8:45 AM-9:45 AM, Lake Michigan, Symposium 6: Once More, With Feeling: Novel Psychosocial Interventions Informed by Basic Affective Science, Symposium. Sheri Johnson; Jasmine Mote; Janelle Painter; Andrew Peckham; Jean Quintero.
Theme and Summary Abstract: Basic affective science is a rich, interdisciplinary field that encompasses a variety of areas — from psychology to neuroscience to economics — to understand the mechanisms behind how, why, and what we experience when we say we are experiencing emotions. This research is particularly applicable to those suffering from mental illness, as practically every mental disorder listed in the DSM-5 includes an emotional dysfunction (e.g., difficulty in emotion regulation, difficulty expressing or exhibiting emotion, experience of negative emotions or lack of positive emotions) that drastically interferes with daily functioning and quality of life. Further highlighting the importance of emotion transdiagnostically, two of the five NIMH Research Domain Criteria (RDoC) include negative valence systems (e.g., responses to acute threat, responses to potential harm) and positive valence systems (e.g., approach motivation, reward learning). Although basic affective science has been increasingly incorporated into clinical research, there remains a paucity of established or novel treatment approaches that draw on basic affective science. This symposium highlights treatment development research on the cutting edge of integrating affective science. By integrating strategies based on basic affective science with cognitive behavioral therapy, these studies address a need in treatment development to address emotional issues through empirically supported methodologies. The studies included in this symposium span diagnoses to show the benefits of these transdiagnostic techniques in a variety of difficult-to-treat mental disorders. In the first presentation, Jean M. Quintero will discuss self-report and behavioral outcomes related to Emotion Regulation Therapy (ERT), a treatment targeting motivational mechanisms related to affect in generalized anxiety disorder (GAD). In the second presentation, Andrew Peckham will describe the Learning Affective Understanding for a Rich Emotional Life (LAUREL) group treatment intervention for people with bipolar I disorder, an intervention designed to increase healthy, low arousal positive emotions in a population where specific types of positive emotions may be harmful or avoided in daily life. In the third presentation, Janelle M. Painter will discuss data relating to an open trial of the Awareness and Coping with Emotion in Schizophrenia (ACES) intervention, a group treatment designed to teach cognitive and behavioral skills with an emphasis on increasing positive emotion in people with schizophrenia. Finally, Sheri L. Johnson will serve as a discussant on this symposium. She will discuss strengths, weaknesses, common themes, and implications of the presented studies, and will offer insight into future directions for treatment intervention informed by basic affective science.
9:15 AM-10:45 AM, Continental B, Symposium 12. Network Analysis: A Symptom Perspective of Psychopathology, Symposium. Laura Bringmann; Julia Langer; Julia Langer; Cheri Levinson; Cheri Levinson; Richard McNally; Thomas Rodebaugh.
Theme and Summary Abstract: Researchers have traditionally used structural equation modeling to test underlying vulnerability models of psychopathology, which theorize that psychopathology stems from an underlying latent variable or common cause (Krueger & Markon, 2006). However, this type of analysis does not allow for examination of how individual behaviors or symptoms might directly cause other behaviors or symptoms. Network analyses address this limitation by allowing researchers to consider disorders as interacting networks of symptoms. From a network perspective, psychopathology arises from direct causal connections between symptoms, instead of from an underlying latent variable (Borsboom et al., 2010). For example, in Major Depressive Disorder the symptoms decreased appetite and losing weight may be highly correlated not because they stem from the same latent variable representing the disorder, but because decreased appetite directly leads to losing weight (Borsboom & Cramer, 2013). This perspective is promising because it suggests that we can use symptom measures to understand how behaviors and cognitions contribute to the development and maintenance of psychopathology (e.g., Post-Traumatic Stress Disorder). Further, we can use network analysis to understand how symptoms of multiple disorders might contribute to each other (e.g., comorbidity between depression and generalized anxiety). This research may ultimately lead to targeted interventions focusing on alleviating specific causal chains of symptoms, which should theoretically lead to decreases in related symptoms. In the current symposium we present research showing how symptoms of a single disorder maintain other symptoms, how symptoms between comorbid disorders relate to each other, and finally, we present a new network analysis technique that could be used in individual clients. First, Dr. Richard McNally presents research on Post-Traumatic Stress Disorder (PTSD) in women with a history of childhood sexual abuse. He shows which symptoms of PTSD are causally important and discusses the clinical implications of these findings. Next, Dr. Thomas Rodebaugh compares a structural equation versus network model of Social Anxiety Disorder. He finds support for a hybrid model and shows that positive affect may fall at the core between social anxiety and depression symptoms. Julia Langer extends this research and examines comorbidity between Social Anxiety Disorder and Major Depressive Disorder in women diagnosed with these disorders. She finds that social avoidance, worthlessness, and moodiness fall in the center of this type of comorbidity. Cheri Levinson presents additional network analyses focused on understanding comorbidity. She examines a network model of social anxiety and eating disorder symptoms and finds that social appearance anxiety may be at the core of this type of comorbidity. She also finds that certain symptoms of these disorders predict each other over time. Finally, Laura Bringmann presents a new type of network analysis, called the time-varying vector autoregressive method. This type of analysis can be applied to individuals to determine whether their networks of psychopathology change over time and, if so, represent the dynamic nature of their network.
