PT - JOURNAL ARTICLE AU - Mary, Alison AU - Dayan, Jacques AU - Leone, Giovanni AU - Postel, Charlotte AU - Fraisse, Florence AU - Malle, Carine AU - Vallée, Thomas AU - Klein-Peschanski, Carine AU - Viader, Fausto AU - de la Sayette, Vincent AU - Peschanski, Denis AU - Eustache, Francis AU - Gagnepain, Pierre TI - Resilience after trauma: The role of memory suppression AID - 10.1126/science.aay8477 DP - 2020 Feb 14 TA - Science PG - eaay8477 VI - 367 IP - 6479 4099 - http://science.sciencemag.org/content/367/6479/eaay8477.short 4100 - http://science.sciencemag.org/content/367/6479/eaay8477.full SO - Science2020 Feb 14; 367 AB - Therapists have discussed for a long time whether attempts to voluntarily suppress the intrusion of trauma memories are helpful to combat the distressing impacts of trauma. Mary et al. studied survivors of the 2015 Paris terrorist attacks who developed posttraumatic stress disorder and those who did not (see the Perspective by Ersche). Using functional magnetic resonance imaging, they investigated the neural networks underlying the control and suppression of memory retrieval. The results suggest that the characteristic symptoms of the disorder are not related to the memory itself but to its maladaptive control. These results offer new insights into the development of post-traumatic stress disorder and potential avenues for treatment.Science, this issue p. eaay8477; see also p. 734INTRODUCTIONOne 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.RATIONALETo 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.RESULTSIn 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.CONCLUSIONWe 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.Mechanisms of memory suppression after trauma.(A) Exposed individuals with or without PTSD were asked to suppress the reexperiencing of neutral intrusive memories. (B) Analyses focused on the functional and causal dependencies between control and memory systems during suppression attempts. (C) Extensive decreased coupling to counteract intrusion was seen in nonexposed and PTSD− groups but not in the PTSD+ group. SFG, superior frontal gyrus; MFG, middle frontal gyrus; IFG, inferior frontal gyrus; CC, cingulate cortex; Hipp, hippocampus; PhG, parahippocampal gyrus; FusG, fusiform gyrus; PCun, precuneus. (D) This decreased coupling was mediated by top-down regulation of involuntary memory processing arising from the right DLPFC.In the aftermath of trauma, little is known about why the unwanted and unbidden recollection of traumatic memories persists in some individuals but not others. We implemented neutral and inoffensive intrusive memories in the laboratory in a group of 102 individuals exposed to the 2015 Paris terrorist attacks and 73 nonexposed individuals, who were not in Paris during the attacks. While reexperiencing these intrusive memories, nonexposed individuals and exposed individuals without posttraumatic stress disorder (PTSD) could adaptively suppress memory activity, but exposed individuals with PTSD could not. These findings suggest that the capacity to suppress memory is central to positive posttraumatic adaptation. A generalized disruption of the memory control system could explain the maladaptive and unsuccessful suppression attempts often seen in PTSD, and this disruption should be targeted by specific treatments.