to downregulate
the larger family in which they radiate and cascade affect, scholars studying emotion dysregulation
dynamically among all members of the system have long pointed out that dysregulated emotion
(Kerig & Alexander, 2013). Parents’ own PTSD processing can take two forms: underregulation and
symptoms, distress, and poor affect regulation can overregulation (Cole, Michel, & Teti, 1994). Just as
compromise their parenting and contribute to chil- the inability to moderate emotions contributes to
dren’s dysregulation and maladaptation to traumatic maladaptation, so lack of access and expression of
events (Lambert, Holzer, & Hasbun, 2014; Marsac, emotions appropriate to an experience “interferes
Kassam-Adams, Delahanty, Widaman, & Barakat, with such adaptive functions as affective communi-
2014; Nugent et al., 2007). Research also supports cation in close relationships and successful problem
an intergenerational transmission of vulnerability to resolution” (Cole et al., 1994, p. 85). In this regard,
PTSD, the mechanisms of which appear to be in new thinking in the field of PTSD has focused on
the realms of both shared biology and socialization the role that specific symptoms play in the distress
processes (Leen-Feldner et al., 2013; Yehuda, regulation process, differentiating between those
Halligan, & Grossman, 2001). that represent attempts to overmodulate emotions
Kerig 271
“acquired CU” endorsed elevated levels of emotion psychological patterns among individuals whose
dysregulation, including nonacceptance of emo- PTSD symptoms are reflective of each of these dif-
tions and lack of emotional clarity. These data are ferent forms of defensive reaction (Gray, 2003;
suggestive of the possibility that some traumatized Koutsikou et al., 2014; Lanius et al., 2014).
youth may wear a “mask” of callousness, beneath
which their functioning is better described as unreg- Developmental Trauma Disorder Proposal
ulated than unemotional (Kerig, Bennett et al., One of the most fully developed conceptualizations
2012), or as exhibiting emotional distress rather of trauma as essentially composing a disorder of
than emotion deficit (Skeem, Johansson, Andershed, dysregulation was a proposal presented to the
Kerr, & Louden, 2007). DSM-5 planning committee by a group of leading
developmental psychopathologists who articulated
Defensive Regulation Model the case for a new diagnosis termed Developmental
Gray’s (1988, 2003) model of the stress response Trauma Disorder, or DTD (van der Kolk, Pynoos
system also emphasizes the role of affective and be- et al., 2009). Citing the conceptual foundations laid
havioral dysregulation in PTSD, a disorder that is down by Terr (1991) and Herman (1994), as well as
conceptualized as arising from an overreliance on a decades of subsequent research, the authors pointed
limited set of regulatory strategies that are no longer to a constellation of symptoms displayed consist
adaptive to the situation. Further, Gray proposes ently by children who had undergone complex trau-
that the prototypical stress-related “flight, fight, matic experiences involving disruptions in caregiving
freeze” (and, more recently added, “faint”; Schauer during their early years, in addition to other
& Elbert, 2010) not only represent different types of Criterion A trauma exposures, such as interpersonal
reactions but also can be understood meaningfully violence. Taken singly, these symptoms could be
as hierarchically sequenced, escalating responses for seen as consistent with a wide variety of diagnoses
regulating emotions and behavior in response to spanning both the internalizing and externalizing
threat. The “freeze” response, as seen in posttrau- spectra, and indeed, children with this complex
matic symptoms such as hypervigilance, behavioral trauma history commonly receive a toxic stew of
inhibition, and emotional constriction, may repre- multiple severe psychiatric diagnoses and accompa-
sent an adaptive initial response that allows us to nying major psychotropic medications. However,
limit our exposure to harm and buy time to appraise the authors argued, these symptoms could be law-
our options. If the threat continues, the next stage fully arranged under the umbrella of dysregulation
of escalation in the stress response system is to and viewed as resulting meaningfully from early
engage in “flight,” seen in symptoms such as avoid- developmental processes disrupted by trauma. The
ance. If flight is not possible, the next defensive re- resulting clarity and parsimony, in which a diverse
sponse is to turn and “fight,” represented by PTSD set of symptoms could be understood as arising
symptoms such as arousal, reactivity, and irritability. from a single pathogenic process, would allow for
Should all previous stress response reactions prove a better identification of the associated change
ineffective, and physical evasion is not possible, processes to be targeted by effective treatments
the next stage in the process is “freeze,” defined by (D’Andrea, Ford, Stolbach, Spinazzola, & van der
attempts to leave the scene psychologically, as Kolk, 2012; van der Kolk, 2005).
evidenced by tonic immobility and dissociation. The DTD proposal identified three domains of
A final stage proposed is that of “faint,” in which, dysregulation, involving key developmental pro-
when all else fails, the system shuts down entirely cesses that are disrupted by childhood trauma in the
and consciousness is abandoned to protect the or- absence of a buffering relationship with a reliable
ganism from experiencing unbearable pain directly attachment figure. First, affective and physiological
(Schauer & Elbert, 2010). dysregulation emerges as an inability to modulate,
As Schauer and Elbert (2010) suggest, these pat- recover from, or tolerate strong emotional states;
terns can be understood as emerging from changes disturbances in regulation of bodily functions or
in the biological circuitry involved, moving from physical sensations; and impaired awareness of
sympathetic activation in the early stages of the or capacity to describe emotions or bodily states.
stress response system to parasympathetic activation Second, attentional and behavioral dysregulation
in the latter stages. Consistent with this model, re- may take the form of either preoccupation with or
search also is beginning to emerge showing differ- diminished capacity to recognize threat, as well as
ent neuropsychological, psychophysiological, and maladaptive attempts at self-soothing, self-harm,
Kerig 273
the Difficulties in Emotion Regulation Scale 2009). An advance offered by this research design
(DERS; Gratz & Roemer, 2004), accounts for the was the creation of an emotion dysregulation latent
association between trauma exposure and post- construct containing measures assessing lack of
traumatic stress symptoms (Bennett, Chaplo, emotional awareness and understanding, dysregu-
Modrowski, & Kerig, 2016), nonsuicidal self-injury lated emotion expression, and rumination.
(Chaplo, Kerig, Bennett, & Modrowski, 2015), Research outside the realm of childhood also
and recurrent involvement in law-violating behav- suggests that emotion dysregulation can act as a
ior (Chaplo, Kerig, Modrowski, & Bennett, 2017). vulnerability for the development of PTSD in the
More compellingly, longitudinal studies confirm aftermath of trauma exposure in emerging adult-
the hypothesis that emotion dysregulation acts as a hood. For example, Bardeen, Kumpula, and Orcutt
mediator of the association between trauma expo- (2013) gathered self-report DERS data from a sample
sure and PTSD, as well as other negative outcomes. of college students prior to a campus shooting.
In a study comparing maltreated and nonmal- Preexisting emotion regulation difficulties predicted
treated school-age children followed over the course the emergence of posttraumatic stress symptoms in
of a year, Kim and Cicchetti (2010) found that ne- the immediate aftermath of the shooting and 8
glect, physical abuse, sexual abuse, experiencing months later; moreover, posttraumatic symptoms
multiple forms of abuse, and early onset of abuse reciprocally predicted increased emotion dysregula-
were related to higher emotion dysregulation as tion over time.
rated by summer camp counselors on the Emotion
Regulation Checklist (Shields & Cicchetti, 1998). Facets of Emotion Dysregulation
Further, over time, emotion dysregulation pre- Related to PTSD
dicted peer rejection and externalizing problems, as A variety of measures with varying underlying
measured by peer nominations and teacher reports, conceptualizations of emotion regulation have been
respectively, which, in turn, exacerbated one an- used to study the association between emotion reg-
other’s negative effects. In a subsequent study fol- ulation, dysregulation, and PTSD. For example,
lowing a similar sample over a 3-year period, this Seligowski and colleagues’ (2015) meta-analysis of
research team found that early-onset maltreatment 57 studies of adults identified 12 measures encom-
was associated with emotional lability and negativity passing eight different aspects of emotion regulation:
at age 7, which predicted emotion dysregulation at general emotion dysregulation, acceptance, experi-
age 8; emotion dysregulation was in turn associated ential avoidance, expressive suppression, reappraisal,
with internalizing problems at age 9 (Kim-Spoon, rumination, thought suppression, and worry. Results
Cicchetti, & Rogosch, 2013). In a study focusing across studies showed the largest effect sizes for an
on a community sample of youth followed over association between PTSD and general emotion
5 years, Heleniak, Jenness, Vander Stoep, McCauley, regulation, rumination, thought suppression, and
and McLaughlin (2016) found that self-reported experiential avoidance.
emotional reactivity and deficient emotion regulation Many studies focusing on adults and adolescents
capacities as measured on the Emotion Reactivity with maltreatment histories have operationalized
Scale (Nock, Wedig, Holmberg, & Hooley, 2008) emotion dysregulation through self-reports on the
mediated associations between childhood maltreat- DERS (Gratz & Roemer, 2004), which assesses six
ment and both internalizing and externalizing dimensions: lack of emotional awareness, lack of
problems. emotional clarity, difficulty controlling behavior
Expanding this research to more general life when upset, difficulty maintaining goal-directed
stressors, in a series of studies following a large behavior, nonacceptance of emotions, and limited
community sample of early adolescents over time, access to emotion regulation strategies. Some re-
McLaughlin and colleagues demonstrated that search suggests that, among these facets of emotion
self-reported emotion dysregulation mediated the dysregulation, difficulty maintaining goal-directed
association between stressful life events and youth behavior, difficulty controlling behavior, lack of
aggression (Herts, McLaughlin, & Hatzenbuehler, emotional clarity, and limited access to effective
2012) and internalizing symptoms (McLaughlin & emotion regulation strategies are those most strongly
Hatzenbuehler, 2009). Further, this team found associated with PTSD among adults with histories
that emotion regulation difficulties accounted for of child abuse–related trauma (e.g., Weiss, Tull,
the association between peer victimization and in- Lavender, & Gratz, 2013). In contrast, in a study of
ternalizing (McLaughlin, Hatzenbuehler, & Hilt, detained adolescents with histories of exposure to
Kerig 275
(Lupien et al., 2009), with potentially significant childhood trauma within similar developmental
consequences for emotion dysregulation across the epochs; moreover, many studies of trauma-exposed
lifespan. There also may be sensitive periods for samples find high rates of retraumatization and
brain structures that make them more individually revictimization that make it challenging to deter-
vulnerable to the effects of traumatic stress at par- mine with any specificity which experiences have
ticular points in development; in addition, these potentiated particular posttraumatic reactions
differences in maturation rates may contribute to (Kerig, 2017).
disruptions in coordination and communication
among regions that ordinarily operate as a cohesive Translational Research Opportunities
network in responding to environmental challenges, The enhancement of adaptive emotion regulation
including the hippocampus, prefrontal cortex, and capacities is encompassed within the leading
amygdala (Cross et al., 2017), with clear implica- evidence-based interventions for child and adolescent
tions for emotion regulation capacity. PTSD (Cohen, Mannarino, & Deblinger, 2017).
Another relatively neglected developmental The scaffolding of healthy regulation capacities is
factor concerns the length of time that has elapsed particularly central to interventions developed for
since the traumatic event(s) and at what point in (Ford, 2015; Ford & Russo, 2006; Ford, Steinberg,
the trajectory of the stress adaptation process that Hawke, Levine, & Zhang, 2012) and adapted to
measurements are taken. For example, in the im- (Cohen, Mannarino, Kliethermes, & Murray, 2012)
mediate aftermath of a traumatic event, cortisol youth with complex PTSD/DTD. However, addi-
levels are generally elevated, whereas with repeated tional research deconstructing these treatment ef-
and prolonged childhood trauma exposure, cortisol fects would be valuable to better inform the field
becomes depleted over the course of the transition about the role of emotion regulation in recovery
from childhood to adolescence (Trickett, Noll, from trauma. For example, in a prospective study of
Susman, Shenk, & Putnam, 2010); therefore, adult combat veterans, Boden and colleagues (2013)
measures taken at different time points may present found that self-reported attempts to manage emo-
contradictory pictures regarding the associations tions through suppression, as measured by the
among traumatic stress, neurochemistry, and Emotion Regulation Questionnaire (Gross & John,
psychological symptoms and behavior. Studies of 2003), were associated with higher levels of PTSD
psychophysiology and neurobiological processes initially and that reductions in emotion suppression
involved in childhood trauma generally have been over time accounted for the beneficial effects of
conducted either in the immediate aftermath of cognitive-behavioral therapy on PTSD symptoms.
exposure to discrete stressors (Kirsch, Wilhelm, & Studies showing similar mechanisms of effect for
Goldbeck, 2011) or in an indeterminately variable child treatment components targeting emotion dys-
period afterward in the case of childhood exposure regulation would be of value. In addition, future
to chronic traumas, such as maltreatment (Cross translational research should be guided by new work
et al., 2017); thus, type of trauma exposure and evidencing typologies of posttraumatic response,
timing of posttraumatic response are inextricably which suggest that different interventions may be
entangled. needed to address different underlying processes
A third developmental consideration arises represented by such distinctions as overmodulation
from the developmental psychopathology concept versus overmodulation of emotions. The development
of stage-salient issues, which suggests that trauma’s of a more nuanced understanding of the posttrau-
effects also will differ as a function of the child’s matic response holds promise for the development
emergent capacities and the prevailing develop- of more targeted and effective treatments.
mental tasks that the child is attempting to master
(Becker-Blease & Kerig, 2016; Kerig, Ludlow, &
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Emily Neuhaus
Abstract
Autism spectrum disorder (ASD) is defined by deficits in social communication and interaction, and
restricted and repetitive behaviors and interests. Although current diagnostic conceptualizations of
ASD do not include emotional difficulties as core deficits, the disorder is associated with emotion
dysregulation across the lifespan, with considerable implications for long-term psychological, social,
and educational outcomes. The overarching goal of this chapter is to integrate existing knowledge of
emotion dysregulation in ASD and identify areas for further investigation. The chapter reviews the
prevalence and expressions of emotion dysregulation in ASD, discusses emerging theoretical models
that frame emotion dysregulation as an inherent (rather than associated) feature of ASD, presents
neurobiological findings and mechanisms related to emotion dysregulation in ASD, and identifies
continuing controversies and resulting research priorities.
283
Lack of attention to emotion dysregulation in that interfere with adaptive function (see Beauchaine,
ASD is all the more striking given that behavioral 2015a; Thompson, 1990). Inherent within this view
difficulties such as aggression, irritability, and self- is recognition that expectations for normative
injury are frequent presenting concerns in clinical emotional experiences and displays differ across
settings, and are often the bases from which both development. As expectations of adaptive function
diagnostic referrals for ASD and need for treatment change, both the degree and frequency of dysregula-
arise (Arnold et al., 2003; Lecavalier, 2006). High tion vary greatly over the course of childhood,
levels of behavior and emotion dysregulation some- adolescence, and adulthood among typically de-
times complicate the diagnostic process for children veloping individuals. For instance, developmental
with ASD (Yee & Millichap, 2015), and constitute a expectations for normative “dysregulation” among
leading source of stress for caregivers of children toddlers differ dramatically from those for older
with ASD (Davis & Carter, 2008). As a consequence, children and adults (e.g., Osterman & Björkqvist,
emotion dysregulation is a frequent target of behav- 2010). As a result, terminology and experimental
ioral and pharmacological intervention efforts in both methods related to emotion dysregulation differ
outpatient and inpatient settings, with dramatically across development as well. During infancy and
increased use of psychiatric services relative to indi- childhood, we often interpret behavioral and emo-
viduals without ASD (Croen, Najjar, Ray, Lotspeich, tional reactivity within the context of temperament
& Bernal, 2006). Together, these findings reveal a (e.g., surgency, reactivity, emotional control,
developmental trajectory marked by pervasive yet soothability), and we use these temperamental con-
poorly documented emotion regulation difficulties structs as markers to index (dys)regulation (e.g.,
across the lifespan for many individuals with ASD. Garon et al., 2009; Putnam, Gartstein, & Rothbart,
In this chapter, I call attention to the role of 2006). By school age, measures of broad dimen-
emotion dysregulation in expression of ASD. I begin sions of internalizing and externalizing difficulties
by considering the prevalence and expressions of are informative, with further differentiation into
emotion dysregulation in both core and associated diagnostic categories such as depression or anxiety
features of ASD. Next, I present theoretical models emerging thereafter.
that integrate these findings, review current under- We also recognize that dysregulation can be
standings of emotion dysregulation in ASD across expressed across a range of both time frames and
neurobiological levels of analysis, and highlight levels of analysis, from momentary fluctuations in
current controversies in the literature. I close with a response to particular stimuli (e.g., event-related
discussion of unanswered questions and suggest pri- changes in skin conductance) to relatively
orities for future studies of emotion dysregulation long-standing patterns of behavior that are stable
in ASD. Given the objectives of this volume, my and resistant to change (e.g., personality traits).
focus is explicitly on emotion dysregulation, so I touch Consistent with this variety in expression across
only briefly on emotion regulation. Although disrup- time and levels of analysis, we consider a range of
tions are likely present in both (White et al., 2014), methodological approaches, from molecular genetic
emotion dysregulation is a transdiagnostic trait, and to subjective experience. This inclusive view of
often precedes and necessitates efforts at emotion emotion dysregulation allows for a more compre-
regulation. Emotion dysregulation may therefore be hensive understanding of emotional experience and
more fundamental to our understanding of these expression among individuals with ASD.
concepts in ASD.
Theoretical Perspectives
Terms and Concepts Historically, mental health concerns among indi-
Despite its broad relevance, emotion dysregulation is viduals with developmental disabilities have been
not universally defined, nor is it clearly and consist poorly recognized due to diagnostic overshadowing,
ently differentiated from the emotional variation in which emotional or psychiatric difficulties are
expected in daily life. Here, I conceptualize dysregu- attributed to the identified disability, and conse-
lation as emotional experiences that differ in inten- quently are overlooked as phenomena warranting
sity, valence, duration, or patterns of reactivity when clinical attention (Kerns et al., 2015; Levitan &
compared to same-age peers without ASD. This is Reiss, 1983). These early misconceptions likely im-
by and large consistent with the definition of emo- peded access to necessary mental health evaluations
tion dysregulation used throughout this volume— and care. Fortunately, views have evolved over time,
patterns of emotional experience and/or expression with growing awareness of emotional difficulties
Neuhaus 285
symptoms are better understood as inherent com- of one’s internal emotional states may interact with
ponents of ASD. Several models that assert such atypical thresholds for sensory input, leading to in-
have been articulated, perhaps most comprehensively creased anxiety when internal and external sensory
by Mazefsky and colleagues (e.g., Mazefsky et al., cues are misinterpreted. In support of this model,
2013; Mazefsky & White, 2014), who developed a imaging studies indicate that neural activation in
model of emotion dysregulation as intrinsic to ASD. sensory and limbic regions in response to auditory
In this framework, a number of ASD-related behav- stimuli correlates with parent-reported anxiety
iors may stem from or represent underlying emotion (Green et al., 2013, 2015). Moreover, the relation
dysregulation. For instance, self-injurious behaviors between ASD and anxiety is mediated largely by a
such as head-banging may be nonverbal indicators of latent factor composed of alexithymia, acceptance
emotional lability (Magnuson & Constantino, 2011). of emotional experience, and uncertainty tolerance
Similarly, repetitive motor movements (e.g., body (Maisel et al., 2016).
rocking, hand-flapping) and sensory-seeking behavior Finally, White et al. (2014) propose a model
(e.g., tactile exploration)—both diagnostic criteria grounded in a developmental psychopathology
for ASD—may be manifestations of dysregulation, framework, whereby emotion dysregulation in ASD
efforts to engage in self-soothing, or both (Mazefsky results from a number of different etiological mech-
et al., 2013). anisms, and is then shaped in its expression (e.g.,
Based on these observations, the Mazefsky et al. anxiety vs. aggression) by a range of psychological
(2013) model describes emotion-related symptoms and social-cognitive moderators. In this view, emo-
among individuals with ASD as unique interactions tion dysregulation is conceptualized as a transdiag-
between emotion dysregulation (conceptualized as a nostic trait common to many forms of psychopa-
transdiagnostic feature of psychopathology) and thology, but both its development and its expression
ASD-specific traits, yielding patterns of lability and are shaped by ASD-specific factors such that it is
dysregulation that are phenomenologically distinct intrinsically related to ASD itself. For example,
from individuals without ASD. According to this ASD may be characterized by heightened physiolog-
model, ASD is characterized by altered physiologi- ical arousal (discussed in more detail in the following
cal functioning and reactivity, as well as atypical section), leading to dysregulation that could take
connectivity among neural regions implicated in any number of forms. When coupled with ASD-
emotion regulation, leading to heightened baseline specific deficits in processing of facial and vocal
levels of negative affect. Layered upon this foun- information, perspective taking, and cognitive
dation are ASD-specific cognitive factors such as flexibility, such dysregulation may take the form of
rigidity, perseveration, deficits in social cognition, intense anxiety and avoidance in social settings,
and idiosyncratic triggers for emotional reactions. since peers’ behaviors and comments can appear
Together, these factors produce dysregulation that is unpredictable and sometimes threatening (White
manifested in unique ways, generating many of the et al., 2014). Emotion dysregulation can be further
behaviors frequently observed in ASD (e.g., sensory exacerbated by the ruminative, perseverative cognitive
seeking, repetitive motor movements). This model style often observed in ASD, resulting in frequent
suggests that individuals with ASD exhibit greater and enduring internalizing symptoms (Burrows,
intraindividual variability in their emotional re- Timpano, & Uddin, 2017).
sponses from day to day, yielding a complex and
seemingly unpredictable constellation of emotional Current Methods and Findings
and behavioral symptoms (Mazefsky et al., 2013). All of the models described specify mechanisms of
Other models link behavior and emotion dys- emotion dysregulation across behavioral and neuro-
regulation to core features of ASD, particularly with biological levels of analysis. Consistent with this, a
respect to internalizing symptoms. In one such variety of research methods currently inform our
model, the combination of atypical sensory process- understanding of emotion dysregulation in ASD
ing, alexithymia (inability to identify and describe and reveal a range of possible mechanisms for the
one’s own emotions), and intolerance of uncertainty emotion dysregulation so often observed in the dis-
forms a pathway to emotion dysregulation (South order. Empirical research has only begun to examine
& Rodgers, 2017). Each of these traits is prominent comprehensive models in a coordinated manner,
among diagnostic criteria for ASD, and together may and most studies focus on single biological systems
operate synergistically to produce anxiety symptoms. rather than integrating mechanisms across biologi-
For example, reduced awareness and understanding cal systems. Given this, we organize findings by
Neuhaus 287
they demonstrate greater variability in daily rhythms familial risk for ASD differ from low-risk infants
(Corbett, Mendoza, Abdullah, Wegelin, & Levine, in their patterns of EEG asymmetry at 6 months
2006). Stressors such as blood draws and magnetic of age, with markedly different trajectories of
resonance imaging exams elicit greater increases in asymmetry over the course of the following
cortisol among those with ASD relative to peers 12 months (Gabard-Durnam, Tierney, Vogel-Farley,
without ASD, with higher cortisol peaks that last Tager-Flusberg, & Nelson, 2015). This body of
longer and return to baseline more slowly (Corbett findings suggests that ASD may be characterized
et al., 2006; Spratt et al., 2012). Among those with by altered patterns of left versus right cortical ac-
ASD, atypical cortisol rhythms are associated with tivity, with possible implications for social and
depression, anxiety, irritability, and repetitive be- emotional functioning. Encouragingly, early evidence
haviors (Bitsika, Sharpley, Sweeney, & McFarlane, suggests that patterns of EEG asymmetry among
2014; Hollocks, Howlin, Papadopoulos, Khondoker, children with ASD may be malleable (at least in
& Simonoff, 2014; Lydon et al., 2015; Mikita et al., some regions), and may more closely approximate
2015; Sharpley, Bitsika, Andronicos, & Agnew, that of typically developing children following ap-
2016). Thus, HPA dysfunction is a clear and con propriate intervention (Van Hecke et al., 2015).
sistent correlate of emotion dysregulation in ASD.