9:45 AM-11:15 AM, Lake Ontario, Symposium 13. Mindful-Based Interventions for Veterans with PTSD: Cognitive, Behavioral, and Neurological Mechanisms of Change, Symposium. Michael Gawrysia; Anthony King; Kyle Stephenson; Helane Wahbeh.
Theme and Summary Abstract: Posttraumatic Stress Disorder (PTSD) is a serious and pervasive public health issue. The US Department of Veterans Affairs (2011) estimates that 3.5% of the general population meets diagnostic criteria for PTSD, compared with estimates of 31% of Vietnam veterans, 22% of Operation Enduring Freedom (OEF) veterans, and 20% of Operation Iraqi Freedom (OIF) veterans. Individuals with PTSD suffer debilitating symptoms that often persist for decades. These symptoms are associated with devastating impacts on the family and high costs to society. Clinical hallmarks include recurrent, intrusive recollections or re-experiencing of the traumatic event, avoidance of external or internal cues that can trigger re-experiencing, emotional numbing, and hyperarousal. Additional symptoms consist of distractibility, hypervigilance, irritability or outbursts of anger, disruption of sleep patterns, increased substance abuse, and exaggerated startle response (APA, 2013). The theoretical and empirical literature suggests that mindfulness-based interventions (MBIs) can be an effective treatment option for PTSD. Several cross-sectional studies have documented an inverse relationship among facets of dispositional mindfulness and PTSD symptoms (Bernstein, Tanay & Vujanovic, 2011; Smith et al., 2011; Wahbeh et al., 2011), and outcome studies suggest MBIs are a feasible and promising intervention for veterans with PTSD (Kearney et al., 2013; Niles et al., 2011). As a result, VA clinics around the country are beginning to employ mindful- based interventions for the treatment of PTSD and associated symptoms. With growing evidence for the overall effectiveness of MBIs among veterans with PTSD, a more detailed examination is warranted. Several mechanisms of change by which MBIs exert their effect on treatment outcome have been proposed, including: a) an increased willingness to tolerate distressing internal events; b) decreased experiential avoidance and thought suppression (Bennett & Wells, 2010; Thompson et al., 2011); c) decreased physiological arousal and stress reactivity (e.g. Delizonna, Williams, & Langer, 2009); d) improved emotion regulation (Wahbeh et al., 2011); and e) greater attentional allocation and reduction of rumination (Lang et al., 2012; Grabovac et al., 2011); Further investigating potential mechanisms of change, including the effects of specific mindfulness practices (e.g., body scan, mindful breathing) and how they interact with various facets of mindfulness (e.g., Nonjudgmental Acceptance, Acting with Awareness) may allow clinicians to tailor elements of the MBI to match the individual being treated. Refined clinical applications could potentially lead to more optimal treatment outcomes, and ultimately, greater dissemination and use of MBIs.
10:45 AM-12:15 PM, Salon A4, Panel Discussion 4. A Critical Discussion of the Implications of RDoC for Depression Research and Treatment, Panel Discussion, W. Edward Craighead; Adele Hayes; Rachel Hershenberg; Michael Kozak; Scott Lilienfeld; Greg Siegle; Edward Watkins.
Abstract Body: The research domain criteria (RDoC) represents a shift in the field. Just as the previous heyday of clinical science heavily favored the randomized clinical trial to elucidate treatment packages that improve DSM-based disorders, the current zeitgeist favors neurobiological methods to elucidate dysfunctional brain systems that underlie psychopathology. This panel provides a platform to discuss the changes in the National Institute of Mental Health (NIMH) funding priorities. We focus on one major implication of RDoC: it will shape the next generation of academic clinical researchers dependent upon obtaining grant funding for tenure. Whether out of agreement, out of necessity, or both, early and midcareer investigators will develop or adapt programmatic lines of research to comply with the funding priorities, making this topic ripe for open and critical discussion. The panel will be organized by its specific focus on the implications of RDoC for the research and treatment of depression (and related disorders and constructs). The discussion will draw upon the expertise of highly respected depression researchers who range in methodological and clinical expertise, grant funding histories, and frank opinions about the topic. Among others, one major topic to be addressed will be the advantages and disadvantages of moving away from “depression” as a unifying construct and moving toward transdiagnostic dimensions, presumed to be more homogenous in nature, that explain clinical phenomena of interest (e.g., rumination). The discussion will be chaired by an early-career depression researcher, who will draw upon the expertise of the panel to address the perennial question of what type of grants early and mid-stage researchers should design that may bridge the science-practice gap and most effectively advance our field. Michael Kozak will represent the perspective of the NIMH and will consider practical suggestions for the design of future studies. Scott Lilienfeld will wrap-up the panel discussion with a macroscopic view of the implications of RDoC on the field (see Lilienfeld, 2015) and integrate the variety of perspectives represented in the discussion.
