Milissa Kaufman, MD, PhD

The Dissociative Disorders and Trauma Research Program, founded in 2013 and led by Dr. Kaufman, focuses on women with experiences of childhood trauma. Dissociative symptoms are associated with trauma spectrum disorders such as post-traumatic stress disorder (PTSD) and dissociative identity disorder (DID). These symptoms may include memory gaps, feelings of detachment from one’s body, emotions, or environment, confusion over one’s identity, and shifts in one’s identity.

Dr. Kaufman’s group aims to identify and understand the brain mechanisms, cognitions, and genes contributing to PTSD and DID and how they relate to both dysfunction and resilience in these disorders. They examine why some people with experiences of trauma develop dissociative symptoms while others do not, why some develop PTSD and others do not, and what brain regions are involved in dissociative symptoms and how they work.

Using cutting-edge statistical, behavioral, and imaging techniques, Dr. Kaufman’s group explores these areas to determine how to identify those at risk for certain trauma related symptoms, how to better identify those who will respond optimally to a particular treatment, and how to tailor individual treatments for the best recovery outcomes. Ultimately, Dr. Kaufman hopes to develop new treatment approaches for these conditions and reduce the stigma surrounding these disorders. Her research goal is to advance the understanding of the genetic, physiological, neural, cognitive, and behavioral mechanisms that underlie trauma spectrum disorders.

In their work evaluating the neurobiological basis of traumatic dissociation in a cross-diagnostic sample of women with histories of childhood abuse and neglect, Dr. Kaufman and her research program focus on the neurobiology of dissociation in women who have experienced childhood trauma. Dissociation is a common reaction to traumatic experiences. At the time of a traumatic event, it may serve as an adaptive function by buffering the impact of overwhelming sensations, emotions, and cognitions. With repeated traumatic experiences, however, dissociation may become conditioned as a primary coping mechanism and occur chronically in response to reminders of the original traumatic event. This response often generalizes to relatively minor daily events. The neurobiology and genetics of dissociation are largely unknown, and the program’s current work aims to characterize these mechanisms in women with the dissociative subtype of PTSD and with DID.

The group is also studying the neurobiology of PTSD dysfunction and recovery following cognitive processing therapy. Previous research has identified negative alterations in self-cognitions (e.g., shame, perceived worthlessness, incompetence) as a strong predictor of PTSD risk, status, and severity. Negative self-processing is associated with alterations in the neural correlates of self-referential processing (e.g., midline cortical structures) and autobiographical memory systems (e.g., medial temporal lobe structures). Using neuroimaging genetic approaches, Dr. Kaufman aims to examine the relationship between traumatic experiences and the neural mechanisms of negative self-referential processing and determine how this relationship changes during PTSD extinction. Concurrently, the research group is examining how the epigenetic profile of different candidate genes predicts, and perhaps changes, in response to recovery from PTSD (and negative self-cognitions) along with its neural correlates. This understanding will further connect genetic biomarkers of risk with neural intermediate phenotypes underlying PTSD symptomatology.