Neuroimaging
Electrophysiology A rich literature documents alterations in amygdala
A long history of research in electroencephalography structure and function among those with ASD.
(EEG) links resting-state neural activity with Although tied initially to social (dys)function in
various forms of psychopathology and individual ASD (see Neuhaus, Beauchaine, & Bernier, 2010
differences in emotion dysregulation. Frontal EEG for a review), the amygdala’s role in emotion-related
asymmetry, often computed as ratios of alpha power processes such as evaluating emotional and motiva-
across hemispheres of the brain, tends to be stable tional significance of stimuli, detecting threats, and
over time and is linked to affective style, approach/ identifying emotions is indisputable (Adolphs, 2003;
withdrawal behavior, and motivational tendencies Grelotti et al., 2002). Accordingly, its contributions
(Davidson, 1998; Coan & Allen, 2003). Relatively to emotion dysregulation in ASD are increasingly
greater activity over left frontal regions is associated evident.
with a greater tendency toward approach (and as- From very early in life, the amygdala follows an
sociated positive emotions; Sutton et al., 2005) and atypical developmental trajectory among children
greater trait positive affect (Tomarken, Davidson, & with ASD. Early on, these children display increased
Henriques, 1990), whereas relatively less left frontal amygdala volumes relative to peers without ASD
activity is associated with withdrawal and depressed (Munson et al., 2006; Sparks et al., 2002), which
mood. Associations with anxiety are more nuanced, correspond to symptoms of anxiety and depression
and it appears that greater left asymmetry is associ- (Juranek et al., 2006). During adolescence, amyg-
ated with anxiety in the form of apprehension and dala volumes are similar across individuals with and
worry, whereas right asymmetry correlates with without ASD, but anxiety symptoms correlate with
anxiety in the form of panic-related symptoms and decreased right amygdala volumes (Herrington
heightened physiological arousal (Heller, Nitschke, et al., 2017). By adulthood, overall amygdala volumes
Etienne, & Miller, 1997; Nusslock et al., 2015). are reduced more broadly in ASD (Pierce et al.,
Based on these relations, variations in frontal EEG 2001). Together, these findings indicate a pattern of
asymmetry index individuals’ propensity to anxiety early overgrowth and subsequent deceleration relative
and dysregulated mood (Davidson, 1998; Nusslock to typical development, with effects on internalizing
et al., 2015). behaviors across development (Schumann & Amaral,
Disruptions to typical patterns of EEG asym- 2006).
metry are observed in autism. Among school-age Amygdala function differs in ASD as well.
children with ASD, left frontal asymmetry is asso- Activation in the amygdala is diminished relative to
ciated with better social functioning but also with peers without ASD across a variety of tasks, includ-
greater anxiety and social stress (Sutton et al., 2005). ing emotion discrimination (Critchley et al., 2000)
Left frontal asymmetry is also associated with and viewing of fearful faces (Ashwin, Baron-Cohen,
higher levels of self-reported anger and obsessive- Wheelwright, O’Riordan, & Bullmore, 2007).
compulsive thoughts and behaviors (Burnette Habituation of amygdala activation to neutral and
et al., 2011). Longitudinally, infants at elevated emotional faces is also slower (Kleinhans et al.,
Neuhaus 289
Constantino, 2017; Beauchaine, Neuhaus, Zalewski, traits such as harm avoidance and reward dependence
Crowell, & Potapova, 2011; Zisner & Beauchaine, (Picardi et al., 2015). In addition, principal compo-
2016). Of particular interest with regard to emotion nents analysis reveals that core features of ASD and
in ASD are DA transporter (e.g., DAT1) and recep- emotional/behavioral concerns load onto two inde-
tor (e.g., DRD2, DRD4) genes. As in the general pendent factors—one composed of emotional and
population, various polymorphisms in DAT1 appear repetitive features and one composed of social-
to modulate symptoms of anxiety, depression, and communication difficulties (Georgiades et al.,
hyperactivity among those with ASD (Gadow, 2011). These findings all raise questions regarding
Pinsonneault, Perlman, & Sadee, 2014; Gadow, the degree to which emotional difficulties should be
Roohi, DeVincent, & Hatchwell, 2008). Also as in differentiated from ASD. Nevertheless, consensus
the general population, DA receptor variants are on whether emotion dysregulation constitutes a
associated with parent reports of externalizing
core symptom of ASD awaits additional research on
symptoms such as oppositionality, and internalizing genetic underpinnings, neural mechanisms, covari-
symptoms related to separation anxiety (Gadow, ation with intervention, and developmental time
DeVincent, Olvet, Pisarevskaya, & Hatchwell, course of ASD and associated behavior and emotion
2010; Gadow et al., 2014). Finally, variants in two dysregulation.
genes involved in degrading serotonin and dopamine Even more foundational to understanding
(the monoamine oxidase [MAO-A] and catechol-O- emotion dysregulation is the issue of how best to
methyltransferase [COMT] genes) may confer vul- assess it among individuals with ASD. In this chapter,
nerability to generalized anxiety (Roohi, DeVincent, I review findings from a variety of methods, encom-
Hatchwell, & Gadow, 2009) and social anxiety passing observational, parent-report, self-report,
(Gadow, Roohi, DeVincent, Kirsch, & Hatchwell, neurobiological, and genetic approaches. Yet limita-
2009), respectively, among children with ASD. tions exist with each of these methods, and these
limitations are likely exacerbated by intrinsic features
Unresolved Controversies of ASD. For example, self-reports of emotional
As outlined previously, a primary issue in under- experiences can be limited due to diminished
standing ASD and other psychiatric syndromes emotional insight and self-awareness, unique inter-
concerns disentangling whether emotion dysregula- pretations of physiological cues related to arousal
tion is part and parcel of the disorder or is a largely and emotion, use of idiosyncratic language to un-
independent trait that interacts with core features of derstand and express internal emotional experiences,
disorders to increase functional impairment. The and difficulties with abstract and/or figurative lan-
latter perspective is consistent with recent models of guage (Ben Shalom et al., 2006; Mazefsky et al.
psychopathology that view emotion dysregulation 2013). Parent and teacher ratings of behaviors and
as a superordinate vulnerability that potentiates emotions can be similarly problematic, and discrep-
expression of most any individual difference (e.g., ancies observed between self- and other-report
negative affectivity, social anxiety, impulsivity; see measures are not easily resolved (e.g., Mazefsky et al.,
Beauchaine & Constantino, 2017; Beauchaine & 2013; White, Schry, & Maddox, 2012). Observational
Zisner, 2017). Clinical features such as intense reac- and neurobiological methods circumvent some of
tions to changes in routines or agenda, ritualized or these concerns but require that participants com-
seemingly compulsive behaviors, diminished eye prehend and comply with task instructions, as well
contact, and social avoidance, among others, can as tolerate stressful protocols (e.g., magnetic reso-
stem from core ASD deficits and/or anxiety and nance imaging scans, blood draws) despite commu-
mood disorders. Thus, diagnostic boundaries are nication and sensory challenges.
not clear. Although current estimates indicate that Further complicating this issue is the question of
the majority of individuals with ASD receive a co- whether emotion-related constructs as they are cur-
morbid psychiatric diagnosis, recent research suggests rently conceptualized have equal validity, structure,
that when psychiatric assessment tools are adapted and neurobiological correlates for individuals with
to account for ASD features, rates of “comorbid” and without ASD. For example, factor analysis of a
diagnoses drop dramatically, from nearly 80% to popular questionnaire to assess anxiety disorders,
approximately 50% (Mazefsky et al., 2012). Twin the Multidimensional Anxiety Scale for Children
studies suggest shared genetic and environmental (MASC; March, Parker, Sullivan, Stallings, &
etiologies between ASD and emotional difficulties Conners, 1997), indicates different factor structure
(Tick et al., 2016), and between ASD and personality for children with ASD relative to their nonaffected
Neuhaus 291
need for better assessment of the construct, including and psychological outcomes (Gotham et al., 2015).
methods and instruments that have been developed Indeed, the transition from adolescence to adulthood,
or adapted specifically to improve validity and relia- and the corresponding transition out of pediatric
bility among individuals with ASD (e.g., Mazefsky health care and public education settings, is a critical
et al., 2016). Through these more specialized and turning point for individuals with ASD and their
comprehensive evaluations, we can better parse families (Taylor & Seltzer, 2010). Lack of attention
boundaries between ASD and comorbid condi- to adulthood and later life for individuals with ASD
tions. Because emotion-related processes can occur is particularly disappointing with regard to emotion-
across various timeframes, assessments must span related processes, as their influences are wide-ranging.
timeframes from momentary events (e.g., sudden Whereas internalizing symptoms can decrease over
responses to discrete stimuli) to longer experiences the course of late adolescence, they tend to plateau
lasting weeks or months (e.g., gradual onset of for some adults with ASD, moderated by factors
mood or anxiety symptoms). Given limitations in- such as cognitive ability and family income (Taylor
herent in measurement, multimodal assessments, in & Seltzer, 2010). Among adults with ASD, contin-
which complementary information is gathered from ued psychiatric symptoms in adulthood are associ-
multiple reporters and methods, will likely offer the ated with poorer physical health, increased familial
richest and most comprehensive information. Central stress, and decreased relationship quality for indi-
to this approach will be inclusion of subjective, viduals and their parents (Hartley, Barker, Baker,
self-report information gathered directly from indi- Seltzer, & Greenberg, 2012; Kring, Greenberg, &
viduals with ASD. Despite potential difficulties with Seltzer, 2008). Thus, understanding risk and protec-
emotional insight, first-hand reports offer access to tive factors, mediators, and consequences of emo-
internal psychological and physical processes that tion dysregulation across the lifespan offers promise
are not otherwise accessible, and recognize the unique for improved quality of life across most, if not all,
experiences of each individual. domains of functioning.
On a foundation of solid assessment, a second Ultimately, my goal in writing this chapter was
priority will be to explore vulnerabilities to and risk to highlight the importance of integrating knowl-
factors for development of emotion dysregulation edge regarding emotion dysregulation into concep-
among individuals with ASD. Decades of research tualizations of ASD, by reviewing emerging theo-
within the context of typical development identify retical models of dysregulation and its relation to
familial, environmental, and psychosocial risk factors core features of ASD, considering research findings
through which individuals’ emotional difficulties spanning multiple levels of analysis, highlighting a
are shaped, including coercive escalation within number of unanswered questions, and suggesting
families (Patterson, 1982), trauma and maltreat- areas for continued investigation. Put most simply,
ment (Mead, Beauchaine, & Shannon, 2010), prob- emotion-related symptoms and challenges represent
lematic peer interactions (Snyder et al., 2005), pa- substantial determinants of current functioning and
rental psychopathology (Kaufman et al., 2017), and long-term outcomes for individuals with autism,
many more. Although one might predict that despite falling outside of historically recognized di-
patterns of risk and resilience would hold constant agnostic boundaries for ASD, influencing social,
among individuals with ASD, this cannot be assumed psychological, and educational outcomes. By ex-
without empirical evidence. It may be that the unique ploring these avenues in a comprehensive and
social, cognitive, and behavioral features of ASD integrated fashion, those who study ASD have the
alter relationships between putative risk factors and potential not only to gain a greater scientific under-
emotion-related outcomes, either amplifying or standing of the disorder but also to have positive,
blunting their effects relative to peers without ASD. meaningful, and enduring effects on the lives of
Finally, further understanding of how emotion affected individuals and their families across the
dysregulation influences long-term ASD trajectories lifespan.
across the lifespan will be essential. Originally iden-
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Abstract
Psychosis spectrum disorders (PSDs) are complex, highly heritable psychiatric conditions with high
economic and societal costs. PSDs have historically been conceptualized as neurocognitive disorders in
which psychotic episodes and impairments in social and emotional functioning are attributed to deficits
in neurocognition. Although cognitive pathways play an important role in the etiology and presentation
of PSDs, recent research suggests that interrelations between cognition and emotion are highly
relevant. Moreover, aberrant emotion regulation likely plays a significant role in the presentation of
PSDs. Emotion dysregulation (ED) may underlie and exacerbate both negative and positive symptoms
in PSDs, such as blunted affect, avolition, disorganized speech and behavior, poor social cognition, and
delusions and hallucinations. Advances in measurement of emotion dysregulation—including self-reports,
behavioral paradigms, neuroimaging paradigms, and neurophysiological assessment—have informed
etiological models of emotion dysregulation in PSDs. This chapter reviews research on emotion
regulation and dysregulation in PSDs. Notably, more severe presentations of emotion symptoms and
greater emotion regulation impairments are associated with worse outcomes in PSDs. It may therefore
be the case that focusing on ED as an early risk factor and intervention target could improve outcomes
and prevention approaches for psychotic disorders.
299
even de novo mutations contributing to vulnera- Emotion and Emotion Regulation
bility (Purcell et al., 2009; Ripke et al., 2014). Abnormalities in PSDs
In turn, these vulnerabilities interact strongly with Multiple forms of affective disturbance are observed
environmental risk factors (e.g., Gottesman & in PSDs (van Rijn et al., 2011, Kring & Elis, 2013).
Gould, 2003). Thus, there is significant incentive Abnormalities in emotion, including blunted affect,
for integrative research that targets etiology, pre- heightened negative emotionality, diminished
vention, and treatment strategies for PSDs. positive emotionality (anhedonia), and increased
Three symptom dimensions characterize schizo- emotional reactivity (lability), are well documented,
phrenia and related disorders, including positive, beginning with the earliest descriptions of schizo-
disorganized, and negative symptoms. These occur phrenia and related disorders (e.g., Bleuler, 1950).
at varying levels of severity across affected individuals Notably, affective difference often precedes the
and conditions (e.g., subthreshold schizotypy to onset and diagnosis of PSDs (Kim et al., 2013;
acute psychosis). In sections to follow, we review Meyer et al., 2014; Kimhy et al., 2016), and patients
emotion dysregulation in contexts of these symptom who experience more severe negative symptoms
dimensions. Core positive symptoms of psychosis have poorer prognoses (Mueser Penn, Blanchard,
include delusions and hallucinations, whereas disor- & Bellack, 1997; Milev, Beng-Choon, Arndt, &
ganized symptoms include disordered behaviors, Andreasen, 2005; Gur et al., 2006; Henry et al.,
disorganized thinking and speech, and generalized 2007; Foussias & Remington, 2010). However, re-
cognitive impairments. Negative symptoms include search on the nature of affective disturbance lags
flattened affect, social withdrawal, decreased motiva- behind studies of cognition (Aleman & Kahn, 2005;
tion (avolition), and decreased attention to emotion van der Velde, Opmeer, et al., 2015). Prior to the
(American Psychiatric Association, 2013). Negative DSM-5, schizophrenia was classified as a “nonaf-
symptoms are associated with poorer concurrent fective” psychosis by the American Psychiatric
and long-term functioning, and are particularly Association (1952, 1968, 1980, 1994). These previous
heritable (Piskulic et al., 2012; Kim et al., 2013; classification schemes may have discouraged re-
Meyer et al., 2014; Schlosser et al., 2015). A large search on affect in PSDs by implying that patients’
part of this review will focus on these important, emotional impairments were a reaction to symptoms
emotion-related symptoms. or experiences of schizophrenia, rather than causal
Although diagnostic criteria include affective or core to the disorder. However, advances in
deficits (American Psychiatric Association 2013), affective science (see, e.g., Kring & Moran, 2008;
PSDs have historically been conceptualized as neu- Kring & Caponigro, 2010) have led to a growing
rocognitive disorders, in which psychotic episodes literature on affective experiences and presentations
and impairments in social, cognitive, and emotional of PSD patients.
functioning are attributed to neurocognitive se- It is now recognized that both emotion regulation
quelae. Large effect sizes are observed in differences and emotion dysregulation may be central to
between people with schizophrenia and healthy PSD severity and treatment outlook (Livingstone,
controls on measures of executive function, working Harper, & Gillanders, 2009; Cohen & Minor, 2010).
memory, and attention (for reviews see Heinrichs & Emotion regulation, as used here, is defined as pro-
Zakzanis, 1998; Green, Kern, Braff, & Mintz, 2000; cesses through which individuals monitor, evaluate,
Pantelis & Maruff, 2002). These cognitive impair- and alter their emotional reactions and experiences
ments are also observed to a lesser extent in in the service of adaptive behavior (e.g., Gross, 2002;
first-degree relatives (for reviews see Sitskoom, Thompson, 1990). Although emotion regulation
Aleman, Ebisch, Appels, & Kahn, 2004; Snitz, has been examined as a component of and vulner-
Macdonald, & Carter, 2006). Cognitive pathways ability to many psychiatric disorders (see Aldao,
are implicated in disorganized thinking and behavior, Nolen-Hoeksema, & Schweizer, 2010), emotion
emotional disturbances, and psychotic symptoms regulation paradigms have only recently found a
(e.g., Brewer et al., 2006; Berenbaum, Kerns, Vernon, foothold in PSD research (Livingstone et al., 2009;
& Gomez, 2008a, 2008b, 2008c; Campellone, Elis, Kimhy et al., 2012; Kimhy et al., 2016). In contrast to
Mote, Sanchez, & Kring, 2016). However, addi- the goal-oriented nature of emotion regulation, emo-
tional consideration and awareness of the intersec- tion dysregulation is conceptualized as emotional pro-
tion of cognition and emotion has furthered current cesses that interfere with healthy emotion regulation
understanding of these disorders. and goal-directed behavior (see Beauchaine, 2015).
Abstract
Several decades of scientific research provide strong evidence that individuals who suffer from e motion
dysregulation, such as that observed in depression and anxiety, are more vulnerable to addictive
behavior. Furthermore, a growing body of studies indicates that chronic use of addictive substances
dysregulates emotional responding. Emerging research also suggests that recurrent drug use and addiction
are associated with deficits in the capacity to proactively regulate negative and positive emotions. This
chapter synthesizes evidence from clinical and neuroscientific studies on effects of addictive behavior
(including misuse of prescription opioids, addiction to cigarettes, and addiction to more powerful
stimulants) on emotion dysregulation to outline an integrative model of emotion dysregulation in
addiction. This model has implications for treatment development and further scientific investigation.
313
and methamphetamine use include cardiovascular Howard, 2016; Goesling et al., 2015; Smith et al.,
disease and other major health consequences, 2015; Edlund et al., 2015; Scherrer, Salas, Lustman,
long-lasting impairment in neural systems that gen- Burge, & Schneider, 2015; Goldner, Lusted,
erate positive affect, incarceration, and crime (e.g., Roerecke, Rehm, & Fischer, 2014; Scherrer et al.,
Chang, Alicata, Ernst, & Volkow, 2007; Enns et al., 2014; Gros, Milanak, Brady, & Back, 2013; Merrill
2017). Given the high prevalence rates of and public et al., 2012; Grattan, Sullivan, Saunders, Campbell,
health effects of opioid, cigarette, and stimulant & Von Korff, 2012; Hooten, Shi, Gazelka, &
addiction, we synthesize evidence from extant stud- Warner, 2011; Fatséas et al., 20109). Early preva-
ies of these drugs and present an integrative model lence estimates indicated that 45% of individuals
of emotion dysregulation in addiction—one that with prescription opioid use disorders met full
yields tractable targets for future research and treat- Diagnostic and Statistical Manual of Mental Disorders,
ment efforts. fourth edition (DSM-IV) criteria for a depressive
or anxiety disorder (Sullivan, Edlund, Steffick, &
Dysregulated Emotions Increase Unutzer, 2005). A more recent survey of over
Vulnerability to Addictive Behavior 26,000 respondents indicated that approximately
Substance use is negatively reinforcing through 80% of individuals who engage in nonmedical use
temporary alleviation of distressing emotions of prescription opioids experience depression and
(Baker, Piper, McCarthy, Majeskie, & Fiore, 2004). anxiety (Green, Black, Grimes Serrano, Budman, &
Such down-regulation of negative affect may increase Butler, 2011). Notably, however, opioids themselves
risk of addictive behavior. An early articulation of have depressive effects, so without longitudinal data
this notion was outlined in the self-medication that include direct assessment of opioid use as a
hypothesis, which posits that individuals with dis- means of self-medication, it is difficult to discern
positional impairments in their capacity to regulate whether dependence and nonmedical use of opi-
psychological distress may be prone to relieve that oids are causes, correlates, or consequences of nega-
distress through substance use (Khantzian, 1997). tive affect.
The self-medication hypothesis posits that specific In the largest longitudinal investigation of this
forms of psychopathology are associated with topic to date, analysis of data from over 34,000
specific forms of drug use, matched according to the adult participants in Waves 1 and 2 of the National
pharmacologic profile of the psychoactive agent and Epidemiologic Survey on Alcohol and Related
putative receptor systems implicated in the disorder. Conditions (NESARC) revealed that baseline mood
Although such specificity lacks empirical support and anxiety disorders predicted the incidence of
(Lembke, 2012), numerous studies support the gen- nonmedical opioid use and opioid dependence sev-
eral notion that individuals use drugs to alleviate eral years later (Martins et al., 2012). These results
negative affect. In fact, onset of affective disorders converge with findings from a sample of prescrip-
often predicts later substance abuse and dependence tion opioid–dependent individuals in acute detoxi-
(e.g., Bolton, Robinson, & Sareen, 2009; Leeies, fication and long-term outpatient treatment, 94%
Pagura, Sareen, & Bolton, 2010; Robinson, Sareen, of whom reported frequent misuse of opioids to
Cox, & Bolton, 2011). This relation may be relieve negative affect (Garland, Hanley, Thomas,
explained in part by allostatic load models of
Knoll, & Ferraro, 2015). In a study of 115 chronic
addiction, which suggest that individuals compul- prescription opioid users, depressed mood was
sively seek and consume drugs to allay dysphoric associated with opioid craving, mediated by thought
mood states stemming from withdrawal and asso- suppression, indicating that attempts to suppress
ciated dysregulation of stress and reward circuitry in distressing and intrusive thoughts may lead to in-
the brain (see the section Drug Use Dysregulates creased craving among opioid users with depressive
Emotional Responding; Koob & Le Moal, symptoms (Garland, Brown, & Howard, 2016).