2:00 PM-3:30 PM, Continental A, Symposium 42. Rumination and Reactivity: Multiple Approaches to Understanding a Transdiagnostic Risk Factor, Symposium, Lauren Alloy; Lori Hilt; Catherine Stroud; Suzanne Vrshek-Schallhorn; Blair Wisco
Theme and Summary Abstract: Rumination (i.e., a repetitive, passive focus on one’s negative emotions and their consequences) is a transdiagnostic cognitive process that has been implicated in the development of depression, anxiety, self-injurious behavior, and binge eating and drinking (Nolen-Hoeksema et al., 2008). According to the Response Styles Theory, rumination may be associated with increased stress reactivity (Nolen-Hoeksema, 1991) and this may be an important mechanism linking rumination to psychopathology. Previous research has found some support for the role of rumination in stress reactivity (e.g., Zoccola & Dickerson, 2012), but the link between rumination and reactivity appears to vary by domain (e.g., neuroendocrine, autonomic nervous system, subjective experience) and by rumination measure (i.e., state or trait; Hilt et al., 2014). Because rumination is a common denominator in the development of psychopathology, it is important to understand the mechanisms underlying this association. In this symposium, we will present a diverse range of studies that approach the question of rumination’s role in stress reactivity. These studies assess stress reactivity in multiple ways including measurement of cortisol (both in response to a laboratory stressor and diurnal rhythms), parasympathetic nervous system, and objective generation of acute and chronic stressors. They were conducted with samples of both adolescents and adults and involve both prospective observational designs and experimental manipulations. Moreover, rumination was assessed in multiple ways (questionnaire, daily diary, and experimental induction) to assess both trait and state levels. This symposium’s focus on rumination fits perfectly with this year’s theme of viewing disorders as products of cognitive and behavioral processes; in line with this, we highlight rumination as a “principle of psychopathology.” In the first paper, Wisco and May examined whether experimentally inducing rumination (versus distraction) would affect parasympathetic nervous system reactivity. They found that a ruminative state led to blunted responding indexed by respiratory sinus arrhythmia (RSA). This effect was seen among both dysphoric and non-dysphoric participants, and suggests a possible physiological mechanism through which rumination contributes to depression. In the second paper, Hilt, Doane and Stroud investigated whether spontaneous and/or habitual use of rumination would alter daily cortisol patterns among adolescent girls. Results indicated that trait rumination was associated with alterations in adolescents’ diurnal cortisol rhythms. Moreover, trait rumination moderated the day-to-day covariation between state rumination and one aspect of the diurnal rhythm, the Cortisol Awakening Response. Such findings suggest that alterations in diurnal cortisol rhythms may be a physiological mechanism linking rumination to the development of psychopathology. In the third paper, Vrshek-Schallhorn, Velkoff, Zinbarg and Adam explored reactivity associated with trait rumination during an acute laboratory stressor (i.e., the Trier Social Stress Test vs. a control task). Findings indicated that rumination was associated with greater shame reactivity, but blunted cortisol reactivity, under stressful conditions. These findings will be discussed in light of prior mixed findings regarding whether rumination leads to increased or decreased cortisol reactivity in the face of acute stress. In the final paper, Stroud and Sosoo examined whether trait rumination predicted reactivity as indexed by objectively- coded chronic and acute stress generation. Findings indicated that rumination predicted increases in acute and chronic stress generation, which led to increases in subsequent depressive symptoms. These findings suggest that adolescents who engage in high levels of rumination may behave in ways that lead to the generation of stressful social environments. Importantly, this study also demonstrates that this reactivity to rumination is a mechanism in the development of depressive symptoms. The discussant, Lauren Alloy, will integrate these four papers, focusing on the link between rumination and different types of stress reactivity. In addition, Alloy will discuss stress reactivity as a mechanism linking rumination to depression and other forms of psychopathology. Finally, in line with this year’s theme of focusing on principles of psychopathology and change, she will address how the current findings inform intervention and prevention efforts targeting rumination.
2:00 PM-3:30 PM, Lake Michigan, Symposium 43. Changing Minds via Cognitive Bias Modification: Expanding to New Populations and Settings, Symposium, Nader Amir; Courtney Beard; Elise Clerkin; Jennie Kuckertz; Meg Reuland; Risa Weisberg
Theme and Summary Abstract: Cognitive models and a wealth of empirical data suggest that cognitive biases maintain emotional disorders. Cognitive Bias Modification (CBM) procedures have directly tested the causal relationship and demonstrated that cognitive biases causally affect emotional vulnerability (see Hallion & Ruscio, 2011; Beard et al., 2012). Researchers have translated these experimental findings into innovative, computerized treatments and have found promising efficacy, but only under certain conditions. Importantly, symptom change most reliably occurs when change in the targeted bias occurs. Consistent with ABCT’s 2015 theme, CBM is a prime example of an approach that first identified a mechanism involved in the maintenance of psychopathology and then developed a treatment to target that mechanism. Moreover, given the unique characteristics of CBM (e.g., computerized, simple, brief, no clinician), it has great potential for dissemination. However, more studies in clinical populations and across different settings are needed before CBM’s potential can be realized. Our symposium will highlight the newest findings in CBM treatment outcome research in clinical samples. The symposium presents studies targeting attention bias (CBM-A), interpretation bias (CBM-I), or a combination (CBM-A- I). Together, the studies describe CBM interventions tested across a wide range of psychopathology, diverse delivery settings (e.g., partial hospital, home), and in children and adults. These studies illustrate the clinical utility of CBM for a wide range of disorders and the feasibility of delivering CBM in real world settings. The symposium will also include studies with null findings, acknowledge the limitations of the existing data, and offer new explanations for failures to replicate across different sites. First, Courtney Beard will present results from the first randomized controlled trial to examine the effectiveness of a transdiagnostic CBM-I in a partial hospital setting. This presentation will highlight the potential use of CBM as an adjunctive treatment in an acute, real world setting. Second, Risa Weisberg will present promising findings from the first open trial of a combined CBM-A-I in individuals with Panic Disorder Third, Meg Meuland will present data comparing a parent-delivered, child-delivered, or combination CBM intervention for adolescents with social anxiety disorder. Fourth, Elise Clerkin will present findings from a randomized controlled trial of CBM-A for comorbid alcohol dependence and social anxiety. The CBM intervention did not successfully change attention bias, and consequently no treatment effects were observed on symptom outcomes. Fifth, Jennie Kuckertz will highlight the importance of examining site differences in CBM effects using data from a multi-site randomized controlled trial of CBM-A for clinically anxious youth. Finally, our discussant, Nader Amir will highlight the strengths, limitations, and future directions of these five studies and of the CBM approach to targeting cognitive vulnerabilities in clinical populations.
