Resilience after trauma: The role of memory suppression

INTRODUCTION One of the fundamental questions in clinical neuroscience is why some individuals can cope with traumatic events, while others remain traumatized by a haunting past they cannot get rid of. The expression and persistence of vivid and distressing intrusive memories is a central feature of posttraumatic stress disorder (PTSD). Current understanding of PTSD links this persistence to a failure to reduce the fear associated with the trauma, a deficit rooted in the dysfunction of memory. In this study, we investigated whether this deficit may additionally be rooted in the disruption of the brain system that normally allows control over memory. RATIONALE To test this hypothesis in a laboratory setting, we implemented neutral and inoffensive intrusive memories paired with a reminder cue in a group of 102 individuals exposed to the 2015 Paris terrorist attacks and in a group of 73 nonexposed individuals (i.e., individuals who did not experience the attacks). The exposed group was composed of 55 individuals suffering from PTSD symptoms (denoted PTSD+) and 47 individuals showing no noticeable impairment after the trauma (denoted PTSD−). We used functional magnetic resonance imaging to measure how the dorsolateral prefrontal cortex (DLPFC), a core hub of the brain control system, regulated and suppressed memory activity during the reexperiencing of these intrusive memories. We focused our analyses on both the functional and causal dependency between control and memory neural circuits during attempts to suppress the reemergence of these intrusive memories. RESULTS In healthy individuals (PTSD− and nonexposed), attempts to prevent the unwanted emergence of intrusive memory into consciousness was associated with a significant reduction of the functional coupling between control and memory systems, compared with situations where the reminder did not trigger such intrusion. In contrast, there was a near-absence of such a decrease in connectivity in PTSD+. Additional analyses focusing on the directionality of the underlying neural flow communications revealed that the suppression of intrusive memories in healthy individuals arose from the regulation of the right anterior DLPFC, which tuned the response of memory processes to reduce their responses. Notably, this regulation was directed at two key regions previously associated with the reexperiencing of traumatic memories: the hippocampus and the precuneus. CONCLUSION We observed a generalized disruption in PTSD of the regulation signal that controls the reactivation of unwanted memories. This disruption could constitute a central factor in the persistence of traumatic memories, undercutting the ability to deploy the necessary coping resources that maintain healthy memory. Such a deficit may explain maladaptive and unsuccessful suppression attempts often seen in PTSD. Our study suggests that the general mental operations typically engaged to banish and suppress the intrusive expression of unwanted memories might contribute to positive adaptation in the aftermath of a traumatic event, paving the way for new treatments.