2001, 2008). These findings parallel research demonstrating that
maladaptive cognitive coping (e.g., catastrophizing)
Evidence from Studies of is associated with opioid misuse (Martel, Wasan,
Prescription Opioids Jamison, & Edwards, 2013) and opioid craving
Studies also demonstrate correspondence between (Martel, Jamison, Wasan, & Edwards, 2014) among
prescription opioid dependence and depression and patients with chronic pain, and that opioid craving
anxiety symptoms (Sullivan, 2016; Mayor, 2016; mediates associations between negative affect and
Scherrer et al., 2016; Arteta, Cobos, Hu, Jordan, & opioid misuse among pain patients (Martel, Dolman,
Abstract
This chapter reviews evidence for the role of emotion dysregulation in the etiology and maintenance of
eating disorders. It examines theoretical models that describe functional relations between emotions
and eating disorder behaviors. Data from self-report questionnaire studies, ecological momentary
assessment, and experimental research designs are considered, with a focus on identifying similarities
and differences in emotion dysregulation across eating disorders. The chapter concludes by describing
a model in which stable (i.e., trait) emotion regulation difficulties increase the likelihood of using
maladaptive strategies, such as eating disorder behaviors, to regulate emotions. Future work must
identify factors that predict whether someone will express trait emotion dysregulation as an eating
disorder versus another psychiatric disorder, and whether emotion dysregulation maintains eating
disorders and can be targeted in treatment.
327
Heatherton & Baumeister, 1991; Polivy & Herman, interpersonal problems then trigger binge eating
1993). Ecological momentary assessment (EMA) re- episodes in daily life, as individuals turn to binge
search largely supports the assertion that negative eating in an attempt to alleviate distress (Polivy &
affect increases prior to and decreases in the hours Herman, 1993). Negative affect reduction occurs
following binge eating and purging (Engel et al., because binge eating provides temporary comfort
2013; Smyth et al., 2007). More recently, scholars and distraction and also may displace distress onto
have posited that restrictive eating and thoughts overeating, with compensatory behaviors then used
about weight, shape, and eating in AN serve similar to undo the “problem” and its anticipated effects on
emotion regulation purposes and may also be used appearance (Hawkins & Clement, 1984). The affect
to prevent the onset of aversive emotions (Schmidt & regulation model is the basis for most research on
Treasure, 2006; Wildes, Ringham, & Marcus, 2010). reciprocal negative affect–ED behavior associations
Patients with AN have difficulty understanding and suggests that binge eating occurs in response to
emotions in others and show impaired emotional stressors in individuals with pre-existing characteris-
expression (Davies et al., 2016; Oldershaw et al., tics, such as emotionally labile temperament and
2011), which may affect their ability to engage in depressive tendencies.
emotion regulation. Broad emotion regulation dif-
ficulties are reported by individuals with EDs (e.g., Escape Model of Binge Eating/Bulimia
elevated scores on Difficulties in Emotion Regulation Nervosa
Scale [DERS] subscales), suggesting that ED behav- A related but distinct maintenance model of binge
iors may function to regulate emotions. eating is the escape model (Heatherton & Baumeister,
This chapter will critically review evidence for 1991). The escape model posits a specific mechanism
associations between emotion dysregulation and EDs. to account for reductions in negative affect during
We begin by describing theoretical models that a binge eating episode—escape from aversive
highlight functional relationships between emotions self-awareness. Individuals with binge eating are
and ED behaviors. We then review research that has hypothesized to self-impose unreasonably high
used self-report questionnaires, with a particular standards and are very aware of shortcomings in re-
focus on the DERS. We also discuss EMA research, lation to these standards. Perceived failures create
which tests tenets of theoretical models explicitly, negative affect, prompting an urge to escape un-
and research that has used experimental paradigms pleasant feelings. Eating provides an avenue for cog-
and laboratory designs to overcome limitations of nitive narrowing (e.g., by focusing on immediate
self-report and causal inference, respectively. We sensations related to the food), and binge eating
finish by synthesizing existing research into an inte- may ensue because the shift from higher to lower
grative framework regarding the role of emotion levels of awareness removes the normal inhibitions
dysregulation in the etiology and maintenance of of eating. However, once a binge episode ends,
EDs and present future directions. awareness returns and individuals experience previ-
ously unwanted thoughts and feelings (e.g., weight
Theoretical Models and shape concerns) that are then addressed through
Several theoretical models that posit functional rela- compensatory behaviors (Heatherton & Baumeister,
tionships between emotions and ED behaviors are 1991). Notably, the escape model is difficult to test
described. given that higher self-awareness is needed to report
on one’s emotions and binge eating (Haedt-Matt &
Affect Regulation Model of Binge Keel, 2011).
Eating/Bulimia Nervosa
The affect regulation model of binge eating has Emotion Avoidance Model of
two tenets: (1) negative mood is a precursor to binge Anorexia Nervosa
eating, and (2) binge eating results in reduction of The emotion avoidance model of AN posits that
distress (Haedt-Matt & Keel, 2011). Hawkins and disordered behaviors and cognitions are driven by a
Clement (1984) state that factors such as being desire to avoid expressing or experiencing physical
overweight, being unassertive, or having an emo- sensations, thoughts, urges, and behaviors related to
tionally labile temperament relate to a negative intense emotional states (Wildes et al., 2010; Wildes
self-image and lead individuals to become preoccu- & Marcus, 2011). Unlike the previously mentioned
pied with dieting and/or a fear of losing control models, the emotion avoidance model considers
over their eating. Stressors such as daily hassles or avoidance of both positive and negative emotional
Abstract
Leading theories and an increasingly large body of empirical work each implicate emotion dysregulation
as a central contributor to the emergence and maintenance of a range of self-injurious behaviors. In
fact, self-inflicted injury (SII) often serves as a maladaptive emotion regulation strategy. In this chapter,
we review shared biological and contextual contributors to both conditions, and discuss mutually
reinforcing influences on their development. Available evidence indicates that emotion dysregulation
and SII are particularly likely to emerge when biologically vulnerable individuals are reared in specific
developmental contexts. However, we cannot yet accurately predict which affective patterns mark
imminent risk for SII. Although research on links between emotion dysregulation and SII has burgeoned
in recent years and associations between these conditions are well established, mediating and moderating
pathways require further exploration. We review recent findings, current methodological barriers, and
directions for future research.
345
peers (e.g., Deutz, Geeraerts, Baar, Deković, & much remains to be learned, as indicated in sections
Prinzie, 2016). Studies consistently find higher where we discuss recent findings, methodological
emotional intensity, deficits in emotional expressivity, barriers to improved understanding of etiology, and
and greater difficulty tolerating emotional distress directions for future research.
among individuals who engage in SII compared
with those without such histories (Iancu et al., 1999; Terms and Concepts
Klonsky, 2009; Muehlenkamp, Peat, Claes, & Smits Self-Inflicted Injury
2012; Nock & Mendes, 2008; Rajappa, Gallagher, Historically, research on SII has been hampered by
& Miranda, 2012). overlapping, vague, and sometimes contradictory
Notably, SII itself often serves as a maladaptive definitions of key constructs (Silverman, Berman,
emotion regulation strategy (Houben et al., 2017; Sanddal, O’Carroll, & Joiner, 2007a, 2007b). Even
Linehan, 1993; Nock & Prinstein, 2004). The most today, few if any terms enjoy universal acceptance.
frequently endorsed reason for engaging in self-harm This has led to significant confusion within the field,
is to escape, circumvent, or otherwise cope with and to difficulties generalizing findings across diverse
aversive affective states (Baetens, Claes, Willem, clinical populations. A key consideration is intent,
Muehlenkamp, & Bijttebier, 2011; Edmondson, defined by the level of conscious desire an individual
Brennan, & House, 2016; Jacobson, Batejan, has to escape from or end his or her life, and the
Kleinman, & Gould, 2013; Chapman, Gratz, & degree to which he or she has resolved to do so
Brown, 2006; Klonsky, 2007; Van Orden et al., (Silverman et al., 2007a). Self-injury can occur both
2015). Retrospective self-report and data collected with and without a desire to die, so separate terms
using real-time sampling indicate that high arousal have evolved to demarcate intent. The term NSSI
and negatively valenced affective states increase refers to acts of bodily harm without conscious intent
prior to, and gradually decrease following, SII to die, whereas ambivalent SII refers to destruction of
(Armey et al., 2011; Claes, Klonsky, Muehlenkamp, bodily tissue associated with uncertain intent to die.
Kuppens, & Vandereycken, 2010; Klonsky, 2009; In contrast, suicide attempts, which may or may not
Nock, Prinstein, & Sterba, 2009). result in death, vary widely from any nonzero level of
Although temporarily effective in regulating intent to certain intention to die. Table 24.1 presents
negative affect, those who engage in SII typically these and additional common SII-related terms.
experience significant deterioration in emotional SII is a deliberately broad term that captures a
state only minutes following an episode (Favazza & continuum of self-injurious behaviors, ranging
Conterio, 1989; Houben et al., 2017; Kamphuis, from NSSI to attempted and completed suicide.
Ruyling, & Reijntjes, 2007). Moreover, SII exacer- Including all self-injurious acts under a general de-
bates emotion dysregulation deficits over time scription has benefits and limitations. Historically,
(Andrews et al., 2013; Gratz & Tull, 2010). In con- important distinctions between various SII behav-
trast, improved emotion regulation contributes to iors were often overlooked (see Linehan, 1997;
SII cessation (see, e.g., Duggan, Heath, & Hu, Muehlenkamp & Gutierrez, 2004), and suicidal
2015; Gratz, Bardeen, Levy, Dixon-Gordon, & Tull, self-harm and NSSI were assumed to serve identical
2015; Slee, Spinhoven, Garnefski, & Arensman, functions, which may or may not be the case
2008; Whitlock, Prussien, & Pietrusza, 2015). (Simpson, 1950; Zilboorg, 1936a, 1936b). For the
Following from these and other findings, many re- past several decades, researchers have sought to
searchers conceptualize SII as a specific manifestation divide SII into meaningful subtypes based on level
of a broader deficit in adaptive emotion regulation of intent, associated function(s), lethality of method,
(Chapman et al., 2006; Gratz & Roemer, 2004; and physical outcomes associated with self-harm
Linehan, 1993). (e.g., Beautrais, Joyce, & Mulder, 1996; Linehan
In this chapter, we review biological and contex- et al., 2006; Zlotnick, Mattia, & Zimmerman, 1999).
tual contributors to emotion dysregulation and SII, Of note, classifying by physical outcome can be prob-
and discuss mutually reinforcing influences on lematic because people who use the same means with
development of these transdiagnostic vulnerabilities similar intent may incur very different results. For
to psychopathology. As demonstrated in the sections example, two individuals may ingest the same dose
to follow, emotion dysregulation and SII emerge of the same harmful substance, with little or no
when vulnerable individuals are reared in specific physical damage incurred by one who is d iscovered
developmental contexts. Although much has been by a relative or friend, versus very serious damage or
learned about these phenomena in recent years, death incurred by another who is not discovered.
Term Definition
Intent Level of conscious desire an individual has to escape from or end his or her life
and the degree to which he or she has resolved to do so.
Self-inflicted injury/self-harm Nonaccidental actions that result in some destruction of bodily tissue or have a
potential effect on bodily functioning.
Nonsuicidal self-injury (NSSI) Self-induced destruction of bodily tissue without any intention to die.
Ambivalent self-inflicted injury Self-induced destruction of bodily tissue and/or deliberate engagement in behaviors
(SII) that place the individual at risk for injury/death (e.g., walking into traffic,
playing roulette with a loaded gun) with uncertain intention to die.
Suicide attempt Self-induced destruction of bodily tissue and/or deliberate engagement in
behaviors that place the individual at risk for injury/death with any nonzero
level of intention to die.
Suicide Intentional self-inflicted injury that results in death.
Thwarted suicide attempt An interrupted suicide attempt, through either discovery by others or losing
access to means of causing injury.
Suicidal threat A verbal or written communication regarding some desire to die and some
degree of intention to act on such desires. This term has fallen out of favor with
many in the field due to its implied associations with manipulation and coercion
(which are frequently unfounded and pejorative).
Suicidal gesture An action communicating some desire to die and some degree of intention to act
on such desires. Typically, such actions are low-lethality behaviors and unlikely
to result in serious damage to bodily tissue. This term has fallen out of favor with
many in the field due to its implied associations with manipulation and coercion
(which are frequently unfounded and pejorative).
Parasuicide An outdated term for nonfatal suicide attempt or NSSI. This term has fallen
out of favor due to implications that parasuicidal behaviors occur due to some
suicidal intent, which is often not the case.
Suicide-related ideations Thoughts about ending one’s life, which may or may not be accompanied by intent.
Passive suicide-related ideations Thoughts about ending one’s life or death without conscious intent or planning
to do so. Often experienced as “unprompted” and without intent.
Suicide-related communications Verbal or written communication regarding some desire to die and some degree
of intention to act on such desires.
Lethality The degree of risk of death associated with specific SII behaviors.
Lethality of means The degree of risk of death associated with specific SII methods/means.
Outcome The level of physical damage resulting from SII.
To complicate matters further, many infer level are sought, and obscure the dimensional nature of
of suicidal intent from the lethality of the method lethality and intent. Moreover, certain populations
selected, even though these are not necessarily related (e.g., youth) may frequently misunderstand which
(Linehan et al., 2006). Many studies also include means are most risky.
people who engaged in low-lethality behaviors On balance, most research has been conducted
such as repetitive cutting, burning, or bruising (e.g., with artificially restricted samples—limiting our
Simpson, 1975), lumping them together with others understanding of continuities in severity of SII and
who engage in more lethal means. Other studies how severity may differ across clinical populations
restrict their samples to participants based on be- (Crowell et al., 2014; Derbidge & Beauchaine,
haviors such as hanging, drowning, and shooting 2014). Those who study personality, mood, and
(e.g., Seiden, 1978). Although neither is necessarily psychotic disorders often examine SII only within
wrong, these sampling strategies can introduce their respective diagnostic group (e.g., Dworkin,
unwanted variability when homogeneous samples 1994; Heisel, Conwell, Pisani, & Duberstein, 2011;
Abstract
Emotion dysregulation has been theorized to either directly or indirectly drive many of the symptoms
associated with borderline personality disorder. In this chapter, several current controversies in this
body of work are reviewed. The chapter presents the role of emotion dysregulation in theories of the
development and maintenance of borderline personality disorder. Further, it reviews the state of
research on emotional responding in borderline personality disorder, focusing on any evidence of
emotional sensitivity, reactivity, and time course. Building on this review, the chapter summarizes
recent advances in the study of difficulties in emotion regulation capacities and strategies in the
context of this disorder. In addition, it outlines the links between emotion dysregulation and other
problems in borderline personality disorder. Finally, this chapter highlights the limitations and future
directions in this line of work.
361
50% of the sample continued to endorse this demands (Gratz & Roemer, 2004). In other words,
criterion six years later (Zanarini, Frankenburg,
emotion dysregulation is characterized by a pattern
Hennen, & Silk, 2003). Thus, emotional dysfunction of emotional expressions or experiences that inter-
appears to be a critical component of BPD. fere with appropriate goal-directed behaviors.
In this chapter, we define relevant terms and Consequently, emotion dysregulation confers
concepts and review theoretical perspectives on vulnerability to a range of internalizing and exter-
emotion dysregulation in BPD. We also discuss cur- nalizing behavior problems (Beauchaine, 2015).
rent controversies in the literature on emotion dys- We can look at emotion regulation and dysregu-
regulation and BPD and present empirical evidence lation from two perspectives. Drawing on the process
supporting each perspective. After synthesizing the model (Gross, 1998), much of the research on emo-
literature and pointing to possible explanations for tion regulation describes the state use of different
discrepancies, we conclude with suggestions for types of emotion modulation strategies, implemented
future research on emotion dysregulation and BPD. at different times across the emotional response.
From this strategy-based approach, specific emotion
Defining Emotions, Emotion Regulation, regulation strategies, such as emotional acceptance,
Emotion Dysregulation, and Related cognitive reappraisal, and problem solving, have
Concepts typically been classified as adaptive in light of their
Two criteria for BPD—affective instability and negative associations with psychopathology symp-
anger—directly reflect disturbances in emotions. These toms (Aldao, Nolen-Hoeksema, & Schweizer, 2010;
emotions, such as fear, anger, shame, and sadness, Garnefski, Kraaij, & Spinhoven, 2001; Gross, 1998).
can be described as short-lived, loosely coordinated Conversely, strategies such as self-criticism, worry,
responses across experiential, physiological, and rumination, suppression, and avoidance are consid-
behavioral domains to a stimulus (Ekman, 1992). ered maladaptive since they tend to be positively as-
Although in typical populations these emotions are sociated with psychopathology (Aldao et al., 2010;
generally adaptive (i.e., by rapidly signaling and Aldao & Nolen-Hoeksema, 2010; Garnefski, Kraaij,
facilitating responses to situational demands), when & Spinhoven, 2001).
these emotions fail to align with situational demands Expanding beyond a focus on strategies, we can
and goals, they require regulation. also focus on dispositional emotion regulation abili-
Before exploring the role of emotion dysregulation ties (Tull & Aldao, 2015). Although we distinguish
in BPD, it is helpful to define emotion regulation. here between emotional responses and regulation,
Despite numerous definitions of emotion regulation, we acknowledge that these are related. We can
most descriptions share several commonalities. consider excessive negative emotionality to be a
Generally, emotion regulation is defined as a multi- consequence of underuse of emotion regulation
faceted construct that involves modulation of strategies, selection of inappropriate strategies, or
emotional experiences and/or expressions (Cole, ineffective use of regulation strategies (Linehan,
Michel, & Teti, 1994; Gross, 1998), alterations to the 1993; Maffei & Fusi, 2016). Conversely, we can also
intensity and/or duration of emotions (Thompson, view intense emotionality as requiring more effective
1994), and regulation of problematic behaviors or extensive regulatory resources. Both excessive
associated with emotions (Cole et al., 1994; Gratz & emotional responding and difficulties modulating
Tull, 2010). This process of emotion regulation fa- emotions are present in BPD, and thus we explore
cilitates goal-directed behavior, even in the context both of these conceptually related yet distinct do-
of strong negative emotions (Gottman & Katz, mains in hopes of better understanding emotion
1989; Linehan, 1993). dysregulation in BPD more broadly.
In contrast, emotion dysregulation involves diffi-
culties in these domains. One prominent multidi- Theoretical Perspectives on Emotion
mensional model suggests that emotion dysregulation Dysregulation and Borderline
can be broadly construed as (1) a lack of emotional Personality Disorder
awareness, understanding, or acceptance of emotions; Across multiple developmental theories of BPD,
(2) difficulties controlling impulsive behaviors in emotion dysregulation is viewed as a critical early
accordance with desired goals when distressed; and etiological mechanism. One prominent model, the
(3) limited access to situationally appropriate emo- biosocial theory, regards emotion dysregulation as
tion regulation strategies to modulate emotional essential, contributing directly to the development
responses in order to meet goals and situational and maintenance of BPD (Linehan, 1993). According
Normative
BPD
Emotional Intensity
E. Regulation
A. Baseline Difficulties regulating.
Higher baseline – Less awareness
negative A B C D E – Less acceptance
emotionality. – Lower perceived
effectiveness
Time – Less cognitive
control
Abstract
377
high levels of distress (Smith, Leffingwell, & Ptacek, behave differently in a context with others
1999; Stone et al., 1998). Similarly, research using (e.g., parent, teacher, spouse). Despite these limita-
both self-report and observational strategies has tions, behavioral observations provide a powerful
illustrated that self-reports are frequently inaccurate measurement strategy for studying emotion
due to information processing biases combined dysregulation—especially when combined with
with the automaticity of overlearned processes effective experimental manipulations (see Cole
(Hawes, Dadds, & Pasalich, 2013; Stone et al., 1998). et al., 2017).
That is, when behaviors are repeated frequently,
they are more likely to occur outside of awareness Theoretical Perspectives
and, in combination with the interpretation of be- Measurement decisions in emotion research can be
haviors, may lead to systematic biases in self-report. linked directly to underlying theoretical issues.
For example, parental observation of their children Emotion dysregulation comprises a set of complex,
is repeated frequently over years, and implicit biases multidimensional, and multilevel processes that are
related to their children may influence parents’ difficult to define and even more difficult to quan-
description of their children’s behaviors. Research tify (Cole et al., 2004, 2017; Zeman, Cassano,
on parenting attributions and practices supports the Perry-Parrish, & Stegall, 2006). Three complemen-
notion that there are biases in the parent report of tary perspectives are presented with an emphasis on
their children. In video-recall procedures, parents how they inform behavioral assessment strategies.
frequently rate their children’s behavior as negative
when observers coded the same behaviors as neutral or Dynamic
positive (e.g., Lorber, O’Leary, & Kendziora, 2003). Emotion dysregulation encompasses a broad range
The contrasting of parent-rated and neutral observer- of processes occurring both discretely (excessive im-
rated codings suggests that parental self-report mediate emotional arousal) and longitudinally (in-
measures would not have captured the phenomenon stability of emotional state over time). Individuals
accurately. Thus, even the best-designed self-report who are dysregulated exhibit patterns of responding
measures are limited by self-perceptions. whereby a mismatch occurs between sociocultural
Behavioral observations and tasks minimize contextual demands and the person’s goals, responses,
limitations inherent to self-report by capturing and/or modes of expression. Finding measurement
behavior objectively and in real time. Trained ob- approaches that sufficiently characterize the com-
servers or automated computer algorithms code plexity of emotion dynamics has proved challenging
behaviors without the perceptual or emotional biases given that individuals have a variety of emotion
that may affect participant reports of emotion regulation strategies and can apply them to different
dysregulation. Despite the advantages of behavioral situations toward achieving their goals. For example,
observation, including flexibility in capturing be- Gross and Jazarieri (2014) highlight problematic
haviors relevant to one’s research question, it is not emotional patterns of intensity, duration, frequency,
without drawbacks. Observational approaches re- and type in the context of the individual’s emotional
quire significant investment of time and resources awareness, emotion-related goals, and strategies.
to design systems with high external validity and From this perspective, capturing the dynamic nature,
generalizability, obtain behavior samples, train coders, flexibility, and pattern of emotion dysregulation
and conduct coding to reliability. Furthermore, de- over time is an essential component of the assess-
pending on the nature of events, desired behaviors ment of emotion dysregulation (e.g., Gross &
may not occur, despite being primed. Because of Jazarieri, 2014; Chow et al., 2005).
variability in individual thresholds for emotional
responses, the need for regulation may vary greatly Functional
within and across individuals (e.g., Cole et al., Researchers must determine whether the primary
2017). If an individual fails to show emotion, we purpose of assessment is to determine the structure
may incorrectly assume that the individual elicited or function of emotion. Although it is not surpris-
emotional control over expressions rather than ing that psychologists would seek to learn what an
concluding that the stimulus was insufficiently emotion is (a structural theory addressing the nature
provocative for emotion elicitation (Cole, Martin, of emotion; e.g., Russell, 1980), researchers and cli-
& Dennis, 2004). Similarly, an individual may nicians also have great interest in what an emotion
regulate emotions effectively in the context of a does. According to functionalist approaches (e.g.,
laboratory setting with an unknown examiner but Barrett & Campos, 1987), a core focus is how
Assessment Strategy Age Range Observation Methods Examples in Research Construct Assessment
Naturalistic observation Infant Infant at home Tonyan (2005) Assess infant emotion regulation (ER) in
home setting
Infant Playroom and high chair J. A. Crowell and Feldman (1988); Evaluates infant regulatory styles with
structured and semistructured Miller, McDonough, Rosenblum, and mother when placed in high chair with low
activities Sameroff (2002); Zeanah et al. (1997) and high challenge tasks
Toddler/preschool Free play alone, with teacher, J. A. Crowell and Feldman (1988); Coping with naturalistic emotional events,
with parent Denham et al. (2003); Eisenberg et al. emotional responses are coded, coding
(1995); Fabes and Eisenberg (1992); interactive behavior (CIB) system
Feldman and Greenbaum (1997)
Toddler/preschool Sibling interactions Volling, McElwain, and Miller (2002) Regulating distress and positive play
b ehavior when distressed
School age Best friend free play Leary and Katz (2005) Assess affective quality, cooperation,
conversational repair skills, etc.