3:15 PM-4:45 PM, Lake Huron, Symposium 51. Neuro-Cognitive Mechanisms in Pediatric Anxiety: Clinical Applications From Cognitive Developmental Neuroscience, Symposium, Michelle Craske; Andrea Gold; Jennifer Lau; Tomer Shechner; Allison Waters
Theme and Summary Abstract: Psychopathology typically emerges during childhood, and may reflect perturbed neurodevelopment (Pine, 2009). Yet, developmental differences in risk, onset, and maintenance of anxiety disorders are poorly understood. Methods from neuroscience permit the study of specific neuro-cognitive systems, and thus may be used to reveal the underling mechanisms of anxiety. This symposium will focus on information-processing functions, specifically threat-related-cognitive biases and fear conditioning and extinction, in an effort to link pediatric anxiety to dysfunction in cognitive mechanisms and in underlying fear circuits. Identifying mechanisms that promote psychopathology that could then be targeted to improve treatment efficacy may promote normative development. Four presentations will underscore how subtle perturbations in neurocognitive mechanisms related to attention, cognitive biases and threat-safety learning are associated with pediatric anxiety and its treatment. Presentation one describes promising results from a randomized control trial of attention training to positive stimuli in clinically anxious children. Presentation two discusses a meta-analysis examining the effects of cognitive bias modification on interpretations biases and pediatric anxiety and will present data from a novel protocol designed to enhance ecological validity and user-engagement. Presentation three examines anxiety and age effects on the functional connectivity between the amygdala and prefrontal cortex (PFC) when appraising and recalling previously learned threat. Presentation four focuses on fear conditioning and extinction in individuals resilient to anxiety in a longitudinal study of early behavioral inhibited temperament. The discussion will integrate these findings, and emphasize the distinctive contribution that developmental cognitive neuroscience research can make towards identifying early biological indicators of anxiety. Identifying these indicators is critical to developing interventions that target the cognitive mechanisms implicated in anxiety disorders.
6:30 PM-8:30 PM, International Ballroom: Friday Night Welcoming Cocktail Party / SIG Exposition and NT/TR SIG Student Poster Competition.
Saturday, November 14, 2015:
8:30 AM-10:00 AM, Salon A1, Symposium 65. Mechanisms of Change and Brain-Based Predictors of Response to Cognitive Behavioral Therapies for Anxiety and Depressive Disorders, Symposium. Phillippe Goldin; Stefan Hofmann; Rachel Jacobs; Heide Klumpp; Greg Siegle.
Theme and Summary Abstract: CBT is well-established as effective in the treatment of depressive and anxiety disorders; however, considerable variation in treatment outcome exists and research has not yet explicated why. This symposium comprises four independent research studies using the methodology of fMRI to examine neural markers of response to CBT and putative mechanisms of change. The first presentation presents resting-state fMRI data from 22 adolescents in partial or full remission from major depressive disorder (MDD) who were randomized to 8 weeks of rumination-focused cognitive behavior therapy (R-CBT) or a control condition. Pre/post connectivity of the Default Mode Network (DMN) was studied as well as task-based fMRI during a rumination induction. Depression was significantly decreased in the R-CBT group relative to control group (p< 0.02). Results suggest that after receiving R- CBT, the DMN may become more distinct from cognitive control networks. In the second presentation, results from a study of 81 individuals with depression who completed Cognitive Therapy will be presented. Results suggest that positive information processing predicts recovery among individuals whose recovery is not better predicted by self- report. After successful Cognitive Therapy, prefrontal regulatory mechanisms were employed more strongly in response to changes during a positive mood challenge. The third presentation presents results from 15 patients with SAD, generalized anxiety disorder, or MDD and examines brain response during attentional control over threat distractors before CBT. A subset of patients also completed an emotion processing task before, during, and after 12 weeks of CBT. Results suggest that individuals with greater baseline activation during attentional control had greater reduction in symptom severity after completing CBT. Data indicate greater attentional control may predict CBT success and regions implicated in the pathophysiology of internalizing disorders may be remediated early in CBT. In the fourth presentation, data from 75 individuals with social anxiety disorder (SAD) who were assigned to 16 sessions of CBT or a waitlist completed an fMRI reappraisal task in which they “reacted” or “reappraised” videotaped actors conveying praise or criticism and provided negative emotion ratings. After controlling for CBT-related responses to praise/criticism, criticism reappraisal predicted an additional 25% of the variance in symptom improvemen,t suggesting CBT involves reappraisal-related brain responses to criticism. The fifth presentation presents baseline resting-state functional connectivity and diffusion-weighted structural connectivity to predict responsivity to CBT among adults with SAD. Amygdala-driven resting state connectivity and probabilistic tractography of the inferior longitudinal fasciculus, together with multivoxel pattern analysis of whole-brain resting-state connectivity demonstrate that each connectomic measure significantly improved the prediction of treatment outcome beyond a clinical measure of initial severity. Collectively, this set of presentations review recent research examining neural predictors of CBT outcome and putative mechanisms of change.
