Dissociative symptoms in traumatized individuals are common, debilitating, and costly. Exposure to traumatic stress is consistently and strongly associated with dissociative symptoms across clinical and community samples of traumatized individuals. Phenomenologically, traumatic dissociation broadly encompasses a range of distinct, yet clinically interrelated symptoms: depersonalization, derealization, amnesia, numbing, intrusive flashbacks, passive influence phenomena, and identity disturbances. Either alone or in various combinations, these symptoms serve as diagnostic criteria and commonly associated features across multiple psychiatric disorders. Traumatic dissociation is also associated with significant personal and societal burden. Traumatized individuals with dissociative symptoms typically have co-occurring psychiatric conditions, high rates of self-destructive behaviors and suicidality, and are disproportionate treatment utilizers. In addition, they are at increased risk for attrition, non-response and relapse following treatment interventions. In the context of posttraumatic stress disorder (PTSD) or complex dissociative disorders (DD), individuals with dissociative symptoms often report histories of childhood abuse and neglect. During such relational trauma, dissociation may serve an adaptive function by buffering the impact of overwhelming threat. With repeated maltreatment, however, dissociation may become a highly generalized and maladaptive conditioned response that impairs functioning. Despite the significant and disabling nature of traumatic dissociative symptoms, little is known about the neurobiology of these processes and targeted interventions do not exist. We seek to identify neurobiological mechanisms of traumatic dissociation across clinical syndromes, testing a model of dissociation that may explain differential neural processing and symptoms in traumatized subjects. To date, neuroimaging studies of traumatic dissociation have been limited in scope: 1) they have focused on largely a single paradigm, 2) they have targeted dissociative symptoms of detachment from the body and environment, which do not cover the wide range of documented dissociative symptoms, and 3) they limit participant samples to one diagnostic category (PTSD). To address these limitations, we propose a novel mechanistic examination of dissociative neural intermediate phenotypes, testing: 1) if dissociation is associated with top-down inhibition in non-trauma related emotion processing evident in both neuroimaging and behavioral measures; and 2) if dissociation is associated with increased cognitive attentional control evident in both neuroimaging and behavioral measures. Successful completion of these Aims will provide a much-needed dataset to further underpin neurobiological theories of dissociation and will inform both risk factors for pathological dissociation and potential neural circuits to target for treatment.

Public Health Relevance

Pathological dissociative symptoms in traumatized individuals are common, debilitating, and costly at both the personal and societal level. This proposal will examine behavioral and brain activity changes related to traumatic dissociation. Results from this proposal will inform how to identify those at risk for these debilitating symptoms, and potential brain regions to target for treatment.

Agency
National Institute of Health (NIH)
Institute
National Institute of Mental Health (NIMH)
Type
Exploratory/Developmental Grants (R21)
Project #
5R21MH112956-02
Application #
9461628
Study Section
Neural Basis of Psychopathology, Addictions and Sleep Disorders Study Section (NPAS)
Program Officer
Borja, Susan
Project Start
2017-04-01
Project End
2019-01-31
Budget Start
2018-02-01
Budget End
2019-01-31
Support Year
2
Fiscal Year
2018
Total Cost
Indirect Cost
Name
Mclean Hospital
Department
Type
DUNS #
046514535
City
Belmont
State
MA
Country
United States
Zip Code
02478
Ratanatharathorn, Andrew; Boks, Marco P; Maihofer, Adam X et al. (2017) Epigenome-wide association of PTSD from heterogeneous cohorts with a common multi-site analysis pipeline. Am J Med Genet B Neuropsychiatr Genet 174:619-630