Structured observation Infant Brazelton Neonatal Assessment Brazelton (1973) State regulation, distress, irritability
System
Infant Bayley Scales of Infant Bayley (1993) Negative affect, frustration, and flexibility
Development
Analog Infant Infant Emotional Challenge Malone, Gunnar, and Fisch (1985) Ability to self-soothe and use others for ER
efforts
Infant Behavior Response Paradigm Garcia-Coll et al. (1988) Latency of cry as presented stimuli become
more intrusive
Infant Still-face paradigm Cohn and Tronick (1983) Infant’s ER to maternal lack of facial
emotional expression
Infant Infant stranger paradigm Mangelsdorf, Shapiro, and Marzolf (1995) Aversion, self-soothe, distraction, avoidance
Infant/toddler/preschool Frustration tasks Buss and Goldsmith (1998); Calkins, Assess infant emotion regulatory responses
Dedmon, Gill, Lomax, and Johnson to frustration (barrier, arm restraint, maternal
(2002); Goldsmith and Rothbart (1999); prohibition) self-soothing, orient, redirect,
Stifter and Braungart (1995) communicate
Infant Mother-infant interaction Feldman, Eidelman, and Play time; maternal touch, affect, talk,
Rotenberg (2004) intrusiveness, adaptation; infant state
(continued )
Table 26.1. Continued
Assessment Strategy Age Range Observation Methods Examples in Research Construct Assessment
Infant High chair task Goldsmith and Rothbart (1996); Assess child’s ability to regulate negative
Graziano, Keane, and Calkins (2010) affect; code using LAB-TAB
Toddler/preschool Frustrating paradigm; negative Cummings (1987); Maughan and Frequency and effectiveness of distraction
emotion barrier Cicchetti (2002) as strategy
Toddler/preschool Disappointment paradigm Cole, Zahn-Waxler, and Danielle (1994); ER efforts when disappointed in presence of
Saarni (1979) audience figure or alone
Toddler/preschool Inhibition of positive emotion Carlson and Wang (2007) Evaluate child’s ability to keep a secret
(inhibit emotion) about an emotionally
positive valence event
Toddler/preschool Separation/strange situation task Ainsworth, Blehar, Waters, and Wall Assess emotionality and ability to regulate
(1978); Ainsworth and Wittig (1969) arousal
Toddler/preschool Delay of gratification, waiting Block and Block (1980); Grolnick, Code emotion regulation strategies: active
task, and separation from de- Bridges, and Connell (1996); Kochanska, distraction, focus on object, passive waiting,
sired object paradigms Murray, and Harlan (2000); information gathering, seeking physical
Marvin (1977) comfort
Toddler/preschool Anger induction: transparent Goldsmith and Rothbart (1999) Assess ability to regulate anger
box procedure
Toddler/preschool Mood induction stimulus for Cole, Jordan, & Zahn-Waxler (1990) Categories based on facial coding system:
children inexpressive, modulated expressive, highly
expressive
Toddler/preschool Entry task with peer Putallaz (1983) ER strategies coded during peer group entry
failure
Toddler/preschool “Beat the Bell” competitive task Cassidy, Parke, Butkovsky, and Braungart Children’s ER when losing a game
(1992); Lütkenhaus, Grossmann, and
Grossmann (1985)
Toddler/preschool Puppet task Cole, Dennis, Smith-Simon, and Assess understanding and elicitation of ER
Cohen (2009) strategies
Toddler/preschool Peer interactions Denham et al. (2001) Evaluated child’s response to a focal child
who expressed emotion
School age Induced distress Fabes, Eisenberg, Karbon, Troyer, and Evaluate child’s response to distress in other
Switzer (1994) (time spent talking, turning speaker off,
facial and vocal distress)
School age Affect regulation in the family Klinnert, McQuaid, McCormick, Examine quality of ER of child and with
Adinoff, and Bryant (2000); Lindahl, mother using positive emotion tasks,
Clements, and Markman (1993) frustrating tasks, conflict discussion
School age Anticipatory disappointment Guttentag and Ferrell (2008) Assess effects of expectations on
and regret disappointment and regret
School age Sadness induction Rice, Levine, and Pizarro (2007) Assess ability to disengage emotionally from
memory for event
School age Peer provocation computer Underwood and Hurley (1999) Assess display rules while playing computer
game game with peer
School age Peer rejection task Reijntjes, Stegge, Terwogt, Kamphuis, Assess ER strategies following peer rejection
and Telch (2006) in a rigged computer game and effect on
subsequent mood
School age Parent–child anger/frustration Melnick and Hinshaw (2000) Assess ER ability to manage anger in face of
induction frustration with parents present
School age Competitive puzzle task Hinshaw and Melnick (1995) Told to mask anger in task with peer
School age Mother–child conflict Melby and Conger (2001) Code positive and negative emotion using
resolution task Iowa family interaction rating system
School age Parent–child emotion Shipman and Zeman (1999) Examine ER in terms of parental validating
interaction task and invalidating response and child’s
response to parent
School age Parent–child interaction task Eisenberg et al. (2005); Suveg et al. Child’s ER strategies were assessed within
(2008) discussion task and coded as (1) cognitive
and behavioral problem-solving approaches
or (2) maladaptive responses
Adolescent Mother–teen problem solving Kobak, Cole, Ferenz-Gillies, Fleming, and Support, communication, dysfunctional
Gamble (1993) anger, avoidance
Adolescent Revealed differences task Strodtbeck (1951) Triadic interaction to resolve differences of
Hauser et al., 1984) opinion; code with Constraining and
Enabling Coding System
Adolescent Mother–teen “talk show” Zimmermann, Mohr, and Spangler Stimulate social evaluative context and elicit
(2009) emotional arousal; code for ER
Adolescent Mother–child interaction Allen et al. (1994) Autonomy and relatedness scales
Beijersbergen, Bakermans-Kranenburg,
Van IJzendoorn, and Juffer (2008)
(continued )
Table 26.1. Continued
Assessment Strategy Age Range Observation Methods Examples in Research Construct Assessment
Adolescent Parent–child interaction Yap, Allen, and Ladouceur (2008) LIFE coding system: Aversive, Dysphoric,
Positive Interpersonal
Adolescent Video recall procedures Ehrmantrout, Allen, Leve, Davis, and Recorded problem-solving task followed by
Sheeber (2011) teen identification of parental emotion in
20-second intervals
Computerized behavioral Adolescent Emotional go/no go Schulz et al. (2007) Emotional modulation of inhibition
tasks
Adolescent Mirror tracing persistence task Renna et al. (2017) Distress tolerance/persistence
Adolescent Paced auditory series Brown, Kahler, and Strong (2002); Distress tolerance/persistence
addition tasks Gronwall (1977); Lejuez, Kahler, and
Brown (2003)
Adolescent Distress tolerance task Nock and Mendes (2008) Distress tolerance/persistence
observing emotion dysregulation in context. This such assessments are conducted in an artificial setting
method provides the most flexibility because there such as a laboratory, although such observations may
are a wide array of settings and paradigms through be conducted in home or school settings. Typically,
which observations can take place. However, this cost, convenience, and control drive decisions to
high degree of flexibility and strength in ecological conduct observations in lab or clinic settings. The
validity for capturing behavior in the setting in strengths of analog observations include the ability
which it naturally occurs is offset by a low level of to have a standard observational setting with a high
experimental control. Given that neutral affect is degree of consistency across participants. Consistency
predominant throughout the day, research using and control standards allow researchers to contrast
observational approaches typically capitalizes on situational contexts (e.g., the strange situation para-
settings and paradigms that accentuate the chance digm measures child behavior with and without a
that emotional content will emerge with sufficient stranger present to observe parent–child interactions
frequency, intensity, and/or duration to obtain in two contexts; Ainsworth, Blehar, Waters, & Wall,
meaningful results. 1978) to examine the effects of specific stimuli or
events on participant behavior. Analog observation
Structured observation tasks involves the use of experimental paradigms that elicit
Researchers who study infants and preschoolers emotional responses and simulate common events.
often use structured observations during emotion Because ethical concerns arise when inducing strong
elicitation tasks to elicit emotion dysregulation. Out negative emotional states in children, these para-
of 13 tasks reviewed by Rothbart, Posner, & Kieras digms typically assess children’s responses to low to
(2006), 11 were suitable to be used with children moderate levels of stressors. We review a few of the
younger than 5 years of age. The most widely used most common analog observation paradigms for as-
structured observational systems are the Brazelton sessing emotion and emotion dysregulation.
Neonatal Behavioral Assessment Scale (BNBAS;
Brazelton & Nugent, 1995) and the Bayley Scales of Strange situation paradigm
Infant Development (Bayley, 1993). The BNBAS The strange situation is a classic paradigm that has
elicits behavioral and reflex responses, recorded with been used to assess parent–child attachment systems
criterion-referenced scoring. Most relevant research since the 1960s (Ainsworth and Wittig, 1969).
from this scale has focused on a range of state This 20-minute procedure exposes the infant to a
clusters and regulation of state clusters to create a series of contexts in which the parent and child are
“proneness to distress” or a “difficultness” factor that together alone, a stranger approaches, the parent
reflects both negative affect and components of separates from the infant, the parent and infant are
emotion dysregulation (Rothbart & Ahadi, 1994). reunited, the parent leaves the infant alone for the
Although assessment of these dimensions varies second separation episode, the stranger enters when
across studies, the construct appears to be relatively the infant is alone, and the parent and infant reunite
robust and stable over the first few months and even for a second time. During the task, the infant’s ex-
into later infancy. Kaye (1978) used the Brazelton ploration behaviors, reactions to caregiver departure
Neonatal Behavioral Assessment Scale to identify and reunion, and behavior toward the stranger alone
a single negative reactivity factor that included are used to categorize the infant’s attachment relation-
three dimensions: irritability to stimuli, rapidity ship with the caregiver as secure, anxious avoidant,
of buildup of negative emotion, and peak of ex- anxious ambivalent, or disorganized. The procedure
citement (i.e., level of distress). The Bayley Scales was designed for infants 8 to 18 months of age and
of Infant Development (Bayley, 2006) is another has been modified for use with older preschool
structured observational measure that includes a children (see Belsky et al., 1994). From the lens of
social-emotional scale. A strength of the Bayley is emotion dysregulation, the task can be deployed to
that the structured observation also has a normative evaluate the ability to regulate arousal and emotional
sample to compare a child’s performance with his or intensity in response to separation, parental sensitiv-
her same-age peers. ity, and parent–child interactions (Cole et al., 2017;
Guo, Leu, Barnard, Thompson, & Spieker, 2015).
Analog observations
Analog behavioral observation involves assessment Face-to-face still-face paradigm
in a contrived environment/circumstance to elicit The face-to-face still-face paradigm is a standardized
emotional reactions and associated processes. Usually, observational strategy designed for infants and their
Abstract
Self-report assessments remain among the most widely used measures for most psychological
constructs, due to their feasibility, ease of administration, low cost, and wide availability. Self-report
measures of emotion dysregulation are no exception. This chapter reviews two predominant
conceptualizations of emotion dysregulation (one of which focuses on dysregulated emotional
responses per se and another that focuses on maladaptive ways of responding to emotions), as well
as the empirical support for extant self-report measures of emotion dysregulation consistent with
both conceptualizations. Based on this review, the chapter concludes that both emotional responses
themselves and an individual’s responses to those emotions may evidence dysregulation and inform
our understanding of normal and abnormal development. Finally, future directions for research in this
area are discussed, including the need for studies examining the clinical utility of targeting responses to
emotions versus emotional experience per se in psychological interventions.
395
emotion dysregulation are likely to remain the most modulation of emotions. Grounded in theory and
common, widely used, and feasible assessments in research on the functionality of emotions (Cole,
both clinical and research settings, the limitations Michel, & Teti, 1994; Ekman & Davidson, 1994;
associated with self-report measures of other R. A. Thompson, 1994) and paradoxical conse-
emotion-related constructs may be less applicable to quences of efforts to avoid or control emotions
measures of emotion dysregulation by virtue of the (e.g., Hayes, Luoma, Bond, Masuda, & Lillis,
nature of the construct itself. 2006), this conceptualization proposes that even
In this chapter, we review two predominant con- intense, reactive, or labile emotions are not inher-
ceptualizations of emotion dysregulation and their ently dysregulated and that responses to emotions
relative clinical utility, as well as the empirical sup- are more important than the quality of those
port for extant self-report measures of emotion dys- emotions.
regulation consistent with both conceptualizations. Although these conceptualizations of emotion
Finally, we discuss future directions for research in dysregulation represent two primary theoretical ap-
this area. proaches to this construct, one additional definition
of emotion dysregulation—often cited in person-
Conceptualizations of Emotion ality disorders literature—warrants discussion.
Dysregulation Specifically, some researchers refer to Livesley and
There are numerous (and often discrepant) concep- colleagues’ research on the factor structure of the
tual definitions of emotion regulation in the litera- Dimensional Assessment of Personality Pathology—
ture, with the relative utility and merits of each de- Basic Questionnaire (DAPP-BQ; Livesley & Jackson,
pendent on the research or clinical question of 2002) when defining emotion dysregulation.
interest (Gratz, Weiss, & Tull, 2015). Thus, it is not However, rather than being grounded in theory on
surprising that there is also not a single agreed-upon emotion dysregulation, the definition stemming
conceptualization of emotion dysregulation, al- from this work reflects simply a label given to an
though the relative lack of attention given to this empirically derived set of intercorrelated lower
construct (vs. emotion regulation) has resulted in order maladaptive personality traits. Namely, in
far fewer conceptualizations of emotion dysregula- their research examining the interrelations and hier-
tion than emotion regulation. In fact, most of the archical structure of 18 specific lower order traits
literature on emotion dysregulation relies on one of underlying personality disorders, a higher order
two primary conceptualizations of this construct. factor emerged that closely resembles borderline
The first conceptualization focuses on putatively personality pathology and is composed of traits cap-
dysregulated emotional responses per se, equating turing emotional, cognitive, interpersonal, and self/
emotion dysregulation with the temperamental identity dysfunction, including anxiousness, affec-
characteristics of emotional sensitivity, intensity, re- tive lability, insecure attachment, submissiveness,
activity, and slow return to baseline (e.g., Newhill, social avoidance, identity problems, and cognitive
Mulvey, & Pilkonis, 2004). According to this defi- dysregulation (Livesley, 2002; Livesley, Jang, &
nition, emotional responses that are particularly Vernon, 1998). As such, this higher order factor
intense, reactive, and long-lasting are inherently captures far more than emotional dysfunction and
dysregulated and may increase risk for maladaptive is instead similar to conceptualizations of BPD
behaviors aimed at regulating these emotions, such (Livesley et al., 1998; Hernandez et al., 2009).
as self-injury or substance misuse (Newhill, Bell, Nonetheless, because of the prominence and saliency
Eack, & Mulvey, 2010). of the emotion-related traits loading on this factor
In contrast, other researchers conceptualize (i.e., anxiousness and affective lability), Livesley and
emotion dysregulation as separate from the quality colleagues labeled this dimension “emotion dysreg-
of the emotional responses themselves (Gratz & ulation” (Livesley et al., 1998). Although labeling
Roemer, 2004; R. A. Thompson & Calkins, 1996), these emotion-related traits as emotion dysregula-
implying that there is a difference between one’s tion is consistent with the first conceptualization of
emotional temperament and emotion dysregula- emotion dysregulation described previously, the
tion. Specifically, Gratz and Roemer’s (2004) con- factor to which this label applies is not specific to
ceptualization focuses on maladaptive ways of emotional dysfunction and is better conceptualized
responding to emotions (regardless of their valence, as BPD-related pathology. Further, an additional
intensity, or reactivity), including deficits in the problem with using this research as the basis of a
understanding, acceptance, and effective use and/or conceptual definition of emotion dysregulation is
Abstract
As emotion is a dynamic construct, ecological momentary assessment (EMA) methods, which gather
data at multiple time points in individuals’ real-world environments, in the moment, are particularly
well suited to measure emotion dysregulation and related constructs. EMA methods can identify
contextual events that prompt or follow an emotional response. This chapter provides an overview of
traditional methods of studying emotion dysregulation and how EMA can be used to capture emotion
dysregulation in daily life, both within and independent of psychiatric diagnoses. It reviews the literature
on emotion dysregulation and related constructs within specific diagnoses (e.g., depression, bipolar
disorder, borderline personality disorder, and eating disorders) and behaviors (e.g., suicide, nonsuicidal
self-injury, and alcohol use). Finally, it discusses future directions in EMA research, as well as its
implications for psychological treatment.
411
emotional stop-signal tasks (Allen & Hooley, 2015; an emotional response. In this chapter, we review
Allen & Hooley, 2018), which assess emotional re- ways in which EMA is well suited to capture emo-
sponse inhibition; and the Trier Social Stress Test tion dysregulation in daily life, both within and in-
(Kirschbaum, Pirke, & Hellhammer, 1993), a stress dependent of psychiatric problems.
induction used to evaluate physiological stress, in-
cluding adrenocorticotropin (ACTH) and cortisol Ecological Momentary Assessment
responses. EMA encapsulates a set of methods employed to
Psychophysiological assessments can also capture better understand the phenomenology of a particu-
emotion dysregulation, if stimulus conditions are lar emotion, behavior, or cognition within the con-
carefully controlled. For example, respiratory sinus text of participants’ real-world experiences (Bolger,
arrhythmia (RSA; also known as heart rate variabil- Davis, & Rafaeli, 2003). These methods are partic-
ity, cardiac vagal control, or vagal tone) appears to ularly useful when researchers are interested in un-
mark emotion regulation capacity in healthy adults derstanding (1) group differences and (2) the natural
(see Balzarotti, Biassoni, Colombo, & Ciceri, 2017, history of individuals through repeated, within-
for review), whereas low resting RSA and RSA with- subject assessments; real-world contexts and influ-
drawal to stressors index emotion dysregulation (see ences on affect, behavior, and cognition; and the
Beauchaine, 2015, for review). Emotional responses temporal sequencing of events to explore causality.
are also evident in the noncontent features of speech, We briefly review the characteristics, benefits, and
such as fundamental frequency (see Giddens, Barron, limitations of EMA next; however, a more thorough
Byrd-Craven, Clark, & Winter, 2013, for review). review can be found elsewhere (Shiffman, Stone, &
Brain-based indices using electroencephalogram Hufford, 2008).
(see Coan & Allen, 2004, for review), event-related In EMA, brief questionnaires and assessments are
potentials (see Hajcak, MacNamara, & Olvet, 2010, presented to participants through a handheld com-
for a review), and magnetic resonance imaging puting device on preselected schedules, optimized
(e.g., Hare et al., 2008; Morawetz, Bode, Derntl, & to capture relevant information about phenomena
Heekeren, 2017) have also been used to explore of interest. EMA descends from paper-and-pencil
emotion regulation. “daily diary” studies (Korotitsch & Nelson-Gray,
As with all measures, traditional methodologies 1999) and other “experience sampling” (Hektner,
have many strengths but are limited in several key Schmidt, & Csikszentmihalyi, 2007), “self-report
ways. First, many rely on aggregate ratings of emo- EMA” (Stone & Shiffman, 1994), or “real time data
tion (e.g., DERS items beginning with “When capture” methods (Stone & Broderick, 2007).
I’m upset…”) and are subject to autobiographical These methods have been in use, in some form,
memory effects, such as random error and systematic since the beginning of structured psychological as-
bias due to heuristics and retrieval (Bradburn, Rips, sessment; however, technological innovations over
& Shevell, 1987). Self-reports also tend to reflect the past two decades have revolutionized our under-
self-conceptualizations, and it is not uncommon for standing of daily experience of affect, behavior, and
respondents to organize or modify responses to reflect cognition. For assessments to be truly “ecological,”
self-perception or worldviews, rather than actual they should occur in real-world environments (i.e.,
events (Ross, 1989). Likewise, responses to behav- participants’ homes), rather than through repeated
ioral tasks are often collected cross-sectionally; these measures in a research context (e.g., a lab). Likewise,
narrow slices of behavior, under specific conditions, the “momentary” component of these methods refers
reduces the generalizability of findings. to the assessment of state, rather than trait, constructs.
When considering how to most accurately meas- For example, an EMA measure of anger would ask
ure emotional experiences, we must recognize that participants to rate how angry they feel right now,
emotions are dynamic. Thinking about emotion as a rather than how they feel in general. Most modern
static construct, in which participants report overall EMA software programs allow for both random and
levels of positive affect (PA) or negative affect (NA), event-cued assessments, where participants choose to
neglects information that could be gained from a complete an EMA when a certain event happens in
moment-to-moment assessment of emotional expe- their lives (e.g., a fight with a partner).
rience (Trull, Lane, Koval, & Ebner-Priemer, 2015).
In contrast, EMA methods allow researchers to Ecological Momentary Assessment Strengths
measure experiences in the moment. These methods EMA has a number of benefits when compared to
can identify contextual events that prompt or follow cross-sectional methods. These methods significantly
Abstract
427
e xternalizing behavior during early childhood (i.e., Hoeksema, 2012). Volitional emotion regulation is
ages 2 to 3) is normal (e.g., Tremblay, 2000), chil- driven by explicit goals, requires conscious effort,
dren who display high levels of externalizing behav- and demands attentional resources. Following from
iors later in childhood are at risk of developing path- this definition, emotion dysregulation refers to inap-
ological outcomes, including delinquency during propriate experience or expression of emotion that
adolescence and an increased likelihood of criminal- interferes with goal-directed behavior (Gratz &
ity in adulthood (Armistead, Wierson, Forehand, & Roemer, 2004; Gross & Thompson, 2007).