9:00 AM-10:30 AM, Salon A5, Symposium 72. Interpersonal Stress as a Candidate Environment for Depression: Neuroendocrine and Genetic Mechanisms, Symposium, Kimberly Dienes; Kate Harkness; Kate Harkness; Lisa Starr; Catherine Stroud; Suzanne Vrshek-Schallhorn.
Theme and Summary Abstract: A large body of evidence suggests that interpersonal stress is an important “candidate environment” for depression. This symposium considers how the effects of interpersonal stress are instantiated, and who is most vulnerable, using cutting-edge neuroendocrine and genetic approaches as well as interview measurement of naturalistic stress. First, hypothalamic-pituitary-adrenal (HPA) axis dysregulation is implicated in the etiology of depression: Depression risk factors are associated with dysregulated cortisol reactivity to lab-based stressors (e.g., Zoccola et al., 2010), and that the magnitude of the Cortisol Awakening Response (CAR) prospectively predicts depression (e.g., Adam et al., 2010). Despite evidence that the HPA axis is particularly sensitive to interpersonal factors (e.g., Dickerson & Kemeny, 2004), insufficient research has examined how interpersonal versus non-interpersonal forms of naturalistic stress predict cortisol reactivity to stress and even moderate the relationship of HPA indices to prospective depression. Second, recent work indicates that genetic risk in the serotonin system confers risk for depression chiefly via vulnerability to interpersonal and not non-interpersonal stress (e.g., Vrshek-Schallhorn et al., 2014). Romantic relationships are an aspect of the interpersonal environment that is particularly important to adolescent depression (e.g., Davila, 2008); exploration of interplay between genetic risk and romantic involvement may shed light on etiological pathways to depression. In addition, efforts to extend GxE tests with interpersonal stress to novel serotonergic polymorphisms beyond 5-HTTLPR, and to examine additive genetic risk consistent with polygenic models, may provide new, more statistically powerful avenues for examining risk for depression under stress. In four talks, this symposium presents longitudinal and controlled experimental evidence for interrelationships between genetic and neuroendocrine markers of stress reactivity and interpersonal stress in relation to depression. First, Kimberly Dienes-Williams will present novel findings demonstrating that interpersonal but not non-interpersonal chronic stress predicts the CAR and cortisol reactivity to the Trier Social Stress Test. Second, Catherine B. Stroud will discuss findings demonstrating that the Cortisol Awakening Response interacts with interpersonal but not non- interpersonal stressful life events to predict increased depression symptoms in a longitudinal study of adolescent females. Third, Lisa Starr will present findings from a longitudinal study that 5-HTTLPR modifies previously established associations between depression and romantic involvement, and that highlight the roles of chronic stress and family discord. Fourth, Suzanne Vrshek-Schallhorn will present longitudinal data showing that additive genetic risk from novel markers in the serotonin system interacts with major interpersonal stressful life events to predict depressive episodes. Finally, Kate Harkness, an expert in life stress and its mechanisms on depression in adolescents and adults, will serve as discussant, connecting these talks with each other and with the existing literature, and developing implications for future research.
9:45 AM-11:15 AM, Lake Ontario, Symposium 78. Innovative Translational Research on Reinforcement Processes: Connecting Basic Lab Research to Inform Clinical Interventions, Symposium, Victoria Ameral; Amy Cameron; Kathleen Palm Reed; Emily Panza; Michael Treadway.
