Our research is dedicated to understanding the neural bases of healthy and pathological emotional processing. Currently we are primarily focusing on identifying neurobiological and psychosocial predictors of risk and resilience following a trauma in both adults and youth, cognition-emotion interactions in anxiety, and the impact of chronic environmental stress on brain structure and function. We are also collaborating with Hanjoo Lee at UWM to investigate changes in brain function following a web-based intervention for obsessive-compulsive and related disorders. We use multimodal neuroimaging and EEG to measure neural indices of these processes.

PREDICTING VULNERABILITY FOR PTSD FOLLOWING TRAUMA

Trauma is common, and fortunately most individuals who experience trauma do not develop PTSD. However is significant minority of those who experience trauma will develop debilitating symptoms of PTSD, depression, and other psychological concerns following trauma. Together with Terri deRoon-Cassini of the Medical College of Wisconsin we are attempting to identify acute post-trauma markers of risk for chronic PTSD. In a recently completed NIMH R01-funded study we examined whether individual differences in fear extinction, cognitive control, uncertain threat, and other measures of brain structure and function measured within two weeks of experiencing a trauma predict which individuals will develop PTSD. With new NIH funding we are currently following up this work with Terri deRoon-Cassini of the Medical College of Wisconsin and Lucas Torres of Marquette University to examine recovery following trauma among Black adults in Milwaukee. Together with Mike Levas of the Medical College of Wisconsin and Ryan Herringa at the University of Wisconsin-Madison we are also conducting this work in youth trauma survivors. In this NIH R01-funded study we are recruiting youth from the Emergency Department at Children’s Hospital of Wisconsin in Milwaukee and assess whether acute post-trauma function and structure in circuits for emotion regulation and cognitive control predicts long-term risk for PTSD and depression.

Learn more by visiting the website for the Milwaukee Trauma Outcomes Project (MTOP).

THE IMPACT OF SOCIOENVIRONMENTAL STRESS AND PROTECTIVE FACTORS ON THE BRAIN AND HEALTH

Through our work on trauma we have observed the profound impact that chronic socioenvironmental stress can have on functioning. Thus, another primary line of research in the laboratory is examining the impact of chronic socioenvironmental stresses, such as neighborhood disadvantage and racial discrimination, and protective factors including social support and neighborhood cohesion on psychological functioning and brain structure and function. This work is done jointly with a number of investigators, including our Milwaukee Trauma Outcomes Project colleagues,  Terri deRoon-Cassini of the Medical College of Wisconsin and Lucas Torres of Marquette University,

fMRI RESPONSE INHIBITION TRAINING FOR OBSESSIVE COMPULSIVE AND RELATED DISORDERS

The UWM Anxiety Disorder Lab, directed by Hanjoo Lee, and the UWM Affective Neuroscience Lab are currently testing computer-based treatment programs designed to help adults (aged 18-60) suffering from problematic repetitive behaviors. This research is conducted by the University of Wisconsin-Milwaukee and is funded by the National Institutes of Mental Health.

Study procedures will be completed through at home computer-based training programs/assessments as well as assessments and brain imaging tasks at the Medical College of Wisconsin over the course of 8-15 weeks. Participants will be randomly assigned to one of the two similar computer-based training conditions designed to help improve symptoms for individuals with OCD, Trichotillomania, or skin picking. Our computer-based treatment program is provided to eligible participants, and each participant will receive compensation for completing the study.

Email ocd-research@uwm.edu to learn more.

ANXIETY & COGNITION-EMOTION INTERACTIONS

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. Together with Hanjoo Lee 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 and gating of information from entering working memory in the face of threat.

PREVIOUS WORK

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.

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.

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