Frame, 1992; Broidy et al., 2003). Contemporary models of psychopathology view
Children who consistently engage in externaliz- emotion dysregulation as a core feature of both in-
ing behavior may be diagnosed with syndromes ternalizing and externalizing problems (e.g.,
including oppositional defiant disorder (ODD)
Beauchaine, 2015).
and conduct disorder (CD; American Psychiatric
Association [APA], 2013). ODD consists of a pat- Emotion Dysregulation in Externalizing
tern of emotional and behavioral symptoms that Behaviors
involve angry and irritable mood, vindictiveness, Externalizing disorders have traditionally been con-
argumentativeness, and defiant behavior. Children ceptualized as problems of behavior and cognition,
with ODD refuse to comply with authority and but behaviors that fall under this domain are inex-
often deliberately provoke others (APA, 2013). CD tricably linked with emotional processes.
consists of a pattern of behavior in which social Disorganization, explosiveness, and defiance are
norms and rights of others are violated. Many, hallmarks of externalizing psychopathology, and
though not all, children and adolescents with CD there is clear evidence that emotion dysregulation is
are aggressive and deceitful. Both ODD and CD associated with aggressive behavior, impulsivity, and
often co-occur with, and are developmental se- substance use (e.g., Beauchaine, 2012; Roberton,
quelae of, attention deficit hyperactivity disorder Daffern, & Bucks, 2012). In fact, undercontrolled
(ADHD; APA, 2013)—a behavioral syndrome behaviors including anger, frustration, and hostility
characterized by hyperactivity, impulsivity, and in- are common among children, adolescents, and
attention. It is not surprising that problems with adults with externalizing disorders, and manifest as
impulsivity, emotional volatility, and self-regulation a difficulty in regulating emotional responses in
are shared features among children with these exter- various situations (e.g., Robins, John, Caspi,
nalizing behavior diagnoses (see Beauchaine, Zisner, Moffitt, & Stouthamer-Loeber, 1996; Roeser &
& Sauder, 2017). Eccles, 2014). There is also a growing body of litera-
ture that identifies associations between externaliz-
Externalizing Disorders and Emotion ing behavior and inadequate self-regulation, includ-
Dysregulation ing problems inhibiting behavior and controlling
Defining Emotion Regulation attentional and cognitive processing (Roberton
Over the past 20 or so years, clinical researchers et al., 2012). Children diagnosed with externalizing
have specified how emotion regulation is associated disorders score significantly lower on measures of
with psychopathology. Current diagnostic manuals attention regulation, inhibition, and effortful con-
in psychiatry reveal that many, if not most, diagnos- trol. They also score higher on impulsivity and dis-
tic criteria contain emotion-related problems (APA, play more negative reactions to disappointment
2013; Mullin & Hinshaw, 2007), and that intense (Eisenberg et al., 2001; Roberton et al., 2012).
and/or prolonged experience of one or more nega- Historically, externalizing syndromes have been
tive emotions is maladaptive. Emotion dysregula- classified as disruptive behavior disorders in the
tion has therefore been cited as a broad, rather than DSM, but evidence suggests that emotion dysregu-
specific, risk factor for psychopathology (e.g., lation is also a core deficit (e.g., Cavanagh, Quinn,
Beauchaine, 2012). Duncan, Graham, & Balbuena, 2017). For example,
A comprehensive discussion of emotion regula- Cavanagh et al. (2017) noted that ODD and emo-
tion is beyond the scope of this chapter but can be tion dysregulation load onto a single factor and sug-
found in other chapters of this volume. Briefly, gested that ODD may be better conceptualized as
however, emotion regulation often refers to the an emotion dysregulation disorder rather than a
adaptiveness with which individuals monitor, evalu- disruptive disorder per se. Others have noted that
ate, and modify the nature and course of their emo- emotion dysregulation becomes more entrenched
tional responses to environmental demands (Nolen- and pervasive among children who progress past
Abstract
Dysregulation of emotions is a core feature of virtually all internalizing disorders. This chapter reviews
the literature on relations between emotion dysregulation and internalizing disorders, with specific
attention to the treatment of emotion dysregulation as a transdiagnostic focus. It describes several
commonly used therapy approaches, considering how each targets emotion dysregulation. It also
reviews the efficacy of programs with regard to reducing maladaptive emotion regulation strategies.
Finally, it outlines how parent emotion dysregulation is targeted in emotion socialization parenting
programs (the Tuning into Kids suite of programs). These programs provide parents with skills to
manage their and their children’s emotions effectively. The chapter finishes with summarizing how
treatments for emotion dysregulation may be strengthened.
443
risk factors. It is well established that individuals & Mead, 2007). For example, early attachment
with depression and/or anxiety experience diffi- relationships provide bases for adaptive (and mala-
culties with emotion dysregulation, including ex- daptive) emotion regulation and shape the way the
periencing negative emotions more frequently, at central nervous system processes emotions (Schore
heightened intensity, and for longer durations than & Schore, 2008). In responsive relationships, chil-
typically developing individuals (Beauchaine, 2015; dren develop skills in identifying, understanding,
Trosper, Whitton, Brown, & Pincus, 2012; Zahn- and regulating emotions, which in turn provides
Waxler, Klimes-Dougan, & Slattery, 2000). At least foundations for healthy emotional functioning
some of these difficulties are underpinned by prob- (Morris, Silk, Steinberg, Myers, & Robinson, 2007).
lems with identifying, understanding, and regulat- Therefore, revisiting family-of-origin messages
ing emotional arousal, all of which can be targeted about emotions may be important to consider when
in interventions (Barlow et al., 2010; Dozois, Seeds, teaching emotion regulation skills to reduce inter-
& Collins, 2009; Weersing, Rozenman, Maher- nalizing disorders.
Bridge, & Campo, 2012). Given shared vulnerabili- In developing our parenting program that tar-
ties to and symptoms of emotional disturbance gets emotional competencies (the Tuning into Kids
across disorders, “transdiagnostic” approaches to [TIK] suite of programs; Havighurst & Harley,
prevention and intervention that target common 2007; Havighurst, Harley, Kehoe, & Pizarro, 2012;
factors have gained traction in the literature (e.g., Havighurst, Harley, Kehoe, & Wilson, 2011;
Aldao, Nolen-Hoeksema, & Schweizer, 2010; Barlow Havighurst, Harley, & Wilson, 2010), we focus on
et al., 2010; Zahn-Waxler et al., 2000). Nevertheless, teaching parents how to respond to their children’s
there remains considerable variation in how skill emotions in ways that help develop emotional com-
deficits are addressed across treatments. Depending petencies. TIK teaches parents emotion coaching,
on underpinning theories, some interventions ad- where parents scaffold children’s learning about
dress different emotional deficits and use different emotions within a supportive, emotionally accept-
methods to target these deficits. ing relationship. By improving emotional commu-
The dominant approach used to address emotion nication in families, we have found that parents,
dysregulation among those with internalizing prob- partners, adolescents, and young children all show
lems is cognitive-behavioral therapy (CBT), which decreases in internalizing difficulties (Havighurst &
focuses on changing disordered patterns of thinking Kehoe, 2017; Havighurst, Wilson, Harley, Prior, &
and behaving by teaching reappraisal and accept Kehoe, 2010; Kehoe, Havighurst, & Harley,
ance regulation skills. However, adaptive cognitive 2014a, 2014b; Wilson, Havighurst, Kehoe, & Harley,
strategies can be difficult to use when an individual 2016). Our approach to treating emotion dysregula-
is emotionally activated, a time when maladaptive tion targets intraindividual aspects of emotion regu-
strategies are most likely to be triggered (Aldao & lation (e.g., recognition, awareness, understanding,
Mennin, 2012; Aldao & Nolen-Hoeksema, 2012; and dampening of one’s own emotions) and aims to
Aldao et al., 2010; Suchy, 2011). Furthermore, CBT improve coregulation of emotions (e.g., interper-
requires cognitive abilities that are not developed sonal emotion regulation; see Havighurst & Kehoe,
fully among very young children (Weiner, Freedheim, 2017 for a detailed review). In addition, we recog-
Stricker, & Widiger, 2003). nize the importance of culture and family of origin
Up to 50% of adult psychiatric disorders first in shaping both nonconscious and conscious emo-
emerge in childhood or adolescence (e.g., Belfer, tion regulation processes, including beliefs and at-
2008), which highlights the importance of developing titudes about emotions and “self-talk” we use during
evidence-based prevention programs. Internalizing emotional moments. Targeting these aspects of
disorders are highly familial, so children with de- emotional competence and recognizing familial and
pression and/or anxiety often have a parent with a cultural factors that shape learning about emotions
similar condition. Familial transmission results is an approach with particular promise for preven-
from biological factors, which create vulnerability tion (Kring, 2010; Trosper, Buzzella, Bennett, &
toward developing disorders (e.g., high sensitivity to Ehrenreich, 2009). By teaching parents how to
emotional stimuli, high reactivity and emotion in- optimally respond to their children’s emotional
tensity, slow return to baseline), environmental risk experiences and expression, parents learn self-talk
factors (e.g., modeling, social learning experiences, strategies that they can use to address their own
instrumental conditioning), and their interactions emotional struggles. Our studies show that a brief
(see Beauchaine, 2015; Beauchaine, Gatzke-Kopp, group parenting intervention can reduce internalizing
Abstract
Developed to treat highly suicidal patients and often associated with the treatment of borderline
personality disorder (BPD), dialectical behavior therapy (DBT) has evolved into a transdiagnostic
treatment addressing emotion dysregulation. DBT is an emotion-focused, comprehensive
cognitive-behavioral treatment including individual therapy, group skills training, between-session
skills coaching (phone coaching), and a therapist consultation team. Several elements of DBT address
emotion dysregulation directly or indirectly, including emotion regulation skills, distress tolerance
strategies to dampen physiological arousal and curb impulses to engage in problematic behaviors, and
individual therapy interventions to reduce emotion dysregulation. Growing evidence suggests that DBT
may address behavioral, cognitive, physiological, and neurobiological aspects of emotion dysregulation.
Future directions should include increasing multimethod research on the effects of DBT on emotion
dysregulation, streamlining treatment, making DBT more efficient and targeted, and conceptualizing
DBT’s place within the spectrum of other emotion-focused transdiagnostic treatments.
463
(e.g., observing and labeling emotional states), in- (e.g., a reciprocal vs. irreverent style or demeanor),
formal exposure to build tolerance of emotions, dis- (2) treatment strategies (e.g., problem solving vs.
tress tolerance strategies to reduce physiological validation), (3) skills coaching, and (4) case man-
arousal, and contingency management strategies to agement (e.g., a balance between modifying the pa-
block problematic behavior (e.g., threats, yelling) tient’s environment and helping the patient solve
while simultaneously eliciting and reinforcing more problems independently). Additionally, in DBT,
adaptive behavior (e.g., effective communication, many existing CBT-oriented coping strategies and
skills use). In this chapter, we discuss a DBT-oriented interventions are packaged as skills, forming the
conceptualization of emotions and emotion dysregu- four core DBT skills modules of mindfulness, inter-
lation, describe how DBT targets emotion dysregu- personal effectiveness, emotion regulation, and dis-
lation, summarize evidence from cutting-edge re- tress tolerance (Linehan, 1993b, 2014). Consistent
search on neurobiological changes in response to with a dialectical framework, some DBT skills
DBT, and discuss future directions. emphasize acceptance (such as mindfulness and dis-
tress tolerance), whereas others emphasize change
Overview of Dialectical Behavior Therapy (such as emotion regulation and interpersonal
When Dr. Marsha Linehan sought to develop a effectiveness).
treatment for highly suicidal individuals with Instead of performing these interventions on cli-
complex mental health concerns, she began with ex- ents, DBT therapists help clients to learn, practice,
isting, evidence-based treatments. At the time, these strengthen, and generalize skills that are effective for
treatments largely included cognitive-behavioral a variety of clinical problems. Forming new habits
therapy (CBT) techniques, including cognitive and reversing entrenched patterns of emotion dys-
therapy, relaxation skills, and behavioral approaches regulation takes consistent practice (e.g., greater
such as skills training, exposure, and contingency client-reported skills use was found to mediate treat-
management. A common thread across CBT inter- ment outcomes; Neacsiu, Rizvi, & Linehan, 2010).
ventions was the notion that clients needed to Thus, among other approaches that help clients gen-
change their thinking patterns and behavior to over- eralize therapy to their everyday lives, DBT guides
come mental health problems. Although CBT clients to become their own therapists.
sometimes yielded good outcomes, many highly As a comprehensive treatment designed for com-
suicidal, complex clients experienced this approach plex, multiproblem clients, DBT addresses several
as invalidating (Linehan, 1993a). These clients had domains within a structured treatment framework.
been suffering from intense emotional turmoil, There are five primary functions of comprehensive
sometimes for many years, and the message that DBT treatment: (1) improving client motivation to
they just needed to change their thoughts and be- change, (2) increasing client capabilities, (3) facili-
haviors seemed overly simplistic and unrealistic. tating generalization of behavioral skills to the
To address the limitations of CBT, Dr. Linehan client’s natural environment, (4) structuring the
began to incorporate specific practices (mindful- client’s treatment and natural environments, and
ness, Zen practice, acceptance) designed to convey (5) maintaining and enhancing clinician motivation
acceptance of clients and help clients accept them- and skills. Structurally, four modes of treatment
selves. Of course, empathy, validation, and self- address these functions, including individual ther-
acceptance alone are inadequate for highly suicidal apy, group skills training, telephone coaching, and a
patients with BPD, who need effective tools for re- therapist consultation team (see Table 31.1 for the
ducing misery and building “a life worth living” structure and functions of comprehensive DBT).
(e.g., a values-driven life that helps the client see In the 27 years since publication of the first ran-
function or meaning in committing to staying alive; domized controlled trial (RCT) supporting efficacy
Linehan, 1993a). Recognizing the need to balance of DBT for reducing parasuicidal behavior (e.g., sui-
acceptance strategies with evidence-based change cide attempts and self-injury; Linehan, Armstrong,
strategies, Linehan cohered this emerging treatment Suarez, Allmon, & Heard, 1991), mounting evidence
with a dialectical philosophy, which emphasizes a has supported DBT as a treatment for BPD. To
balance and synthesis between acceptance and date, over 20 published RCTs have examined stand-
change. The DBT therapist seeks to incorporate ac- ard DBT (including individual therapy, telephone
ceptance and change dialectically in all aspects of consultation, group skills training, and the DBT
treatment delivery, including (1) therapeutic style consultation team), and over 15 published RCTs
Abstract
This chapter discusses themes that emerged while editing the Oxford Handbook of Emotion Dysregulation
and outlines directions for future research. Although the term emotion dysregulation has at times
been used amorphously in the literature, most authors now define the phenomenon as experiences
and expressions of emotion that interfere with situationally appropriate, goal-directed behavior. Situational
embedding of emotion dysregulation is important given very different expectations of appropriate
emotional expression across contexts and cultures. Despite emerging consensus regarding emotion
dysregulation as a construct, several challenges lie ahead. Major tasks for the field are to (1) abandon
implicit notions of emotion dysregulation in favor of formally operationalized definitions, such as
that provided earlier; (2) maintain a clear distinction between emotion dysregulation versus mood
dysregulation; (3) map transdiagnostic features of emotion dysregulation across functional domains
of behavior such as those instantiated in the Research Domain Criteria matrix and, where appropriate,
syndromes in the Diagnostic and Statistical Manual of Mental Disorders; (4) further develop prevention
and treatment programs that systematically target emotion dysregulation across development; and
(5) extend emotion dysregulation research to stigmatized groups in an effort to identify mechanisms
of mental health disparities. Chapters in this volume address these issues and advance the science
of emotion dysregulation in new and exciting ways.
477
among constructs that are sometimes conflated, Ackerman, & Izard, 1995; John & Gross, 2004);
including emotion, mood, emotion regulation, and and (3) research on development of emotion regula-
emotion dysregulation. Although contributing au- tion, including normative trajectories and family
thors were careful in this regard, it remains common dynamics that support or disrupt emergence of
in the field to use the terms emotion and mood inter- healthy regulation (e.g., Morris, Silk, Steinberg,
changeably. Notably, however, emotions differ from Myers, & Robinson, 2007; Pang & Beauchaine,
mood in terms of both eliciting events and duration 2013; Vasilev, Crowell, Beauchaine, Mead, & Gatzke-
(Beauchaine & Cicchetti, 2019). Emotions (e.g., Kopp, 2009). These examples highlight a small frac-
desire, anger, disgust) last for short intervals (seconds tion of the voluminous literature on emotion reg-
to minutes), are elicited by specific stimuli, and ulation and emotion regulatory processes. Readers
motivate behavioral action or inaction (see Fox, who are interested in expended discussion regarding
2018). In contrast, moods (e.g., anhedonia, depres- theory, definitions, and measurement of emotion
sion, mania) are more persistent (hours to weeks), regulation are referred to comprehensive reviews
are imbued by broader internal and external milieus, (e.g., Adrian, Zeman, & Veits, 2011; Cole, Martin,
and bias behavior, cognition, and emotion over time & Dennis, 2004; Sheppes et al., 2015).
(Fox, 2018). Although emotions can affect mood In contrast to the situationally functional nature
and mood can bias the valence of emotions, mood of emotion regulation, emotion dysregulation im-
and emotion are distinguishable phenomena. For plies failure to dampen strong emotional responses
example, depressed individuals sometimes show less to achieve situational objectives. This may include
emotional reactivity to sadness-eliciting stimuli than inappropriate/ineffective use of emotion regulation
healthy controls (Rottenberg, 2005). Thus, mood skills and strategies. Thus, emotion dysregulation is
dysregulation is not synonymous with emotion dys- often conceptualized at least in part by difficulties
regulation (see also Sheppes, Suri, & Gross, 2015). with emotion regulation (e.g., Gratz & Roemer,
For this reason and others, consistent definitions 2004). A common result of this conceptualization is
are critical when distinguishing between mood a view of emotion regulation and dysregulation as
and emotion. distinct endpoints along a single dimension, which
oversimplifies both constructs.
Emotion Regulation Versus Dysregulation In this volume, we urged authors to use a single
The study of emotion regulation dates back further definition of emotion dysregulation to provide con-
in time than the study of emotion dysregulation. sistency across chapters. According to this perspec-
Consequently, there are widely used definitions of tive, emotion dysregulation is characterized by “a
emotion regulation that are well established and pattern of emotional experience and/or expression
guide scientific inquiry. Thompson (1994) defined that interferes with appropriate goal-directed be-
emotion regulation as “extrinsic and intrinsic pro- havior” (Beauchaine, 2015a, p. 876). This defini-
cesses responsible for monitoring, evaluating, and tion, which we discuss in further detail elsewhere
modifying emotional reactions, especially their in- (Beauchaine & Cicchetti, 2019; Beauchaine &
tensive and temporal features, to accomplish one’s Haines, 2019), underscores several important as-
goals” (pp. 27–28). Similarly, Gross (1998) defined pects of emotion dysregulation, beginning with an
emotion regulation as “processes by which individu- emphasis on emotion rather than mood, as outlined
als influence which emotions they have, when they earlier. A critical aspect of this definition is its ag-
have them, and how they experience and express nostic stance vis-à-vis evolutionary functions of
these emotions” (p. 275). These definitions form the emotions. Instead, it focuses on “appropriate” goal-
foundation of several intersecting lines of research directed behavior. Thus, the definition is embedded
on emotion regulation, including (1) laboratory emo- in situational functionalism—not evolutionary func-
tion elicitation research in which participants are tionalism. Many emotions and behaviors that may
directed to regulate or not regulate emotions accord- have conferred selective advantages in our evolution-
ing to specific instructions (e.g., Ehring, Tuschen- ary environments of adaptation have no bearing on
Caffier, Schnülle, Fischer, & Gross, 2010; Gross & fitness in our contemporary environments (Mead,
Levenson, 1993; Gyurak, Gross, & Etkin, 2011); (2) Beauchaine, & Shannon, 2010). In fact, certain be-
explorations of individual differences in emotion haviors such as impulsivity may have been adaptive
regulation and its associations with temperament, in specific evolutionary contexts but place individu-
personality, and/or psychopathology (e.g., Aldao, als at situational disadvantage in classrooms, work
Nolen-Hoeksema, & Schweizer, 2010; Cicchetti, environments, and so forth.
Note: Figures and tables are indicated by an italic “f ” and “t” respectively, following the page numbers.
487
anterior cingulate cortex (ACC) (Continued ) attention core affect and 190
in cognitive control 72 defined 15 individual differences in arousal 61
in depression 256 emotion in relation to 40–44 internalizing spectrum disorders
in emotion regulation 91, 137 late positive potentials and 169, 170, and 256
in motivated behavior 20 170f psychosis spectrum disorders and
overmodulation and 271 motivated behavior and 17 304–306
in reappraisal of negative emotion 4 psychosis spectrum disorders and 300 synchrony during conflict
respiratory sinus arrhythmia and 155 salience network and 187 conversations 105
trait anxiety and 87 selective 73 avoidance emotions 2–4, 6, 88
undermodulation and 271 attentional biases
antidepressant medications 47, 142, addiction and 316, 318–319 B
161n1, 173 autism and 30 Babkirk, S. 171
antisocial behavior 238–242, 436 borderline personality disorder Babuscio, T. 319
antisocial personality disorder (ASPD) and 365, 370 BAM (Becoming a Man) program 434
92, 227, 239 childhood maltreatment and 251–252 Bardeen, J. R. 274
anxiety disorders. See also specific conditions congruent mood state and 43 Barlow, D. H. 447, 473
addiction and 314 emotion regulation and 41, 213 Barrett, Lisa Feldman 5–6, 28–30
attentional biases and 41 vulnerability to 208 BAS (behavioral activation system) 414
autism and 283, 285, 286 attentional deployment 40, 73, 132–133, BASC (Behavioral Assessment System
brain regions related to 20, 188, 189, 135, 302, 447 for Children) 429
192–193 attention-deficit/hyperactivity disorder basic emotions
emotion dysregulation and 47, 254 (ADHD) in affective neuroscience 185
family influences on 102–103, 251–253 delinquency associated with 242, 243 eating disorders and recognition of 335
functional connectivity deficits and 4, developmental progression from 238, hyperactivation of 19
188 241, 243, 428 locationist perspective on 7
gender differences and 92, 443 dopaminergic function and 227, 228 LPP potentiation to 170
late positive potentials and 173 emotional lability and 58 motivated behavior directed by 17–18
maladaptive motivated behavior environmental influences on 242 neural structures in promotion of 3, 6
and 21–22 ontogenic process perspective on 238, Pankseppian model of 15–16, 20
in older adults 78, 79 242, 243f regulatory strategies vs. 93–94
predictive factors 19 parent training interventions for 431 basic emotion theory 6, 28, 185
prenatal exposure to 143 prefrontal cortex development and 240 Baumeister, R. F. 30, 469
prevalence of 443 respiratory sinus arrhythmia and 156 Bayley Scales of Infant Development 385
regulatory strategies and 136 risk factors for 87 BDNF (brain-derived neurotrophic factor)
respiratory sinus arrhythmia and 156, trait impulsivity and 238–240, 242 gene 209, 257
157, 257 treatments for 431, 434, 435 Beauchaine, Theodore P. 1, 87, 89–90,
serotonergic function and 225 Attention Network Task 411 128, 153, 227, 237, 465, 477
trait anxiety and 78, 85, 87, 89 attributional biases 5, 102, 104, 434 Becerra, R. 398
treatments for 173, 203, 432, 449–452 attunement 143–145 Bechara, A. 69–70
approach emotions 2–4, 6, 88, 227 Atzil, S. 149 Becker, S. P. 271
Armey, Michael F. 352–353, 411 autism spectrum disorder (ASD) 283–292 Beckes, Lane 27, 32
arm restraint task 386 attentional biases in 30 Becoming a Man (BAM) program 434
ASD. See autism spectrum disorder behavioral difficulties and 284 BED (binge eating disorder) 327–333,
ASEBA (Achenbach System of Empirically comorbidity and 283, 285, 290, 291 336–338
Based Assessment for School-Age diagnostic formulation of 283, behavioral activation system (BAS) 414
Children) 429–430 285–286 behavioral assessments 377–389.