Theme and Summary Abstract: Processes related to reinforcement have long been associated with the development, maintenance and treatment of psychopathology. For example, mechanisms related to appetitive control such as reward processing characterize a number of disorders (e.g., depression, Pizzagalli et al., 2008), and inform well- supported treatment techniques, including behavioral activation (Jacobson et al., 1996). Mechanisms related to aversive control such as distress tolerance have also been gaining increased attention as maintenance factors and treatment targets (Leyro et al., 2010; Brown et al., 2008). Despite the vast research literature investigating appetitive and aversive control (i.e., positive versus negative reinforcement) processes, these processes are often examined in isolation from one another and the link between basic lab findings and implications for treatment is not fully developed. The primary aim of this symposium is to provide a forum to showcase innovative work conducted across a number of basic research and clinical settings, and to discuss how consideration of the entire context can inform our understanding of psychopathology and our design of effective clinical interventions. The presentations in this symposium consider reinforcement processes using a variety of methodological approaches, ranging from neuroimaging to behavioral tasks to participant self-report. Further, as these processes are conceptualized as transdiagnostic markers of psychopathology, the role of the appetitive versus aversive control will be discussed across a number of clinical presentations. The symposium will begin with Treadway and colleagues' investigation of the neural architecture underlying the relationship between stress and reward processing deficits. Using a combination of imaging and behavioral techniques, this study extends our understanding of the neural etiopathophysiology of stress-linked reward processing deficits found in disorders such as major depression. Next, Panza and colleagues will present their findings on the negative automatic reinforcement functions of comfort eating behavior, showing the impact of state rumination on the negative reinforcement function of comfort eating. The third presentation, by Ameral and colleagues, will evaluate the differential impact of responsiveness to rewards and the perceived ability to tolerate distress on quality of life in a sample of clinically depressed and healthy control volunteers. Finally, Cameron and colleagues’ study will present data on an intervention targeting values, or the intrinsically reinforcing properties in daily life, for borderline personality disorder. This study provides evidence linking changes in rule-governed behavior to changes in both symptom severity as well as valued living. Taken together, these studies will provide an opportunity to consider the complex interplay of reinforcement processes and provide a forum for the discussion of future directions for such work.
10:15 AM-11:45 AM, Continental C, Symposium 80. Cognition and Emotion in Psychopathology: From Mechanisms to Treatment, Symposium, Arielle Baskin- Sommers; Christopher Beevers; Daniel Foti; Robin Nusslock; William Vanderlind
Theme and Summary Abstract: The capacity for self-regulation is a key predictor of psychological and physical well being, whereas self-regulatory failure is associated with significant psychiatric and somatic morbidity. The harmful manifestations of poor self-regulation are diverse and encompass a range of maladaptive behaviors including substance abuse, suicidal behavior, and risky health behaviors, which together are related to causes of almost two- thirds of all deaths in the United States. Substantial research has linked cognitive processes, such as action control, behavioral flexibility, and decision-making to chronic failures in self-regulation. Although substantial research links cognitive deficits to chronic failures in self-regulation, our knowledge of how affective factors, such as distress and reward, interact with cognitive factors to promote psychopathology remains poorly understood. Given the strong evidence that both cognitive and affective factors play key roles in the etiology of psychopathology, this gap in knowledge poses a significant roadblock to the development of effective intervention and prevention strategies. The present symposium will focus on recent research investigating cognitive-affective factors implicated in self-regulation from a transdiagnostic perspective. The overarching aims are to identify cognitive and affective factors associated with the onset and maintenance of various forms of psychopathology and to examine the efficacy of paradigms aimed at modifying such processes in the service of treating clinical disorders. The first talk, presented by Mr. Vanderlind, identifies cognitive processes associated with emotion regulation difficulties and examines how these constructs contribute to depressive symptomology. The second talk, presented by Dr. Foti, highlights the role that action monitoring and reward processing play in the interaction between personality traits and internalizing symptoms (i.e., depression and anxiety). The third talk, presented by Dr. Robin Nusslock, reviews neurophysiological and neuroimaging research on the role of reward processing in unipolar depression and bipolar disorder. Data reveal that aberrant reward processing is a common mechanism contributing the onset of these disorders; however, the nature of its role distinguishes the two forms of psychopathology. The final talk, by Dr. Baskin- Sommers, will present data on a new cognitive remediation program designed to address specific cognitive-affective processes implicated in chronic failures of self-regulation, including substance abuse and personality disorders. Following these presentations, the discussant of the symposium, Dr. Beevers, will summarize these new findings with regard to how examination of cognitive processes and self-regulator mechanisms can inform the development of target treatment programs.
1:45 PM-2:45 PM, Lake Ontario, Symposium 108. Reward Processing Predictors of Depression Treatment Response: Initial Presentation of a Clinical Trial, Symposium, Stacey Daughters; Gabriel Dichter; Moria Smoski; Erin Walsh
Theme and Summary Abstract: Though there are many effective interventions for Major Depressive Disorder (MDD), there is significant heterogeneity in treatment response. One obstacle to improved treatment response is the lack of biomarkers to predict which patients will respond to a given treatment. In MDD, the mesocorticolimbic reward processing system is of particular interest, given its linkages to antidepressant treatment response in preclinical models and to anhedonia. The aim of this symposium is to present results of a recently concluded NIMH-funded trial examining functional neuroimaging predictors of response to an open trial of Behavioral Activation (BA) psychotherapy for MDD. Participants (MDD=38; Controls=20) underwent functional neuroimaging during reward processing tasks before receiving Brief Behavioral Activation Treatment for Depression (BATD). Greater understanding of patient characteristics that predict response to BA may inform dissemination efforts by increasing confidence in the appropriateness of this intervention for specific patients. Neural mechanisms of reward processing are well-suited to be a predictor of response to BA because BA encourages patients to reduce avoidance and expose themselves to reinforcing situations. Consistent with the posited effects of BA on reward processing, the overall study aim was to examine relations between neural responses to rewards and response to BATD in patients with MDD. Analyses tested competing hypotheses of whether BATD functions best as a means of ameliorating deficits in reward processing (i.e., greater reward network dysfunction predicts better treatment response) versus capitalizing on preserved strengths (i.e., preserved reward network function predicts better treatment response.) The first presentation within the symposium, delivered by Dr. Smoski, will focus on study design, participant characteristics, and clinical response. Consistent with the study’s focus on the Research Domain Criteria (RDoC) construct of positive valence systems, key outcome variables will focus on treatment effects on anhedonia, in addition to depression symptoms more broadly. The second presentation, delivered by Dr. Walsh, investigates whether functional connectivity while participants attempted to upregulate positive affect predicted treatment response. Functional connectivity with signal nodes of the salience network distinguished participants with MDD from nondepressed controls, and connectivity with those nodes is used as a predictor of treatment response. The third presentation, delivered by Dr. Dichter, investigates whether activation in mesocorticolimbic reward regions during reward anticipation and reward outcomes predicted treatment response. Compared to controls, MDD participants differed in endurance of neural response to reward; drop-off in activation in the left OFC, right putamen, and bilateral striatum over the course of the fMRI task predicted change in depressive symptoms following treatment. BA is effective in reducing depressive and anhedonic symptoms, however, there may be unique challenges in treating patients with disturbed reward functioning. This calls for further study on how to disseminate effective interventions for anhedonia.
