Our research is dedicated to understanding the neural bases of healthy and pathological emotional processing. Over the past decade our research program has three main foci: individual differences in affective and cognitive processes associated with anxiety, trauma, and depression, understanding cognitive-affective processes in disinhibitory psychopathology, and characterizing the essential stimulus properties of environmental cues that signal threat. We use multimodal neuroimaging, psychophysiological, behavioral, genetic, and self-report tools to examine these questions. Current research topics include:
Individual Differences in Emotional Reactivity and Emotion Regulation
Our earliest work was aimed at characterizing basic individual differences in the intensity and time course of emotional responding. For example, do some people show slower recovery from unpleasant stimuli? Are these individuals at greater risk for anxiety and depression? Across a series of studies using EEG, fMRI, and peripheral psychophysiology we found that speed of onset and time course of emotional recovery are aberrant in those who are experiencing symptoms of anxiety or depression. More recently we have examined how specific genes are related to individual differences in the time course of emotional recovery. Our research over the past several years builds on these initial findings – what are the mechanisms that impair emotional recovery in anxiety and depression?
We are also continuing our work in this area by examining contextual influences, such as stressful contexts, on emotion regulation and regulation of behavior.
Anxiety & Trauma: Emotion Regulation, and Cognitive-Affective Processing
Anxiety is characterized by rapid expression and slow decay of negative affect, in many cases anxiety symptoms persist well-beyond the presence of perceived potential threats. We have explored several potential models for understanding deficits in downregulating negative affect in anxiety and related conditions, including impaired extinction of conditioned fear and impaired attentional control in the face of threat, resulting in threat unnecessarily occupying valuable working memory stores. Together with Terri deRoon-Cassini of the Medical College of Wisconsin, we are currently examining whether impaired extinction and attentional control prospectively predict development of PTSD in recently trauma-exposed individuals. Our initial work in this area shows that maladaptive engagement of circuitry subserving emotion regulation within two weeks of a traumatic event robustly predicts severity of PTSD symptoms six months later. We will be continuing to pursue this work with an NIH R01.
In other work in this domain we are investigating proactive and reactive control deficits in anxiety, as well as how worry impacts working memory functioning.
Depression: Rumination and Reward Processing
Research on depression in the laboratory has focused on rumination, one key process that may impede successful downreguation of emotion among those who are depressed. We have recently demonstrated aberrant functional connectivity of key networks such as the default mode, executive, and salience networks, in individuals with depression that were most prominent not when ruminating, but when instructed not to ruminate and engage in a externally-focused task. We are currently combining this work with our anxiety work on working memory in hopes of clarifying the role of impairments in certain aspects of working memory in rumination.
In a separate line of work we have shown that individuals who are current euthymic, but have a history of depression are less motivated by reward – compared to those with no history of depression they do not improve cognitive performance (in this case visual selective attention) as robustly when monetarily rewarded for their performance.
Disinhibitory Psychopathology: Emotional Reactivity and Cognition-Emotion Interactions
In collaboration with colleagues who investigate disinhibitory psychopathology we have examined the role of emotion and cognition-emotion interactions in psychopathy and aggression. Working with Joe Newman of the University of Wisconsin-Madison and Kent Kiehl of the Mind Institute and University of New Mexico, we found that in contrast to prominent models of psychopathy that posit a global amygdala-based fear deficit, incarcerated psychopaths showed intact amygdala responses to fear when task demands ensured the fear stimulus was attended to. Through work with Alex Burt at Michigan State University we found that negative affect was uniquely linked with aggression, but not rule-breaking antisocial behaviors.
Stimulus Properties Facilitating Detection of Threat
When we see something that frightens us, how do we know to be afraid? What is it about that stimulus that signals threat? This line of research is designed to answer such questions, primarily through isolating the most basic, essential features of a visual stimulus capable of signaling threat. In a series of studies conducted together with Joel Aronoff of Michigan State University we found that a downward-pointing V shape, stripped of all contextual cues (literally a “V”) functions much like a typical contextually-laden threat stimulus. The downward V shape