ASPD (antisocial personality disorder) 92, electrophysiology and 288 See also behavioral observation;
227, 239 emotional lability and 58, 283, 286 specific assessments
Aspinwall, L. G. 93 future research directions 291–292 computerized 387–389
Asselbergs, J. 420 genetic influences on 289–290 of externalizing spectrum
associative learning 3, 4, 227 methodology for study of 286–292 disorders 429–430
Atchley, Rachel M. 313 neuroimaging studies and 288–289 future research directions 389
attachment figures 31 psychophysiology and 287–288 multiple levels of analysis in 63, 380
attachment theory respiratory sinus arrhythmia and 156 for schizophrenia 303
adaptive-basins model and 31–32, 34 theoretical models of emotion theoretical perspectives on 378–379
development of 141 dysregulation in 284–286 Behavioral Assessment System for
disorganized attachments 32, 100–101, autobiographical memory 46, 170, 176, Children (BASC) 429
108, 252, 363 192, 412, 420 behavioral expression 14–16, 19, 21, 90, 133
elements of 31 automated computer vision and machine behavioral inhibition system (BIS) 414
on emotion dysregulation 100–101 learning (ACVM) 480 behavioral observation
insecure attachments 100, 120, 144, 252 autonomic nervous system (ANS) advantages of 55, 378
internalizing spectrum disorders activation without emotion 33 analog tasks 379, 385–387
and 252 autism and 287 analytic approach to 62–63
488 index
of children and adolescents 56–62 borderline personality disorder C
coding systems for 117, 387 (BPD) 361–372 Cabanac, M. 17
of context-inappropriate emotion brain regions related to 20, 91, 365–367, Cacioppo, J. 69–70
57–58, 62 370, 466, 470–472 Caffier, D. 337
of duration of emotion 59–60 characteristics of 361–362, 429, Calkins, S. D. 120
of emotional lability 58–59, 63 466–467 callous-unemotional (CU) traits 58–59,
of emotion dysregulation 55–63, comorbidity and 367, 372 156, 271–272
205, 253, 430 ecological momentary assessment Campbell-Sills, L. 447
length and number of 60–61 of 367, 417–418 Campitelli, G. 398
limitations of 63, 290, 378, 412 emotional responding in 364–368 candidate epigenetic studies 224–225, 231
methodology for 380, 381–384t emotion dysregulation within 58, 129, candidate gene studies 109, 207t,
naturalistic 380, 385 225, 466–467 208–210, 214
structured tasks 385 future research directions 371–372 Cannon, T. D. 212
Bell, Spencer 313 gender differences and 92 Carroll, K. M. 319
Bell, Ziv E. 153 graphical depiction of emotion Carter, J. C. 331
Benight, C. C. 273 dysregulation in 371, 371f cascading systems 30–33, 34f
Bennett, D. C. 271, 275 late positive potentials and 176 Castaldo, R. 156
Bents, H. 331 parent–child interactions and 120 catechol-0-methyltransferase (COMT)
Berg, K. C. 334 posttraumatic stress disorder and 367 gene 90, 208, 209
Beri, S. 226 regulatory strategy use in 364, categorization, in theory of constructed
Berk, Michele 377 368–370 emotion 190, 192
Berner, L. A. 334 respiratory sinus arrhythmia and 156 Cavanagh, M. 428
Bernston, G. 69–70 self-inflicted injury in 361, 363, 416, CBT. See cognitive-behavioral therapy
biases. See also attentional biases 417, 470–471 CD. See conduct disorder
attributional 5, 102, 104, 434 serotonergic function and 225–226 Cecil, C. A. M. 269
in brain development 29 theoretical perspectives on 362–364 central nervous system 15, 155, 185, 225,
in heritability estimates 205 treatments for 367, 370, 451, 463–471 287, 444
information processing 378, 449 Bowlby, J. 31, 32, 100, 141, 266 Chaplo, S. D. 275
in older adults 72, 73, 75, 77 Boyle, C. L. 123 Chapman, Alexander L. 463
Pavlovian 5 BPD. See borderline personality disorder Chentsova-Dutton, Y. E. 93
recall 333, 418 Bradley, B. 265 Child Behavior Checklist (CBCL) 429,
self-referential 171, 172, 176 brain. See also affective neuroscience; 434, 436
binge eating disorder (BED) 327–333, neuroimaging; specific parts childhood abuse
336–338 of brain dissociation and 55
Binion, Grace 115, 118 evolution of 186 epigenetics and 269
biological pathways. See also limbic- functional patterns of activity in 187 internalizing spectrum disorders
hypothalamic-pituitary-adrenal axis neurodevelopment 29, 35, 239–241, and 251–252
alteration through DNA 285, 292, 349 invalidating environment and 122
methylation 224 triune brain concept 185–186 orbitofrontal cortex and 241
candidate epigenetic studies of 225 brain-derived neurotrophic factor (BDNF) respiratory sinus arrhythmia and 158
epigenetic studies with 224–230 gene 209, 257 risk factors for 144
neurotransmitter systems 225–228, Brammer, S. 429 self-regulation and 103
267 Brazelton Neonatal Behavioral Assessment childhood maltreatment. See also
biometrical model 204–206, 207t, 212 Scale (BNBAS) 385 childhood abuse
biosocial theory 117, 176, 362–363, 432, Bremner, J. D. 267 allostatic load and 228
466, 474n1 Brennan, Patricia A. 427 context-inappropriate emotion
bipolar disorder. See also depression; mania Bridgett, D. J. 156 and 57–58
context-inappropriate emotion and 57 Brockmeyer, T. 331 emotion dysregulation in aftermath
ecological momentary assessment Brody, G. H. 231 of 273–274
of 415 Brown, April L. 427 familial dysfunction and 89, 270
genetic influences on 212 Brown, E. J. 122 genetic interactions with 209, 257, 258
L-HPA axis dysfunction and 228 Brown, Mindy 221 internalizing spectrum disorders
valuation of emotion in 134 Buckner, J. D. 419 and 251, 253, 254
BIS (behavioral inhibition system) 414 bulimia nervosa (BN) 327–338 salience network activation and 256
BN. See bulimia nervosa characteristics of 327 childhood trauma 265–276. See also
BNBAS (Brazelton Neonatal Behavioral ecological momentary assessment posttraumatic stress disorder
Assessment Scale) 385 of 332–335, 418 biopsychosocial processes in 268–270
Boden, M. T. 276 experimental research on 335–338 callous-unemotional traits and 271–272
body–mind training 435 self-report assessments and 329–332 conceptualizations of 266–268
body regard 353–354 socioemotional processing and Developmental Trauma Disorder
Bohlmeijer, E. T. 452 335–336 proposal and 272–273
Boker, S. M. 213 theoretical models related to 328 emotion dysregulation in aftermath
Bolger, N. 413 Butler, E. A. 92 of 265, 273–275
index 489
childhood trauma (Continued ) DERS score improvement computerized behavioral tasks 387–389
future research directions 275–276 following 401 COMT (catechol-0-methyltransferase)
over-/undermodulation subtypes for eating disorders 331 gene 90, 208, 209
and 271 late positive potentials and 173 conduct disorder (CD)
children and adolescents. See also family; limitations of 464 characteristics of 428
parent–child interactions for maladaptive motivated behavior 22 developmental pathway to 238, 241
abuse of (see childhood abuse) for posttraumatic stress disorder 276 dopaminergic function and 227
attachment theory and 31–32, 100–101 principles of 432, 444, 449 environmental influences on 242
autistic (see autism spectrum disorder) for psychosis spectrum disorders 307 functional connectivity deficits
cognitive control in 42 cognitive change 40–42, 73, 132, 133, and 240
context-inappropriate emotion in 301–302, 447 gender differences and 92
57–58 cognitive control. See also executive neural deficits related to 91
dissociation among 55 functioning prefrontal cortex development
duration of emotion in 59–60 age-related changes in 71–73 and 240, 241f
eating disorders among 327 borderline personality disorder respiratory sinus arrhythmia and 156,
emotional lability in 58–59, 253, 350 and 368–369 257
emotional modulation of LPPs in brain regions related to 72–73, 185, risk factors for 87, 89
170–171 255–256 trait impulsivity and 239
in environments of adaptation 3 emotion in relation to 45–46, 72–73 treatments for 434
gender-specific socialization in socioemotional selectivity theory 70 conflict
practices and 92 cognitive deconstruction 469 adaptation to 45, 46
maltreatment of (see childhood cognitive-interpersonal maintenance coercion theory and 117
maltreatment) model of anorexia nervosa 329 escalation of 58, 88, 93, 119
motivated behavior in 18 cognitive motor group 192, 195n5 externalizing spectrum disorders
observation of (see behavioral cognitive reappraisal and 242
observation) addiction and 318–320 in interaction models 119
prefrontal cortex response in 4 age-related changes in use of 74 marital 101, 104
respiratory sinus arrhythmia in borderline personality disorder and 368 resolution of 46, 87, 350
156–158 brain regions related to 42, 318 in romantic relationships 145–146
self-inflicted injury by 345–346, 352 defined 41, 133, 254, 301 skills for management of 463, 468
self-regulation by 56, 102–104 detached 74 conflict discussion task 93, 146, 148, 386
trauma and (see childhood trauma) eating disorders and 332 Conkey, Lindsey C. 361
treatment strategies for 432–435, 449, effectiveness of 59 Conners’ Rating Scales (CRS) 429
480–481 in emotion coaching 457 Conradt, Elisabeth 108, 221
Children’s Emotion Management late positive potentials and 169–170, constructed emotion theory 5, 183–184,
Scales 430 170f, 172–176 189–194
chromatin 222, 230 limitations of 42, 135 constructionism
Cicchetti, Dante 249, 273, 274 operant reinforcement and 118 in affective neuroscience 183–184,
cigarettes 175, 313–315, 317–319 positive 74, 79 189–194
Clement, P. F. 328 psychosis spectrum disorders and 301, convergence and divergence with
Clore, G. L. 30 302 functionalism 6–8
Coan, J. A. 32 as therapeutic technique 41, 46–47, implications for emotion
cocaine 175, 313–314, 319–320 437 dysregulation 5–6
Coccaro, E. F. 205 cognitive reframing. See cognitive innateness vs. 29
coercion theory 117, 121 reappraisal principles of 4–5
cognition Cohn, A. M. 429 psychological 188, 189, 191
attention (see attention) Cole, Pamela M. 53 theory of constructed emotion 5,
constructionist accounts of 4 common pathway model 206 183–184, 189–194
decision making (see decision making) comorbidity context, in emotion dysregulation 2, 27,
eating disorders and 330 of anxiety and depression 173 35, 75–76
emotion in relation to 39–47, 72 autism and 283, 285, 290, 291 context-inappropriate emotion 57–58, 62
learning (see learning) borderline personality disorder Cooper, J. L. 330
memory (see memory) and 367, 372 core affect theory 5, 7, 28, 54, 190
psychopathology and 136–137 emotion dysregulation as 285 coregulation 88, 350, 444, 448
in psychosis spectrum disorders genetic and environmental core limbic group 191, 192, 195n3
304–305 influences 212 Corner, Geoffrey W. 141
serotonin and 225 internalizing–externalizing 62, 158, 285 C-PTSD (complex posttraumatic
spontaneous 55 psychosis spectrum disorders and 299 stress disorder) 267
cognitive-behavioral therapy (CBT) regulatory deficits and 206 Cross, D. 265, 269
ACS score improvement competitive games with peer Crowell, Sheila E. 85, 119, 158, 209, 221,
following 402 confederates 386 225, 345, 363, 477
for children and adolescents 434, 449 complex posttraumatic stress disorder Crowther, J. H. 352–353
cognitive reappraisal in 41, 46–47, 437 (C-PTSD) 267 CRS (Conners’ Rating Scales) 429
490 index
Csikszentmihalyi, M. 413, 414 regulatory strategies and 135 emotion dysregulation as
Cukrowicz, K. C. 147 respiratory sinus arrhythmia and 156, conceptualized in 465–467
Culbert, K. M. 335 161n1, 257 empirical support for 464–465,
cultural influences 2, 90, 93, 479, rumination and 41 470–472
481–482 salience network dysregulation in 193 future research directions 472–474
Cummings, E. M. 104 serotonergic function and 225, 226 interpersonal processes and 149
CU (callous-unemotional) traits 58–59, suicidal ideation and 79, 172 metaphor use in 474n1
156, 271–272 symptoms of 171, 227, 254 modes and functions of 464, 465t
Cyders, M. A. 332 treatments for 432, 450–452 neurobiological changes following
DERS. See Difficulties in Emotion 470–472
D Regulation Scale for parent–child interactions 124
Damasio, A. R. 30 detached reappraisal 74 physiological issues addressed by
DAPP-BQ (Dimensional Assessment development. See also socioemotional 468–469
of Personality Pathology–Basic development principles of 432, 450–451
Questionnaire) 396–397 brain-related 29, 42, 88 for psychosis spectrum disorders 307
Darwin, Charles 6, 101, 141 defined 15 for self-inflicted injury prevention 354
Davidson, R. J. 176 of emotion dysregulation 100–103, skills training component of 433, 434,
Davies, P. T. 104 116–121 463–464, 467–469
Davis, B. 386–387 motivated behavior and 18 stepped-care models of 474
DBT. See dialectical behavioral therapy neurodevelopment 29, 35, 239–241, streamlining 473
DeBaryshe, B. 117 285, 292, 349 Diamond, L. M. 93
decision making normative patterns of 230 diathesis-stress model 108, 109
age-related changes in 77, 79, 80 developmental perspective differential susceptibility 103, 108–110
emotion in relation to 30, 31, 44–45 on behavior assessment 379 Difficulties in Emotion Regulation
improvement strategies 434 on emotion dysregulation 88, 89, Scale (DERS)
maladaptive 183 251–253, 349–351 age-related effects and 77
somatic marker hypothesis on 30–31, on externalizing spectrum alternate versions of 401, 411
45 disorders 429 in behavioral observation 56
systemic biases in 44 on internalizing spectrum borderline personality disorder and 472
Decker, S. E. 319 disorders 251–253, 259 core emotion difficulties assessed by
Deckersbach, T. 398 on psychopathology 86, 87, 89, 257 348, 430
DeClaire, J. 453, 457 resilience in 86 eating disorders and 329–331, 338
default mode network (DMN) 192–194, on treatment strategies 431 empirical support for 400–401
289 Developmental Trauma Disorder phenotype assessment and 213
defensive regulation model 272 (DTD) 272–273 posttraumatic stress disorder and
DeGarmo, D. S. 242 DeWall, N. C. 30 274–275
degeneracy 28, 29, 194 Diagnostic and Statistical Manual of Mental self-inflicted injury and 354
Delahanty, D. L. 273 Disorders, 5th edition (DSM-5) digital phenotyping 420
delusions 300, 304–306 discrete order approach of 237 Dimaggio, G. 225
deoxyribonucleic acid (DNA) eating disorders in 327 Dimensional Assessment of Personality
composition of 208, 222 emotional symptoms of Pathology–Basic Questionnaire
double helix structure of 222, 223f psychopathology in 71, 127 (DAPP-BQ) 396–397
methylation 208, 222–231, 269 internalizing spectrum disorders in 251, disappointing gift paradigm 118, 386
transcription 208, 222, 269 445 discrete emotion theories 54
depression. See also bipolar disorder on nonsuicidal self-injury disorder 348 discrimination 266, 481–482
addiction and 314 on psychosis spectrum disorders 299, disorganized symptoms 300, 301
autism and 283, 285 306 dissociation 55, 267, 271, 272, 361, 367
brain regions related to 20, 256 on suicidal behavior disorder 348 distraction
cognitive control deficits and 45 trauma and PTSD in 195n2, 266, cognitive resources and 73–74
ecological momentary assessment 267, 270 effectiveness of 40, 59, 133
of 414–415 dialectical behavioral therapy late positive potentials and 177
emotional lability and 58 (DBT) 463–474 limitations of 41
family influences on 102, 104, 251–253 ACS score improvement following 402 operant reinforcement and 118
gender differences in 92, 443 behavioral issues addressed by distress tolerance
genetic influences on 212 467–468 assessment of 389
late positive potentials and 171–173 for borderline personality borderline personality disorder and 369
learned helplessness and 134 disorder 370 invalidating environment and 118
L-HPA axis dysfunction and 228 for children and adolescents 433–435, laboratory-based assessment of 213
medications for 47, 142, 161n1, 173 481 serotonergic function and 90, 208, 209
in older adults 78–79 cognitive issues addressed by 469–470 strategies for 451, 463, 467
postpartum 147, 149 DERS score improvement distress tolerance test (DTT) 389
prenatal exposure to 142 following 401, 472 Ditzen, B. 148
prevalence of 443 for eating disorders 331 Dixon-Gordon, Katherine L. 361
index 491
DMN (default mode network) 192–194, socioemotional processing and dual-process model of 30
289 335–336, 338 evolutionary perspective on 2–3, 6–8
DNA. See deoxyribonucleic acid state–trait emotion interactions in 335 functionalist accounts of 2–4, 6–8,
Docherty, Anna R. 299 theoretical models related to 328–329 54, 60
domain-relevant approach to treatments for 329, 331 generation of (see emotion generation)
emotion 27–31, 33–35, 34f ECI (Emotion Context-Insensitivity) as information 30–34, 44–45
domain specificity of emotion 27–29, model 171 interpersonal levels of 92–93
31, 35 ecological momentary assessment intrapersonal levels of 89–92
domestic violence. See intimate (EMA) 411–420 measurement challenges 250
partner violence of addictive behavior 321 mechanistic perspective on 13–14
dopamine advantages of 412–413 modal model of 41
anhedonia and 227, 239, 349 of bipolar disorder 415 mood vs. 33, 445, 447–478
autism and 289–290 of borderline personality disorder 367, motivated behavior and 14, 20, 21
in developmental theory 89 417–418 neural bases of 185–189, 191–193
in emotion dysregulation 227–228 of cognitive reappraisal 302 overmodulation of 270–272, 275, 276
in reward processing 7, 228 of depression 414–415 Pankseppian model of 15–17
trait impulsivity and 239 of eating disorders 328, 332–335, 338, regulation of (see emotion regulation)
variation in receptor genes 32, 109 418–419 social behavior regulation through
Doussard-Roosevelt, J. A. 154 of emotional inertia 213 27–35
Doyle, C. 273 of emotion socialization 119 socialization of (see emotion
Drabant, E. M. 90 incorporation in multimethod socialization)
DRD4 gene 109, 110, 227–228 research 214 theories of (see emotion theories)
drug abuse. See substance use disorders of individual differences in emotional undermodulation of 270–272, 275,
DSM-5. See Diagnostic and Statistical trajectory 413–414 276
Manual of Mental Disorders, limitations of 413 Emotion-Affect Regulation Interview 430
5th edition overview 411 emotional awareness
DTD (Developmental Trauma psychophysiological measures and 414 borderline personality disorder
Disorder) 272–273 of self-inflicted injury 352–354, and 368, 467
DTT (distress tolerance test) 389 416–417 default mode network and 289
dual-generation interventions 121–123 self-report assessments and 116 individual variations in 134
dual-process model of emotion 30 of specific emotions over time 414 lack of 274, 330, 348, 362
Dudeney, J. 104 of stress response 413–414 parenting interventions for 454
Duncan, L. E. 211 of substance use craving 419–420 psychosis spectrum disorders and 301,
duration of response metric 176 unobtrusive 420 304, 305, 307
Dvorak, R. D. 403 ecological momentary interventions emotional behavior
dyadic processes. See also parent–child (EMIs) 420 abrupt changes in 58–59, 62–63
interactions Edelbrock, C. 237 afunctional 2, 3, 479
emotion in 63, 141 EDs. See eating disorders age-related changes in 76–78
at interpersonal level of emotion 92–93 Edwards, Weston Layne 27 in children and adolescents 32
romantic relationships 145–148 EFT (emotion-focused therapy) 449–450, context-inappropriate 57–58, 62
in self-regulation development 433 455 duration of emotion 59–60, 78, 80
dynamic systems theory 54, 55, 60 Egeland, B. 120 organism-wide 17
Ehrmantrout, N. 386–387 emotional clarity
E Eimer, M. 170 borderline personality disorder and
eating disorders (EDs) 327–339. Eisenberg, N. 104 363, 368, 467
See also anorexia nervosa; Elbert, T. 272 eating disorders and 330, 331, 336
bulimia nervosa elderly persons. See aging lack of 272, 274, 275, 348, 354
binge eating disorder 327–333, electroencephalography (EEG) 19, 184, schizophrenia and 305
336–338 193, 288, 291, 319 emotional competence 57, 122, 430,
in DSM-5 327 electrophysiology 153–154, 288, 317 444–447, 453
ecological momentary assessment Elliot, A. J. 414 emotional go/no-go tasks 388–389, 411
of 328, 332–335, 338, 418–419 EMA. See ecological momentary emotional inertia 213
emotion dysregulation in prediction assessment emotional lability
of 254 EMIs (ecological momentary autism and 58, 283, 286
experimental research on 335–338 interventions) 420 behavioral observation of 58–59, 63
future research needs 339 emotion callous-unemotional traits and 58–59
gender differences in 327 basic (see basic emotions) in children and adolescents 58–59,
integrative model for 338–339 cognition in relation to 39–47, 72–73 253, 350
mood manipulation and 337–338 constructionist accounts of 4–8, 29 defined 58
prevalence of 327 definitions of 14–15, 33, 167, 184, 445 functional connectivity deficits and 4
psychophysiology and 336–337 domain-relevant approach to 27–31, negative reinforcement of 157, 158
regulatory strategy use in 332 33–35, 34f psychopathology and 58, 59, 397
self-report assessments and 329–332 domain specificity of 27–29, 31, 35 respiratory sinus arrhythmia and 116
492 index
emotional reactivity constructionist accounts of 5–6 definitions of 39–40, 70, 87, 154, 204,
addiction and 317, 319, 320 context in 2, 27, 35, 75–76 300, 362, 411, 478
age-related changes in 70, 75 cultural influences on 93, 479, executive functioning and 72
borderline personality disorder 481–482 functionalist accounts of 4, 101–103
and 363, 365–368, 371, 372, 466 definitions of 3, 39, 71, 128, 154, genetics (see genetic influences)
cultural influences on 93, 479 250, 411, 478–479 implicit vs. explicit 70, 80, 137
defined 128 developmental perspective on 88, 89, interpersonal (see interpersonal
depression and 213 251–253, 349–351 processes)
family influences on 104 eating disorders and (see eating molecular genetics and 208–212, 257