2:00 PM-3:30 PM, International North, Symposium 114. The Neurocognitve Underpinnings of Anxiety: Implications for Theory and Treatment, Symposium, Eugenia Gorlin; Lauren Hallion; Elizabeth Lewis; Saren Seeley; Shari Steinman; David Tolin
Theme and Summary Abstract: Recently, there has been a surge of interest in the neural and cognitive mechanisms that underlie anxiety and related disorders. This interest is in line with the Research Domain Criteria (RDoC) and has significant implications for advancing theory and improving outcomes. A clear understanding of neurocognitive mechanisms can help identify etiological factors, differentiate disorders with distinct neural pathways, evaluate cognitive models of anxiety, and suggest new targets for treatment. For example, research linking impairments in cognitive functioning to symptoms has led to the growing popularity of computerized cognitive training (CCT; e.g., cognitive bias modification). Although CCT can produce large effect sizes for improvements in cognition, the effect on symptoms is smaller than initially hoped (Hallion & Ruscio, 2011). This discrepancy suggests that CCT may not optimally target the mechanisms responsible for psychiatric disorders. Similarly, although CBT often produces large effect sizes, not everyone improves, and recurrence is common. To be optimally effective, interventions should directly target the mechanisms that underlie symptoms. To that end, this symposium will describe new developments in the cognitive and neural underpinnings of anxiety and related disorders. Lauren Hallion will demonstrate impaired cognitive but not motor inhibition in GAD. Saren Seeley will describe mechanisms of attentional change during Emotion Regulation Therapy for GAD. Gena Gorlin will link motivational and neurocognitive factors to recurrence of suppressed thoughts and anxiety. These three talks highlight advances in executive control research. Elizabeth Lewis will describe neural activity during cognitive, social, and emotional tasks in GAD and social anxiety disorder. Shari Steinman will demonstrate impaired sensorimotor gating in females with OCD. These two talks highlight neural circuitry that may underlie anxiety. Finally, David Tolin, an expert in mechanism and treatment research in anxiety and related disorders, will serve as discussant.
2:00-3:00pm, Conference Room 4D: SIG meeting
Description: This year we are honored to have ABCT President-Elect Michelle Craske as our featured speaker. If you share our interest in advancing treatment through translational application of neuroscience and other multidisciplinary methodologies, we welcome you to come join the discussion!
Click here for the flyer for this year's SIG meeting. 3:30 PM-4:30 PM, Williford B, Panel Discussion 27. Bridging Basic Science and Treatment Research on Emotional Reactivity in Depression: Theoretical Questions, Methodological Issues, and Pathways for Moving Forward, Panel Discussion, Lauren Bylsma; Sona Dimidjian; Kari Eddington; Daniel Foti; Jackie Gollan; Rachel Hershenberg
Abstract Body: As CBT researchers have moved to identify mechanisms that cause and maintain psychological problems, the field of depression research has increasingly focused on emotional reactivity to environmental stimuli as one critical mechanism. In this panel, we focus on the evidence for how depressed individuals react to positive stimuli (as captured in the laboratory) and positive life events (as captured via experience sampling methodologies). On the one hand, experience-sampling methodologies offer support for mood-brightening. Mood-brightening refers to the phenomenon that, when measured in daily life, depressed compared to non-depressed participants self-report larger decreases in negative affect following positive events and comparable increases in positive affect (Bylsma et al., 2011). This finding has been referred to as "somewhat curious," insofar as it does not fit with the predominant model of emotional reactivity in depression, emotion context insensitivity, which suggests that depressed individuals demonstrate attenuated reactivity to both positive and negative laboratory-based stimuli at multiple units of analysis (e.g., physiological reactivity to film clips; Bylsma et al., 2008). That said, mood-brightening effects converge with the evidence for behavioral activation (BA), as the hypothesized mechanism of change is that symptoms of depression improve once patients continue to place themselves in rewarding environmental contexts. Our panelists are experts in the study of emotion, motivation, and depression who vary in their research methodologies. We draw out both convergent and discrepant evidence that has arisen based on distinct methodologies at differing units of analysis—discrepancies that are rarely integrated in the literature. The panel's goals are to critically discuss (a) how to conceptually integrate differing findings, particularly between lab-based studies (Foti, Bylsma) and experience sampling methodologies (Bylsma, Eddington); (b) how to consider the implications of this basic-science research on intervention (from bench to bedside; Eddington, Gollan); and (c) how to consider how emerging data on BA can inform basic science research on emotional reactivity (from bedside to bench; Gollan, Dimidjian).
