The Lab’s Core ideology

Central Values: Guiding principles by which we navigate.  These are values we would have regardless of the job, and even if they were a competitive disadvantage.

  • Passion fueled by creativity, perseverance, and good (self-deprecating) humor

  • Connection – to cultivate a culture of belonging and openness through both knowing others and the privilege of bearing witness to peoples’ stories

  • Ambition – a strong desire to achieve with a healthy dose of humility

Core Purpose: our lab’s reason for being

  • To understand the adaptability of the human mind and body, so that we can help those impacted by childhood abuse.

Mission

The Dissociative Disorders and Trauma Research Program, founded in 2013 by Dr. Milissa Kaufman and now jointly directed by Dr. Kaufman and Dr. Lauren Lebois, focuses on individuals 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.

We aim to identify and understand, in a clinically nuanced manner, the phenomenology, brain mechanisms, cognitions, physiology, and genes contributing to PTSD and DID and how they relate to both dysfunction and resilience in these disorders.

Using statistical, behavioral, and imaging techniques, we aim to document people's experience of trauma and its consequences, to understand the heterogeneity of post-traumatic adaptations, and to identify those who will respond optimally to a particular treatment. Ultimately, we hope to reduce the stigma surrounding these experiences and improve the quality of assessment and treatment that people receive.


Participating in the study was the first time I felt like anything good came out of my terrible experiences.
— Research Participant

FOCUS AREAS

The Search for Biological Markers and Mechanisms of Trauma-related Dissociation

Exposure to traumatic stress is consistently and strongly associated with dissociative symptoms for a subset of the population.  Phenomenologically, dissociation encompasses a range of distinct, yet clinically interrelated symptoms: depersonalization, derealization, amnesia, numbing, intrusive flashbacks, agency/ownership loss over thoughts, emotions, and bodily experiences, and identity disturbances.  These symptoms, individually or in various combinations, serve as diagnostic criteria across multiple psychiatric disorders including posttraumatic stress disorder (PTSD) and dissociative identity disorder (DID).  However, the biological markers and mechanisms of dissociation remain largely unknown.  Understanding these mechanisms could yield tractable new points of intervention for patients – for example, novel neurobiological targets to engage in future psychotherapeutic, pharmacological, neurofeedback or neuromodulatory interventions. 

Our research suggests that trauma-related dissociation is associated with several distinct neurobiological and psychophysiological mechanisms, varying based on the type of dissociation examined (e.g., Lebois et al., 2021, American Journal of Psychiatry; Lebois et al., 2022, American Journal of Psychiatry; Lebois et al., 2022, Neuropsychopharmacology; Seligowski et al., 2019, Depression & Anxiety).  We were also the first to show that self-reported dissociative symptoms could be accurately predicted solely based on patterns of brain functional connectivity (Lebois et al., 2021, American Journal of Psychiatry). Furthermore, we found that dissociative symptoms and their neurobiological correlates predicted more severe future posttraumatic stress symptoms in a large-scale, prospective longitudinal study (Lebois et al., 2022, American Journal of Psychiatry). 

This body of work represents a significant advancement in our understanding of dissociation, its neural underpinnings, and its physical manifestations.  By integrating these insights, we have increased awareness of the need to assess for dissociative symptoms and intervene early in clinical and medical settings.  This research not only emphasizes the importance of early intervention but also paves the way for developing more targeted treatment strategies that leverage our neurobiological understanding of trauma-related dissociation.

 

Empirical Research on Dissociative Identity Disorder

Dissociative Identity Disorder (DID) has long been one of the most stigmatized psychiatric disorders in the world.  Paradoxically, DID is both an ingenious adaptive response to inescapable childhood maltreatment, and it is associated with significant financial, personal and societal costs. Research supports a powerful relationship between chronic, early childhood abuse and the development of DID.  The diagnosis is well-validated psychometrically and prevalence is higher than generally appreciated – with a 1.1% lifetime prevalence – more prevalent than schizophrenia.  Despite this, even among mental health clinicians and researchers, beliefs about DID often are not based on the scientific literature and the condition remains understudied.  For instance, skepticism, misunderstanding, and lack of professional education about DID all contribute to striking rates of underdiagnosis and misdiagnoses.  Consequently, individuals with DID typically wait an average of 6-12 years to receive appropriate treatment.

Our research has contributed to the growing body of empirical studies on DID. We have identified distinct neurobiological correlates associated with the disorder (Lebois et al., 2021, American Journal of Psychiatry; Lebois et al., 2022, Neuropsychopharmacology).  Additionally, we have documented a range of distorted bodily perceptions in individuals with DID (Merker et al., 2021, Journal of Psychiatric Research) and high levels of anxiety sensitivity related to concern over losing control of their mind (Pan et al., 2022, Journal of Psychiatric Research).  Furthermore, we have observed altered performance on emotional and self-face perception tasks in DID (Lebois et al., 2020, Journal of Psychiatric Research; Lebois et al., 2019, Journal of Trauma & Dissociation).

This research represents substantial progress in our understanding of DID. By identifying both self-report and objective behavioral task-based markers of dissociation, we have begun to lay the groundwork for more accurate assessments and more effective treatment strategies. These markers and others we are studying offer the potential to not only confirm the presence of dissociation but also to monitor clinically meaningful indicators of recovery or relapse over time. Our research stands as a testament to the critical importance of rigorous, evidence-based investigation in transforming the diagnosis, treatment, and ultimately the lives of those affected by DID.

 

Enhancing Early Identification and Intervention for trauma-related Dysfunction. 

Early identification of trauma-related dysfunction is critical for successful interventions.  Neurophenotypes, or brain-based markers, of PTSD can serve as objective indicators of PTSD subgroups to propel the development of predictive models for PTSD susceptibility.  However, progress in this area has been limited due to the challenges associated with collecting large-scale, prospective, longitudinal data. 

Our team has contributed to the AURORA Study and the psychiatric genomics consortium for PTSD, aiming to identify neurophenotypes of PTSD through large-scale prospective and meta/mega-analyses.  So far, we have found smaller hippocampal volume, altered white matter microstructure organization, altered intrinsic functional connectivity after trauma, sex/ancestry-specific genetic risk loci for PTSD, and distinct functional brain-based biotypes after trauma.  Drs. Kaufman and Lebois also chair the newly established international Enhancing Neuro Imaging Genetics Through Meta Analysis (ENIGMA) dissociation working group, and hope to bring together neuroimaging genetic dissociation researchers worldwide.

This work has significantly enhanced our mechanistic understanding of posttraumatic sequelae using well-powered samples.