late positive potentials and 172, disorders) motivations for engagement in 128
174–176 functionalist accounts of 4, 101–103, parenting interventions for 455–456
posttraumatic stress disorder and 271 110, 348 process model of (see process model of
psychosis spectrum disorders and genetics and (see genetic influences) emotion regulation)
300, 303 intergenerational transmission of 143, socioemotional development and 431
reduction of 448 146, 149, 221 stages of 88, 130–136, 131f
startle response and 287 interpersonal processes and strategies for (see regulatory strategies)
to stressors 257, 317 (see interpersonal processes) validity of construct 250
temperament and 284 motivated behavior and 18–19 as valuation system 129–130, 130f
emotional responding multidimensional model of 362 Emotion Regulation Checklist 56, 58,
addiction and 316–317, 320, 321 neuroimaging of (see neuroimaging) 274, 430
blunting of 57 patterns of behavior indicative of Emotion Regulation Questionnaire 74,
in borderline personality disorder 56–60 276, 302
364–368, 371, 372 personality disorders (see specific emotion socialization
cognitive control over 42 disorders) childhood maltreatment and 270
in decision making 44 reinforcement of (see operant ecological momentary assessment
in depression 171 reinforcement) of 119
dopamine pathways and 227 in relationships (see relationships) family processes in 61, 117, 479–480
in dyadic interactions 63 self-injury (see self-inflicted injury) internalizing spectrum disorders
maladaptive 18–19, 71 stigma and 304, 305, 481–482 and 104, 257
manipulation of 40–42 trauma (see trauma) invalidating environment and 122–123
quantification of 176 treatments for (see treatment training interventions 121, 453
socioemotional development and 453 strategies) emotion theories
emotional security hypothesis 104 emotion-enhanced memory 43 basic emotion theory 6, 28, 185
emotional sensitivity 349, 350, 363–365, Emotion Expression Scale for constructed emotion theory 5,
396–398, 451, 466 Children 430 183–184, 189–194
emotional stop-signal tasks 412 emotion-focused therapy (EFT) 449–450, core affect 5, 7, 28, 54, 190
emotional systems 15–20, 30, 46 455 discrete 54
emotional well-being emotion generation domain-relevant approach in 29
aging and 69–72, 75–77, 79, 80 integrated theory of 87 dynamic systems 54, 55, 60
autism and 283 models of 8, 86–87, 128 future research directions 35
cognitive reappraisal and 133 psychopathology and 250 EMSP (emotion-modulated startle
defined 69 regulation processes during 40, 73 paradigm) 337
self-care for 455, 456 situation–attention–appraisal–response endophenotypes 32, 212, 214, 239, 415
supportive interactions and 148 perspective on 86 Engel, S. G. 333, 335, 419
emotion-as-social-information model 31 subcortically mediated 4, 86, 87, 91, English, T. 448
emotion avoidance model of anorexia 320 environmental influences
nervosa 328–329 as valuation system 129–130, 130f differential susceptibility to 103,
emotion coaching 104, 121, 157, 270, emotion induction procedures 387 108, 109
444–445, 453–457 Emotion Management Scales 56 epigenetics and 221, 224
Emotion Context-Insensitivity (ECI) emotion misregulation 47, 129 on externalizing spectrum disorders
model 171 emotion-modulated startle paradigm 241–243
emotion dysregulation. See also (EMSP) 337 on phenotypes 206
psychopathology emotion paradox 303 on prefrontal cortex
in addiction (see addiction) Emotion Reactivity Scale (ERS) 398 neuromaturation 240–241
aging and (see aging) emotion regulation on respiratory sinus arrhythmia 156
assessment of (see behavioral addiction and 317–321 epigenetics 221–231
assessments; ecological momentary aging and 70–75 biological pathways in 224–230
assessment; self-report assessments) brain regions related to 91 childhood trauma and 268–269
attachment theory on 100–101 cognitive control and 72–73 controversies and challenges to
in autism (see autism spectrum disorder) conceptualizations of 55, 167, 428, study of 230–231
as comorbidity 285 446, 465 defined 29, 221, 258
conceptualizations of 53–55, 88, 167, context in 2, 27, 35, 128 DNA modifications and 208, 221
300, 396–397, 428, 446, 465–466 cultural influences on 93, 479 history of 224
index 493
epigenetics (Continued ) first-order syndromes 238 Froeliger, Brett 313, 316
in intergenerational transmission of functional connectivity deficits and 4 frontoparietal network 190, 192, 193
emotion dysregulation 143, 221 gender differences in 92, 291 frustration tasks 120, 252, 386
internalizing spectrum disorders genetic influences on 90, 142–143, 206 Fruzzetti, A. E. 329
and 258, 259 prefrontal cortex neuromaturation functionalism
methodology for study of 224–225, and 239–241 on behavior assessment 378–379
229–231 prevention strategies for 435–436 convergence and divergence with
overview of processes in 222–224 resilience against 91 constructionism 6–8
stress and 106, 107 respiratory sinus arrhythmia and critiques of 5–8
temperament and 86 156–160 on emotion dysregulation 4, 101–103,
epigenome-wide association studies trait impulsivity and 87, 89, 238–240, 110, 348
(EWASs) 224, 225, 229, 230 242–243 evolutionary 2–3, 6–8
equifinality 19, 429 treatments for 430–437 locationist basic emotion perspective
error-related negativity (ERN) 193 of 7
ERS (Emotion Reactivity Scale) 398 F on relational processes of emotion
escape model of binge eating/bulimia face-to-face still-face paradigm 54, 60
nervosa 328 385–386 situational 478–479
essentialism 185 facial expressions variant uses of term 2–4
event-related potentials (ERPs) 168, 176, amygdala in perception of 186–187 functional magnetic resonance
193. See also late positive potentials deficits in processing 283, 304, 446 imaging (fMRI)
evolution emotion transmission through 144 addiction and 317, 319
of brain 186 evolutionary role of 141 advantages of 184
conservation of emotion across 15, 16 mood states influenced by 448 amygdala habituation to emotional
facial expressions and 141 of negative emotion 63, 85 stimuli in 209
innate processes and 29, 30 in somatic marker hypothesis 30 in behavioral observation 430
natural selection in 6 family. See also children and adolescents; history of neural studies with 6
of social behavior 155 parent–child interactions internalizing spectrum disorders
teleological misconceptions of 5, 6 appraisal processes influenced by 102 and 255, 256
evolutionary functionalism 2–3, 6–8 in emotional socialization processes 61, limitations of 7
EWASs (epigenome-wide association 117, 479–480 mechanisms of 184
studies) 224, 225, 229, 230 emotion dysregulation influenced by on neural activation changes following
executive functioning 103–104, 479–480 DBT 470–472
brain regions related to 4, 192, 431 in genetic studies of emotion overmodulation and 271
defined 45 regulation 204–206, 212 functional neuroimaging 19, 21, 184
emotion regulation and 72 internalizing spectrum disorders and functional polymorphisms 208
environmental influences on 241 251–253, 444
in overriding motivational marital conflict within 101, 104 G
tendencies 19 Family Stress Model 101, 104 Gable, S. L. 414
in psychosis spectrum disorders 300, Fani, N. 265 GAD (generalized anxiety disorder) 89,
305 Fast Track program 436 156, 173, 192–193, 256, 285
respiratory sinus arrhythmia and 155, fear conditioning 43, 186 Garland, Eric L. 313, 316
156 Feldman, R. 105, 149 GCTA (genome-wide complex trait
in theory of constructed emotion felt security 31, 34 analysis) 207t, 211–212
190–191 females. See gender differences GEDM (General Emotion Dysregulation
trauma exposure and 268 Fields-Olivieri, Margaret A. 53 Measure) 397–398
experience sampling 56, 58, 306, 353, Filene, J. H. 123 gender differences
412–413, 448 Filipp, S. H. 148 in anxiety disorders 92, 443
experimental research 105, 145, 335–339, Fischer, S. 332 in depression 92, 443
419 Fitzgerald, J. M. 174 in eating disorders 327
exposure therapy 173, 449 5-HTTLPR. See serotonin transporter- in interaction models 119
The Expression of the Emotions in Man linked polymorphism in internalizing and externalizing
and Animals (Darwin) 141 FKBP5 gene 209, 229, 269 disorders 92, 291
expressive suppression 40, 73–75, 78, flashbulb memories 43 in schizophrenia 299
133, 301 fMRI. See functional magnetic resonance socialization and 92
externalizing spectrum disorders 237–244. imaging in supportive interactions 148
See also specific conditions Forbes, Courtney N. 395 in treatment strategies 436–437
behavioral assessments of 429–430 Forest, M. 230 Gene–Environment interaction
characteristics of 427–428 Fox, D. 147 theory 363
context-inappropriate emotion in 57 Fraga, M. F. 230 General Emotion Dysregulation Measure
developmental perspective on 429 Franklin, J. C. 352 (GEDM) 397–398
dopamine pathway and 227–228 French, L. 211 generalized anxiety disorder (GAD) 89,
duration of emotion in 59 Fresco, D. M. 446 156, 173, 192–193, 256, 285
environmental influences on 241–243 Frewen, P. A. 271 genes, defined 208
494 index
genetic influences 203–214. See also Haynos, A. F. 329, 331, 334 functional connectivity deficits and 4
epigenetics; molecular genetics heart rate variability. See respiratory prefrontal cortex development and 156,
on autism 289–290 sinus arrhythmia 240
differential susceptibility and 108, 109 Heleniak, C. 274 trait impulsivity and 85, 87, 89
DNA methylation and 230–231 Heller, A. S. 135 Incredible Years program 121, 431, 432
on emotional modulation of LPPs 168 Hellhammer, D. H. 148 infant cry, emotion transmission
on externalizing spectrum disorders 90, Hendler, T. 149 through 143–144
142–143, 206 heritability. See genetic influences inferior frontal gyrus (IFG) 4, 91, 192,
future research directions 206, 212–214 Herman, J. L. 267 256, 271, 320
in intergenerational transmission of Herpertz, S. C. 471 informal exposure strategies 469
emotion dysregulation 143, 221 hidden regulators 31 information processing biases 378, 449
on internalizing spectrum disorders 90, Hierarchical Taxonomy of Psychopathology insular cortex 4, 20, 91
142–143, 205, 206, 257–258 (HiTOP) initiative 306 integrative body–mind training 435
at intrapersonal level of emotion 89–90 hippocampus integrative cognitive-affective therapy
on psychosis spectrum disorders activation across anxiety 189 (ICAT) 331
299–300, 306 in addiction 320 interaction models 116, 119–120
temperament and 85 amygdala influences on 43 internalizing spectrum disorders
twin studies on 204–206, 212, glucocorticoid receptors in 228 249–260. See also specific conditions
230–231, 269, 290, 415 in internalizing spectrum disorders 256 affective neuroscience on 255–256
genome-wide association studies septo-hippocampal system 3, 6, 90, 349 characteristics of 445
(GWASs) 207t, 210–211, 214 histone modification 208, 222, 223 developmental perspective on 251–253,
genome-wide complex trait analysis Hofer, Myron 31 259
(GCTA) 207t, 211–212 Hofmann, S. G. 448 in DSM-5 251, 445
genomic imprinting 222–223 Hogendoorn, S. M. 449 duration of emotion in 59
genotypes 29, 90, 208, 253, 257, 289 Holliday, Robin 224 economic burden of 443
Gibson, E. L. 414 Holmes, A. 170 emotion socialization and 104, 257
Giorda, R. 226 Holzman, J. B. 156 epigenetics and 258, 259
glucocorticoid receptor genes 31–33, 107, homeostasis family influences on 251–253, 444
224–225, 228–229, 258, 269 defined 15 first-order syndromes 238
goal-corrected behavioral systems 31 hedonic 316 functional connectivity deficits and 4, 91
Goldstein, R. Z. 169–170 as innate process 30 gender differences in 92, 291
Good, G. E. 429 motivated behavior and 15, 17 genetic influences on 90, 142–143,
Goodman, M. 471–472 regulation of 28, 32, 34f, 86, 190 205, 206, 257–258
Gottman, J. M. 105, 145, 453, 457 Hope, Nora H. 463 late positive potentials and 172
Gratz, Kim L. 120, 329, 348, 354, 395, Horowitz, M. J. 270 methodology for study of 253–254
396, 400, 403, 411, 446 Horvath, Sarah A. 327 overview 249–251
Gray, J. A. 90–91, 272, 414 Hostinar, Camelia E. 249 peer influences on 253
Gross, James J. 33, 59, 73, 87–88, 127, Houben, M. 353 psychophysiology and 256–257
141, 203–204, 378, 446–449, 478 Hubbard, J. A. 386 regulatory strategies and 254
Grosse, M. 331 Hunkele, K. 319 resilience against 91, 259–260
Gruber, J. 307 Hunter, J. 413, 414 respiratory sinus arrhythmia and
GWASs (genome-wide association Huntington’s disease 222 156–160
studies) 207t, 210–211, 214 hypothalamic-pituitary-adrenal (HPA) trait anxiety and 87, 89
axis 209, 210, 225, 256–258, treatments for 444, 448–458
H 287–288 International Classification of Diseases-11
Haedt-Matt, A. A. 333 hypothalamus 16, 191, 225, 228 (ICD-11) 266, 267, 270, 273
Hahn, Hunter 477 interpersonal levels of emotion 92–93
Haines, Nathaniel 1 I interpersonal processes 141–149.
Hajcak, Greg 167, 169–170 ICAT (integrative cognitive-affective See also parent–child interactions
Halberstadt, A. G. 446 therapy) 331 affiliative bonds and 142–143, 145–149
Haliczer, Lauren A. 361 ICD-11 (International Classification of age-related changes in 77
hallucinations 300, 305 Diseases-11) 266, 267, 270, 273 behavioral observation of 61
Ham, J. 105 identification stage of emotion borderline personality disorder and 363
Hamer, M. 414 regulation 88, 130–131, 131f, 134 in coregulation 88, 350, 444, 448
Harlow, H. F. 28, 141 IFG (inferior frontal gyrus) 4, 91, 192, cultural influences on 93
Harrison, A. 331 256, 271, 320 dyadic interactions 92–93
Hatzenbuehler, M. L. 481 illness, partner support during 147 in emotion transmission 143–145
Havighurst, Sophie S. 122, 443 implementation stage of emotion future research directions 149
Hawes, D. J. 104 regulation 88, 131, 131f, 135 maladaptive 183
Hawkins, R. C. 328 impulse control. See also addiction overview 141–142
Hawkley, L. 69–70 in borderline personality disorder 429 regulatory strategies and 55
Hawn, Sage E. 203 dialectical behavioral therapy for 434 in romantic relationships 145–148
Hayes, S. C. 452 eating disorders and 330 in socioemotional development 142
index 495
intimate partner violence 57, 107, depression 171–173 Maiti, A. K. 154
144–146, 429 distraction and 177 major depressive disorder. See depression
intrapersonal levels of emotion 89–92 duration of 168–169 males. See gender differences
invalidating environment model 117–118, eating disorders and 175–176 maltreatment. See childhood maltreatment
122–123, 363, 466 emotional modulation of 168–171, 175 mania 53, 134, 156, 227. See also bipolar
irreverence therapy style 470 future research directions 175–177 disorder
memory and 170, 176 Maniaci, M. R. 148
J posttraumatic stress disorder and Martin, Christina Gamache 115
Jazaieri, Hooria 127, 378 173–174 MASC (Multidimensional Anxiety
Jenness, J. L. 274 potentiation by stimuli 168, 169f Scale for Children) 290–291
Johansen, E. B. 238–239 substance use disorders and 174–175 Mattson, Whitney I. 13
Johnson, A. M. 104 suicidal ideation and 172 Maxwell, S. E. 214
lateral paralimbic group 191, 195n4 Mazefsky, C. A. 286
K Latzman, R. D. 120 McCauley, E. 274
Kadosh, K. C. 29 Lavender, J. M. 329, 330, 333 McGlone, F. P. 170
Kaliush, Parisa R. 85 LD (linkage disequilibrium) 207t, 211 McHugh, R. K. 317
Kaminski, J. W. 123 learned helplessness 134 McLaughlin, K. A. 274
Kämmerer, A. 331 learning. See also operant reinforcement McMain, S. F. 474
Kanakam, N. 205 associative 3, 4, 227 McRae, A. F. 230–231
Karmiloff-Smith, A. 29 defined 15 McRae, Kateri 39
Karnik, Niranjan S. 427 emotion as learning signal 30, 31 Meaney, M. J. 224
Kaufman, Erin A. 345 motivated behavior and 17 medial PFC group 191–192
Kaye, K. 385 observational 252 medial posterior group 191–192
Kayser, J. 171 social 100, 259, 449 memory
Keane, S. P. 120 LeDoux, J. 30, 448 age-related changes in 78
Keel, P. K. 333 Lee, S. H. 212 autobiographical 46, 170, 176, 192,
Kehoe, Christiane 443 Leshin, Joseph C. 183 412, 420
Keller, M. C. 212 Leve, C. 386–387 defined 15
Kendler, K. S. 206 Levenson, R. W. 105, 145 emotion-enhanced 43
Kensinger, E. A. 72–73 LiKamWa, R. 420 late positive potentials and 170, 176
Kerig, Patricia K. 265, 271, 275 limbic-hypothalamic-pituitary-adrenal mood-congruent 43–44
Khaled, Mona 141 (L-HPA) axis motivated behavior and 17
Kiel, E. J. 120 autism and 287 in psychosis spectrum disorders 303,
Kieras, J. 385 dysfunction of 228, 287 305
Kim, H. 90 epigenetic bases of functioning working 45–46, 78, 169, 241, 268, 300
Kim, J. 274 228–229 men. See gender differences
Kirschbaum, C. 148 glucocorticoid receptor and 224 Mence, M. 104
Klauer, T. 148 hyperresponsivity of 269 Mendelson, T. 436
Kleiman, E. M. 416 measurement of functioning 110 Menin, D. S. 446
Knutson, N. M. 242 physiological synchrony and 105 Merwin, R. M. 331
Kober, H. 192 stress and 106–107, 144–145, 228, 268 mesolimbic system 14, 87, 90, 227,
Kohlhoff, J. 104 trauma-related effects on 265, 275–276 239, 349
Kostaras, D. 147 Lindquist, Kristen A. 183 meta-emotion philosophy (MEP) 454,
Kostaras, X. 147 Linehan, Marsha M. 117, 129, 176, 349, 455
Kovacs, M. 104 363, 429, 432, 464, 466 methamphetamine 313, 314, 319, 320
Krause, E. D. 147 linkage disequilibrium (LD) 207t, 211 Miller, D. J. 413
Kring, A. M. 307 Links, P. S. 416 Miller, M. A. 414
Kumpula, M. J. 274 Liu, Y. 420 mind–brain correspondence 189
Kuppens, P. 213 Livesley, W. J. 396 mindfulness-based interventions 321,
load sharing 32–33 432–438, 450, 456, 480–481
L Lobo, I. 174 mirror tracing persistence task
Ladouceur, C. D. 119 locationist basic emotion perspective 7 (MTPT) 388
Lane, N. D. 420 Lonsdorf, T. B. 209 Misri, S. 147
Lane, R. D. 155 LPPs. See late positive potentials modal model of emotion 41
Lanius, R. A. 271 Lynam, D. R. 413 Modrowski, C. 275
late positive potentials (LPPs) 168–177 Lynch, T. R. 147, 470 modularity hypothesis 29
affective chronometry and 176 molecular genetics
anxiety disorders and 173 M emotion regulation studies in
attention and 169, 170, 170f MacDonald, D. E. 331 208–212, 257
borderline personality disorder and 176 Mackler, J. S. 120 methodology for study of 206, 207t,
cognitive reappraisal and 169–170, MacLean, P. D. 185–186 208–211
170f, 172–176 MacNamara, A. 169–170, 173, 174 overview 207–208
cultural influences on 93 main-effects models 118–121, 124, 352 specific gene variants in 206, 208
496 index
monitoring stage of emotion regulation Nelson, Eric E. 13 theoretical perspectives on 117–118
88, 131–132, 131f, 136 Nelson-Gray, R. O. 434 transactional models and 117, 120–121,
Montirosso, R. 226 nervous system. See specific branches 123
mood-congruent memory 43–44 Neuhaus, Emily 283 opioids 313–318, 351
mood disorders. See also specific conditions neuroconstructivism 29 opposite action strategy 467–468
autism and 285 neurodevelopment 29, 35, 239–241, 285, oppositional defiant disorder (ODD)
emotion dysregulation and 47 292, 349 characteristics of 428
family influences on 251 neuroimaging. See also affective developmental pathway to 238, 241
predictive factors 19 neuroscience; functional magnetic dopaminergic function and 227
regulatory strategies and 136 resonance imaging environmental influences on 242
serotonergic function and 225 addiction and 317 gender differences and 92
treatments for 450–451 age-related changes and 70 risk factors for 89
mood vs. emotion 33, 445, 447–478 autism and 288–289 treatments for 431, 434
Moore, K. E. 435 on cognitive reappraisal 42 orbitofrontal cortex (OFC)
Moore, S. A. 120 cortical subdivisions identified by 4 in addiction 318
Morie, K. 319 defined 184 age-related changes in use of 72, 73
Morningstar, Michele A. 13 emotion-specific patterns in 20 in borderline personality disorder 366
morphological systems 30–33, 34f functional 19, 21, 184 childhood abuse and 241
Morris, A. S. 118 psychosis spectrum disorders and 302, in cognitive control 72, 73
motivated behavior 13–22 304 conduct disorder and 240, 241f
attention and 17 neuroticism 41, 192, 205–208, 304, in emotion regulation 91
controversies regarding 20–21 338, 413 impulsivity inhibition by 240
defined 14 neurotransmitter systems 225–228, 267. in lateral paralimbic group 191
development and 18 See also specific neurotransmitters in motivated behavior 17
emotion and 14, 20, 21 neurovisceral integration theory in reappraisal of negative emotion 4
future research directions 21–22 (NIT) 155 in reward pathway 315, 317
homeostasis and 15, 17 Nicholson, A. A. 271 in self-regulation 349
learning and 17 nicotine use. See cigarettes Orcutt, H. K. 274
maladaptive 18–19, 21–22 Niedtfeld, I. 472 overmodulation of emotion 270–272,
memory and 17 Nieuwenhuis, S. 169 275, 276
methods for study of 19–20 NIMH (National Institute of Mental Overstreet, Cassie 203
overview 13–14 Health) 53–54, 212, 255, 306 oxytocin receptor (OXTR) gene 33,
in Pankseppian model 15, 16 Nock, M. K. 352, 417 90, 209
social behavior and 17–18 Nolen-Hoeksema, S. 332, 436
MTPT (mirror tracing persistence nonfunctional polymorphisms 208 P
task) 388 nonsuicidal self-injury. See self-inflicted paced auditory serial addition task
Muehlenkamp, J. J. 352–354 injury (PASAT) 336, 388
Multidimensional Anxiety Scale for Nugent, N. R. 352–353 Pachankis, J. E. 481
Children (MASC) 290–291 Pagliaccio, D. 209
multifinality 267, 429 O pain-offset relief hypothesis 351
multiple levels of analysis Oberlander, T. F. 224 panic disorder 134, 156, 157, 256
advancements in 348, 480 Obradović, J. 120 Panksepp, Jaak 8, 13, 15–17, 20, 21,
for age-related changes 80 O’Brien, Jacqueline 115 86–87, 91
in behavioral assessments 63, 380 observational learning 252 paranoia 303, 305, 361
in developmental processes 86, 94 observational research. See behavioral parasympathetic nervous system (PNS).