Sunday, November 15th, 2015:
8:30 AM-10:00 AM, Continental C, Symposium 131. Beyond Reaction Time Bias: Neural, Physiological, Ecological, and Clinical Correlates of Information Processing Mechanisms, Symposium, Kristy Benoit Allen; Rudi De Raedt; Jennie Kuckertz; Jennie Kuckertz; Rebecca Price; Bethany Teachman
Theme and Summary Abstract: Altered patterns of information processing (e.g., attention) are posited to be critical mechanisms of psychopathology in cognitive-behavioral models. The manner in which individuals attend to and process the complex array of stimuli in their environment may influence conscious cognitions, perceptions, and behavior, leading to risk for psychological distress across a large range of traditional diagnoses. For example, selective focus on negative information may lead to overestimation of the dangers and misfortunes present in the world, promoting negative affective states. Traditionally, information processing constructs have been studied using methodologies drawn from the field of cognitive science (e.g., reaction time measures of attention). More recently, a wider array of techniques drawn from cognitive neuroscience, psychophysiology, and clinical science have been applied to further explicate the nature and correlates of information processing dimensions. The promise of this multidisciplinary work is that it will not only improve our understanding of psycholopathological mechanisms, but also point the way to novel, dissemination ready (e.g., computer-administered) treatment strategies targeting information processing dimensions directly. The authors in this symposium will describe findings pertinent to better understanding information processing mechanisms of psychological distress, across diagnoses and developmental periods. First, Price and colleagues will describe a study in which laboratory-assessed vigilance to threat (assessed via reaction times) and related brain connectivity measures (assessed via fMRI) were linked to real-world avoidance behavior (assessed via Ecological Momentary Assessment) among 78 clinically anxious youth. Next, Benoit Allen and colleagues will describe long-term clinical consequences of information processing mechanisms in anxious youth and their mothers, using eyetracking and pupil dilation (a psychophysiological index of neural reactivity) collected in both mother and child during an attentional task. Third, Kuckertz and colleagues will describe neurocognitive predictors of response to an Attention Bias Modification intervention using event-related potentials (ERPs) and behavioral data as markers of attentional mechanisms. Finally, de Raedt et al will describe the experimental effects of cognitive control modulation (via neuromodulation of the prefrontal cortex) on psychophysiological responses to a stressor, helping to validate a causal role for information processing in psychological vulnerability. As discussant Bethany Teachman will underscore, these studies exemplify the utility of applying multidisciplinary methods to better understand the nature of information processing mechanisms and to clarify the role they play in real-world psychological dysfunction and recovery.
9:00-10:30 AM, Williford A, Symposium 134. Clinical applications of economics and learning theory in the context of social anxiety, depression, and suicidality. Andrew Valdespino, Thomas Rodebaugh, Dahlia Mukherjee, Andrew Valdespino, Greg Siegle, Alexandre Dombrovski.
Recent advances in the study of human decision making leverage computational models of optimal choice and learning. These models reduce complex interactions to a comparatively simple framework and isolate parameters controlling approach/avoidance behavior and even social exchanges. This allows one to dissect behavioral processes characteristic of psychopathology with the upshot of informing precise targets for intervention. Such interventions could focus on basic principles that cut across disorders and increase prospects for dissemination and impact. In this symposium we present novel applications of formal learning theory and behavioral economic methodologies that yield new insight into specific cognitions and behaviors that characterize social anxiety disorder, depression, and suicidality. The presentations reveal how specific dimensions (i.e., reinforcement learning, reward computations, and specific social interaction styles) elucidate shared pathogenetic processes for these psychopathologies. Andrew Valdespino (Virginia Tech) will begin by introducing how quantitative decision-making models, which constitute the overarching methodological theme across presentations, can provide insight into psychopathology. Andrew Valdespino will also present data suggesting that altered learning and updating of the beliefs of interaction partners may characterize social anxiety. Dr. Thomas Rodebaugh (Washington University in St. Louis) will follow by presenting data from a behavioral economic social interaction task, revealing that SAD is characterized by reduced sensitivity to interpersonal context. Findings presented in these first two talks suggest that targeting interpersonal-specific cognitions and behaviors, such as learning others’ beliefs, as well as increasing flexibility of responding in relationships, might provide additional inroads for treatment targets. Dahlia Mukherjee (University of Pennsylvania) will present data leveraging a computational behavioral model of reinforcement learning, which reveals that depression is characterized by domain-specific deficits in learning stimulus-outcome contingencies. Alex Dombrovski (University of Pittsburgh) will present data suggesting that unplanned suicidal behavior is characterized behaviorally by the neglect of decision-relevant information, which is paralleled by altered paralimbic expected value representations. Research presented in these final two talks implicates the neglect of positive reward bearing information as a common etiological risk factor for both suicidality and depression.
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