for endophenotypes 212 observation See also respiratory sinus arrhythmia
importance of 479 obsessive-compulsive disorder activation in DBT 469
interpersonal 92–93 (OCD) 156, 173, 193, 285 addiction and 316
intrapersonal 89–92 ODD. See oppositional defiant disorder autism and 287
Multisystemic Therapy 430 OFC. See orbitofrontal cortex phylogenetic account of 155, 157
multivariate pattern-based analyses Oland, A. A. 104 physiological synchrony of 259
(MVPA) 187 older adults. See aging in stress response 272, 448
mutuality in romantic relationships 147 On the Origin of Species (Darwin) 6 withdrawal to unthreatening social
ontogenic process perspective 238, 242, stimuli 157
N 243f paraventricular nucleus 4, 228
Nanney, D. L. 224 operant reinforcement 115–124 parent–child interactions. See also emotion
National Institute of Mental Health clinical interventions for 121–123 socialization
(NIMH) 53–54, 212, 255, 306 future research directions 123–124 affiliative bonds and 142–143
naturalistic observation 380, 385 interaction models and 116, 119–120 aversive 104, 117, 119, 120
natural selection 6 main-effects models and 118–120 behavioral observation of 57–59,
negative symptoms 300, 301 measurement tools 116–117 61–62
negative urgency 332, 335, 338, 339, in parent–child interactions 115–116 clinical interventions for 121–123
417, 420 replication across lifespan 116 coercion theory and 117, 121
index 497
parent–child interactions (Continued ) phobias 156, 173, 285 in cognitive control 72, 73, 185,
differential susceptibility and 108, 110 physical touch, emotion transmission 255–256
disorganized attachments 32, 100–101, through 143 in cognitive reappraisal 42
108, 252, 363 physiological hyperreactivity in emotion regulation 91, 137
emotion transmission in 143–145 hypothesis 144 impulsivity inhibition by 240
insecure attachments 100, 120, 144, physiological stress 143–145, 148, 149 in internalizing spectrum disorders 256
252 physiological synchrony (PS) 104–106, medial PFC group 191–192
interaction models for 116, 119–120 109, 110, 259 motivated behavior and 14
in invalidating environment 117–118, Plomin, R. 211 neuromaturation of 42, 88, 239–241
122–123 PMT (parent management training) in reappraisal of negative emotion 4
main-effects models for 118–120 432–434, 437, 480–481 respiratory sinus arrhythmia and
operant reinforcement in 115–124 PNS. See parasympathetic nervous system 155–156
physiological synchrony and 105–106 polygenic risk score (PRS) 207t, 211, 304, in reward pathway 315
self-regulation and 349–350, 433, 480 306 in self-regulation 349
in socioemotional development 350 polymorphisms trait anxiety and 87
transactional models for 117, 120–121, in candidate gene studies 208–210 process model of emotion regulation
123 defined 208 129–137
traumatic events and 269–270 DRD4 gene 109, 227–228 future research directions 136–137
parenting interventions 121, 431–434, 5-HTTLPR 90, 120, 208–209, regulatory strategies in 40, 132–133,
444–445, 452–458, 480–481 226–227, 257, 289 204, 362, 447
parent management training (PMT) FKBP5 gene 209, 229, 269 stages of regulation in 88, 130–136,
432–434, 437, 480–481 functional 208 131f
Paris, J. 474 nonfunctional 208 valuation system within 129–130, 130f
Parsons, J. T. 481 single nucleotide 208–211, 222, Promoting Alternative THinking
Parvaz, M. A. 169–170 223f, 231 Strategies (PATHS) program 436
PASAT (paced auditory serial addition polyvagal theory 155, 291 prospect theory 44
task) 336, 388 population stratification 210 Provenzi, L. 226
PATHS (Promoting Alternative THinking Porges, S. W. 154–155, 291 PRS (polygenic risk score) 207t, 211,
Strategies) program 436 positive reappraisal 74, 79 304, 306
Patterson, G. R. 117, 242 positive symptoms 300, 301 PS (physiological synchrony) 104–106,
Paul, S. 173 Posner, M. I. 385 109, 110, 259
Pavlovian bias 5 postpartum depression 147, 149 PSDs. See psychosis spectrum disorders
peers posttraumatic stress disorder (PTSD) psychoanalytic theory 203, 455
deviant affiliations 241, 242 amygdala activation in 188 psychological constructionism 188,
emotional responses to acceptance by 18 biopsychosocial processes in 268–270 189, 191
internalizing spectrum disorders borderline personality disorder and 367 psychological flexibility 133, 451–452
and 253 brain regions related to 193 psychopathology. See also emotion
operant reinforcement and 116 clinical interventions for 122 dysregulation; specific conditions
in reinforcement of gender-specific complex 267 aging and 78–79
processes 92 dissociation and 267, 271 brain regions related to 20
rejection by 253, 274 in DSM-5 195n2, 267, 270 classification of 237
social difficulties with 241 emotion dysregulation and 274–275 cognition and 136–137
periaqueductal gray 20, 191, 271 FKBP5 gene expression in 229, 269 developmental perspective on 86, 87,
peripheral nervous system 15, 28, 190, functional connectivity deficits and 188 89, 257
191, 257 in ICD-11 267, 270, 273 diagnostic criteria for 71, 127
Perry, N. B. 120 late positive potentials and 173–174 duration of emotion and 59
personality disorders. See specific disorders respiratory sinus arrhythmia and 156, emotional lability and 58, 59, 397
Perth Emotional Reactivity Scale 269 externalizing (see externalizing spectrum
(PERS) 398–399 symptoms of 173–174, 267 disorders)
PFC. See prefrontal cortex theoretical models of emotion factor analysis of symptoms 237–238
phasic dysregulation model 270 dysregulation in 270–273 gender-specific trajectories 92
phenotypes treatments for 276, 469 genetics (see genetic influences)
behavioral 29, 224 vulnerability to 269–270, 274 Hierarchical Taxonomy of
defined 204 Potenza, M. N. 319 Psychopathology initiative 306
differential susceptibility factors Pots, W. T. M. 452 internalizing (see internalizing spectrum
and 108 Powers, A. 265 disorders)
DNA methylation 231 Prader-Willi syndrome 223 late positive potentials and 171–175
of early-onset depression 172 Prakash, Ruchika Shaurya 69 psychosis (see psychosis spectrum
endophenotypes 32, 212, 214, 239, 415 prefrontal cortex (PFC) disorders)
environmental influences on 206 in addiction 318, 320 recovery from 41
genetic-related variances 29, 204–208 age-related changes in use of 72, 73 respiratory sinus arrhythmia and
infant 89 in borderline personality disorder 155–161, 257, 269
rise of 222, 224 365, 366 theoretical models for 153–154
498 index
psychophysiology. See also event-related internalizing spectrum disorders psychopathology and 155–161, 257, 269
potentials; respiratory sinus and 254 in psychophysiological assessments 412
arrhythmia maladaptive use of 135, 254, 362, quantification of 154, 155f, 159–160,
autism and 287–288 368–370, 447 160f
behavioral observation of 61 in process model 40, 132–133, 204, self-inflicted injury and 158, 257, 351
childhood trauma and 272, 276 362, 447 social and developmental influences
cognitive reappraisal and 41 in psychosis spectrum disorders on 156–158
eating disorders and 336–337 301–302, 305–306 task selection and 158–159
ecological momentary assessment response-focused 73, 88, 301, 447, 448 theoretical models for 154–156
and 414 response modulation 73, 132, 133, 447 response-focused regulatory strategies 73,
hyperreactivity to children’s distress situation modification 40, 73, 132–133, 88, 301, 447, 448
and 144 447 response modulation 73, 132, 133, 447
internalizing spectrum disorders situation selection 40, 73–74, 132, 135, reward pathway 227, 315–317
and 256–257 136, 447 ribonucleic acid (RNA) 208, 222, 223
measurement guidelines in 160 spontaneous use of 60, 368 Richmond, Julia R. 395
psychosis spectrum disorders stopping 136 Richter, Curt 17
(PSDs) 299–307. See also specific switching 45, 46, 132, 136 Riggs, Arthur 224
conditions Reis, H. T. 148, 414 Rini, C. 147
cognitive deficits in 304–305 Reitz, S. 470 rise time to peak metric 176
in DSM-5 299, 306 relationships 99–110. See also family; risk-as-feeling hypothesis 44
emotion abnormalities in 300–304 parent–child interactions; peers risk distribution 32–33
future research directions 307 age-related changes in 77, 99 Roemer, L. 329, 348, 354, 396, 400,
genetic influences on 299–300, 306 in attachment theory 32, 100–101 411, 446
methodology for study of 306 differential susceptibility and 108–110 Rogge, R. D. 148
neuroimaging studies of 302, 304 dyadic interactions and 92–93, ROI (region-of-interest) analysis 6, 189
prevalence of 299 145–148 romantic relationships 40, 116, 145–148
regulatory strategy use in 301–302, in functionalist emotions theory 93, Rothbart, M. K. 385
305–306 101–103 Rottenberg, J. 171
symptom dimensions of 300, 302–306 future research directions 109–110 Rowsell, M. 331
treatments for 307 as hidden regulators 31 RSA. See respiratory sinus arrhythmia
psychotropic medications 272, 367 physiological synchrony and 104–106, rumination
PTSD. See posttraumatic stress disorder 109, 110 borderline personality disorder and 369
romantic 40, 116, 145–148 childhood maltreatment and 251
R stress neurobiology and 106–107, defined 41, 302
Racine, Sarah E. 327, 330, 331 109, 110 eating disorders and 332, 334
Rains, J. C. 452 Rendina, H. J. 481 effectiveness of 133
Rajappa, K. 354 Repetti, R. 145, 146 as emotion misregulation 47
Ramsey, E. 117 Research Domain Criteria (RDoC) functionalist view of 102
Ramsook, K. Ashana 53 53–54, 212, 255, 306, 479, 481 older adults and 78
Rappaport, Lance M. 203 resilience psychosis spectrum disorders and 302,
Rasmussen, A. M. 268 in aftermath of trauma 275 305–306
rationalization strategy 447 in developmental perspective 86 Russell, V. A. 238–239
Raz, G. 192 promotion of 259–260
RDoC (Research Domain Criteria) respiratory sinus arrhythmia and 91, S
53–54, 212, 255, 306, 479, 481 156 Saarni, C. 446
reappraisal. See cognitive reappraisal social mechanisms of 94 Safren, S. A. 481
recall bias 333, 418 respiratory sinus arrhythmia (RSA) Sagvolden, T. 238–239
reciprocity therapy style 469–470 153–161 salience network (SN) 5–6, 187–188,
recovery time metric 176 addiction and 316 191–194, 256
region-of-interest (ROI) analysis 6, 189 age-related changes in 161n2 Satpute, A. 5–6
regulatory strategies. See also cognitive autism and 287, 291 SAVI (strength and vulnerability
reappraisal; distraction; in behavioral observation 430 integration theory) 70–71, 79
self-regulation; suppression defined 91, 154, 350, 479 Saxbe, Darby 141, 145, 146
age-related changes in use of 71, 73–76 differential susceptibility and 108–109 SBT (social baseline theory) 32–33
antecedent-focused 73, 88, 301, 447, emotional lability and 116 Schachter, S. 86
448, 455 in interaction models 119 Schatten, Heather T. 411
attentional deployment 40, 73, measurement issues related to Schauer, M. 272
132–133, 135, 302, 447 160–161 Schilling, E. A. 413
behavioral observation of 55, 59–60 methodological considerations in schizophrenia
cognitive change 40–42, 73, 132, 133, study of 158–161 cognitive deficits in 304–305
301–302, 447 neural substrates of 155–156 dopaminergic function and 227
coregulation 88, 350, 444, 448 overview 153–154 emotion abnormalities in 300, 301, 303
ineffectiveness of 60, 135 physiological synchrony and 105–106 gender differences in 299
index 499
schizophrenia (Continued ) loss through trauma 268 SOC-ER (selection, optimization, and
genetic influences on 299–300 neurological influences on 91, 156 compensation with emotion
methodology for study of 306 parent–child interactions and 349–350, regulation) framework 70, 71, 79
polygenic risk for 211 433, 480 social anxiety disorder 136, 173, 188,
regulatory strategy use in 305 reward pathway and 315–316 193, 285
respiratory sinus arrhythmia and 156 self-regulation shift theory (SRST) 273 social baseline theory (SBT) 32–33
salience network dysregulation in 193 self-report assessments 395–404. social behavior
symptom dimensions of 300, 303–305 See also specific assessments antisocial behavior 238–242, 436
schizotypal personality disorder 305 advantages of 56, 167, 395 defined 15
Schnell, K. 471 age considerations for 116, 253, 379 elicitation of prosocial behavior 2
Schreurs, K. M. G. 452 autism and 290, 292 emotion as regulator of 27–35
Schröder-Abé, M. 146 eating disorders and 329–332 evolution of 155
Schwarz, N. 30 future research directions 403–404 motivated behavior and 17–18
Schweizer, S. 332 in genetic studies 205, 213 social-ecological niche 28, 32–33
Selby, E. A. 334, 419 limitations of 74, 377–378, 395–396, socialization
selection, optimization, and compensation 412 emotion (see emotion socialization)
with emotion regulation (SOC-ER) of maladaptive responses to emotions gender and 92
framework 70, 71, 79 400–402 of RSA reactivity 158
selection stage of emotion regulation 88, overreliance on 275, 438 of stress neurobiology 106–107, 109
131, 131f, 134–135 parent–child interactions and 117, 119, social learning 100, 259, 449
selective attention 73 123 socioemotional development
self-care behaviors 451, 455–457 psychosis spectrum disorders and 302 adaptive-basins model on 30–32
self-inflicted injury (SII) 345–355. regulatory strategy use and 72, 75 attachment theory on 31
See also suicide and suicidal ideation of temperamental emotional emotional responding and 453
autism and 286 vulnerability 397–400 emotion regulation and 431
in borderline personality disorder 361, Seligowski, A. V. 274 future research directions 34–35
363, 416, 417, 470–471 separation anxiety disorder 89, 285, 445 heuristic view of 28
categorical conceptualizations of separation distress 31, 34 individual differences in 85–86
346–348 septo-hippocampal system 3, 6, 90, 349 interpersonal processes in 142
by children and adolescents 345–346, serotonin 225–227, 289 parent–child interactions in 350
352 serotonin transporter-linked physiological synchrony in 106
conflict escalation and 58, 119 polymorphism (5-HTTLPR) 90, socioemotional selectivity theory
development perspective on 349–351 120, 208–209, 226–227, 257, 289 (SST) 70, 71, 79
ecological momentary assessment of Shader, Tiffany M. 159, 237 somatic marker hypothesis 30–31, 45
352–354, 416–417 Shalev, A. Y. 266, 268 Speed, Brittany C. 167
emotional interaction patterns and 93 Sharma-Patel, K. 122 SRET (self-referential encoding task) 171,
future research directions 355 Shaw, D. S. 104 172, 176
L-HPA axis dysfunction and 228 Sheeber, L. 386–387 SRST (self-regulation shift theory) 273
methodology for study of 352–354 Shipman, K. L. 270 startle responses 267, 287, 317, 337, 367
moderating and mediating influences Shoji, K. 273 stepped-care treatment models 474
on 353–354 SII. See self-inflicted injury Steptoe, A. 414
motivations for 346, 351 Silk, J. S. 104 stigma 304, 305, 481–482
neurobiological factors associated Singer, J. 86 stimulants 313–314, 319–320
with 470–471 single nucleotide polymorphisms (SNPs) stop codon 208
prevention efforts 354–355 208–211, 222, 223f, 231 STOP skills 451, 467
respiratory sinus arrhythmia and 158, situated conceptualization 5 Stoycos, Sarah A. 141
257, 351 situational functionalism 478–479 strange situation paradigm 120, 252, 385
serotonergic function and 90, 209 situation–attention–appraisal–response strength and vulnerability integration
terminology related to 346, 347t perspective 86, 447 theory (SAVI) 70–71, 79
theoretical perspectives on 348–352 situation modification 40, 73, 132–133, stress. See also posttraumatic
treatments for 450–451 447 stress disorder
self-medication hypothesis 314 situation selection 40, 73–74, 132, 135, age-related changes in 75–76
self-referential biases 171, 172, 176 136, 447 buffers against 101, 143
self-referential encoding task (SRET) 171, Skowron, E. A. 158 cigarette use and 315
172, 176 Skuban, E. M. 104 diathesis-stress model 108, 109
self-regulation Smith, G. T. 332 EMA of response to 413–414
active coaching of 104 smoking. See cigarettes emotion regulation and 55, 75–76
by children and adolescents 56, SN (salience network) 5–6, 187–188, Family Stress Model 101, 104
102–104 191–194, 256 L-HPA axis in response to 228
constructive forms of 100 SNPs (single nucleotide polymorphisms) neurobiology of 106–107, 109, 110,
cortical structures in 4, 186, 349 208–211, 222, 223f, 231 257, 268
environmental influences on 241 SNS. See sympathetic nervous system of overriding motivational
improvement strategies 435 Snyder, J. J. 117 tendencies 19
500 index
physiological effects of 143–145, 148, overreliance on 302, 303 treatment strategies
149 psychosis spectrum disorders and acceptance and commitment
in postpartum period 147 301–302, 305 therapy 401, 451–452
psychotic symptoms related to 306 as PTSD coping strategy 270 CBT (See cognitive-behavioral
of separation distress 31, 34 of thoughts 73–75, 447 therapy)
Trier Social Stress Test 148, 317, 412 Surguladze, S. A. 209 for children and adolescents 432–435,
stress contagion 106, 145, 146 Svaldi, J. 337 449, 480–481
stria terminalis 4, 315 Swart, M. 209 DBT (See dialectical behavioral
Stroop tests 193, 336, 365–366, 402, switching 45, 46, 132, 136 therapy)
411, 436 sympathetic nervous system (SNS) developmental perspective on 431
structured observation 385 activation without emotion 34 emotion-focused therapy
substance use disorders (SUDs) assessment of activity in 105 449–450, 455
brain regions related to 227 autism and 287 exposure therapy 173, 449
dopaminergic function and 227 hyperreactivity in 268 for externalizing behavior
ecological momentary assessment mobilization in response to problems 430–437
of 419–420 threats 157 future research directions 437–438
environmental influences on 242 physiological synchrony of 259 integrative cognitive-affective
late positive potentials and 174–175 psychosis spectrum disorders and 303 therapy 331
maladaptive motivated behavior suppression and 63, 133 for internalizing spectrum
and 21–22 synchrony 142–144, 148–149. disorders 444, 448–458
in older adults 78 See also physiological synchrony mindfulness-based interventions 321,
prefrontal cortex development and 240 432–438, 450, 456, 480–481
respiratory sinus arrhythmia and 156 T Multisystemic Therapy 430
risk factors for 89 Tager, D. 429 parenting interventions 121, 431–434,
trait impulsivity and 239 Tchanturia, K. 331 444–445, 452–458, 480–481
treatments for 452 teleological explanations 3, 5, 6 special considerations for 436–437
suicide and suicidal ideation temperamental emotional stepped-care models 474
autism and 283, 285 vulnerability 363, 397–400 transdiagnostic 473–474, 481
behavioral observation and 63 Thayer, J. F. 155 Trickey, D. 269
borderline personality disorder theory of constructed emotion (TCE) 5, Trier Social Stress Test 148, 317, 412
and 361, 416 183–184, 189–194 triune brain concept 185–186
depression and 79, 172 Thiruchselvam, R. 177 Trompetter, H. R. 452
ecological momentary assessment Thompson, M. 271 Tronick, E. 105
of 416 Thompson, Ross A. 58, 99, 101, 478 Trupin, Eric 434–435
late positive potentials and 172 Thorp, S. R. 147 tryptophan hydroxylase-2 (TPH2)
L-HPA axis dysfunction and 228 thought suppression 73–75, 447 gene 209
serotonergic function and 90, 225, TIK (Tuning into Kids) program 122, Tull, Matthew T. 120, 395
226 444–445, 453–458 Tuning into Kids (TIK) program 122,
suicide and 283 TIP skills 451, 469 444–445, 453–458
treatments for 450–451 tobacco use. See cigarettes Tuschen-Caffier, B. 337
Sunderland, M. 456 touch, emotion transmission twin studies 204–206, 212, 230–231,
support through 143 269, 290, 415
behaviors related to 148 TPH2 (tryptophan hydroxylase-2)
during illness 147 gene 209 U
mobilization of 102, 291 trait anxiety 45, 78, 85–90, 192–193 Uhlmann, A. 320
parental 101–107, 117–122, 270 trait impulsivity 85–89, 238–243, 451 undermodulation of emotion 270–272,
in romantic relationships 145–148 Tranel, D. 69–70 275, 276
for self-inflicted injury prevention 354 transactional models 117, 120–121, 123, unified protocol (UP) treatment 473, 481
self-regulatory 106, 350 329 Uusberg, Andero 127
in transition to parenthood 147–148 transcription 208, 222, 269 Uusberg, Helen 127
suppression translational research 276, 301, 307,
addiction and 318, 319 472–474 V
age-related changes in use of 74–75 trauma Vachon, D. D. 413
borderline personality disorder childhood (see childhood trauma) vagal tone. See respiratory sinus
and 369 conceptualizations of 266–268, 272 arrhythmia
brain regions related to 302, 318 Developmental Trauma Disorder Valle, L. A. 123
cultural influences on 93 proposal 272–273 van der Kolk, B. A. 268
defined 74, 254, 301 evidence-based treatments for 122 van der Oord, S. 434
eating disorders and 332 late positive potentials and 173–174 Vander Stoep, A. 274
expressive 40, 73–75, 78, 133, 301 physiological effects of 265 Van Kleef, G. A. 31
functionalist view of 102 PTSD (See posttraumatic stress Vansteelandt, K. 417
genetic influences on 41 disorder) variable number tandem repeats
observability of 63 Treasure, J. 331 (VNTRs) 208
index 501
Vater, A. 146 W working memory 45–46, 78, 169, 241,
ventral striatum Wallace, Gemma T. 299 268, 300
components of 90 Walton, E. 230
in core limbic group 191 Wardle, J. 414 Y
motivated behavior and 14, 16 Waters, Sara F. 99, 105–106 Yap, M. B. 119
in reward pathway 227 Webster-Stratton, Carolyn H. 121, 431 Yates, T. M. 120
trait impulsivity and 239 Weinberg, A. 172, 205 Yehuda, R. 229
upregulation of responses in 318 Weisman, O. 143 Yerkes-Dodson Law 130
ventral tegmental area (VTA) 3, 6, 16, 20, West, J. 435
90, 227–228, 315 Wheeless, Linnie E. 395 Z
video-recall procedures 378, White, S. W. 286 Zajonc, R. B. 27
386–387 Whitmoyer, Patrick 69 Zalewski, Maureen 115, 118
violence. See childhood abuse; intimate Wichers, M. 415 Zarolia, Paree 39
partner violence Wildes, J. E. 330, 331 Zettle, R. D. 452
Vlisides-Henry, Robert D. 85 Winiarski, Dominika A. 427, 436 Zhang, L. 30
VNTRs (variable number tandem Winnicott, D. W. 100 Zhong, L. 420
repeats) 208 Wolz, I. 330 Zisner, A. 87, 89–90
Vohs, K. D. 30 women. See gender differences Zwi, M. 431
502 index