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      Fear conditioning and early life vulnerabilities: two distinct pathways of emotional dysregulation and brain dysfunction in PTSD

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          Abstract

          The newly proposed criteria for posttraumatic stress disorder (PTSD) in the Diagnostic and Statistical Manual (DSM-V) include dysregulation of a variety of emotional states including fear, anger, guilt, and shame, in addition to dissociation and numbing. Consistent with these revisions, we postulate two models of emotion dysregulation in PTSD in which fear is not the prevailing emotion but is only one of several components implicated in a dysregulated emotional system that also mediates problems regulating anger, guilt, shame, dissociation, and numbing.

          We discuss whether there is a relationship between fear and other emotion regulation systems that may help further our understanding of PTSD and its underlying neurocircuitry. Two pathways describing the relationship between fear and other emotion regulation systems in PTSD are proposed. The first pathway describes emotion dysregulation as an outcome of fear conditioning through stress sensitization and kindling. The second pathway views emotion dysregulation as a distal vulnerability factor and hypothesizes a further exacerbation of fear and other emotion regulatory problems, including the development of PTSD after exposure to one or several traumatic event(s) later in life. Future research and treatment implications are discussed.

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          Most cited references131

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          The neural bases of emotion regulation: reappraisal and suppression of negative emotion.

          Emotion regulation strategies are thought to differ in when and how they influence the emotion-generative process. However, no study to date has directly probed the neural bases of two contrasting (e.g., cognitive versus behavioral) emotion regulation strategies. This study used functional magnetic resonance imaging (fMRI) to examine cognitive reappraisal (a cognitive strategy thought to have its impact early in the emotion-generative process) and expressive suppression (a behavioral strategy thought to have its impact later in the emotion-generative process). Seventeen women viewed 15 sec neutral and negative emotion-eliciting films under four conditions--watch-neutral, watch-negative, reappraise-negative, and suppress-negative--while providing emotion experience ratings and having their facial expressions videotaped. Reappraisal resulted in early (0-4.5 sec) prefrontal cortex (PFC) responses, decreased negative emotion experience, and decreased amygdala and insular responses. Suppression produced late (10.5-15 sec) PFC responses, decreased negative emotion behavior and experience, but increased amygdala and insular responses. These findings demonstrate the differential efficacy of reappraisal and suppression on emotional experience, facial behavior, and neural response and highlight intriguing differences in the temporal dynamics of these two emotion regulation strategies.
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            Neurobiological basis of failure to recall extinction memory in posttraumatic stress disorder.

            A clinical characteristic of posttraumatic stress disorder (PTSD) is persistently elevated fear responses to stimuli associated with the traumatic event. The objective herein is to determine whether extinction of fear responses is impaired in PTSD and whether such impairment is related to dysfunctional activation of brain regions known to be involved in fear extinction, viz., amygdala, hippocampus, ventromedial prefrontal cortex (vmPFC), and dorsal anterior cingulate cortex (dACC). Sixteen individuals diagnosed with PTSD and 15 trauma-exposed non-PTSD control subjects underwent a 2-day fear conditioning and extinction protocol in a 3-T functional magnetic resonance imaging scanner. Conditioning and extinction training were conducted on day 1. Extinction recall (or extinction memory) test was conducted on day 2 (extinguished conditioned stimuli presented in the absence of shock). Skin conductance response (SCR) was scored throughout the experiment as an index of the conditioned response. The SCR data revealed no significant differences between groups during acquisition and extinction of conditioned fear on day 1. On day 2, however, PTSD subjects showed impaired recall of extinction memory. Analysis of functional magnetic resonance imaging data showed greater amygdala activation in the PTSD group during day 1 extinction learning. During extinction recall, lesser activation in hippocampus and vmPFC and greater activation in dACC were observed in the PTSD group. The magnitude of extinction memory across all subjects was correlated with activation of hippocampus and vmPFC during extinction recall testing. These findings support the hypothesis that fear extinction is impaired in PTSD. They further suggest that dysfunctional activation in brain structures that mediate fear extinction learning, and especially its recall, underlie this impairment.
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              The role of the amygdala in fear and anxiety.

              M DAVIS (1992)
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                Author and article information

                Journal
                Eur J Psychotraumatol
                Eur J Psychotraumatol
                EJPT
                European Journal of Psychotraumatology
                Co-Action Publishing
                2000-8198
                2000-8066
                10 December 2010
                2010
                : 1
                : 10.3402/ejpt.v1i0.5467
                Affiliations
                [1 ]Department of Psychiatry, The University of Western Ontario, London, Ontario, Canada
                [2 ]Department of Psychology, The University of Western Ontario, London, Ontario, Canada
                [3 ]University Medical Center, Utrecht, The Netherlands
                [4 ]Traumatic Stress Studies, Mount Sinai School of Medicine, NY, USA
                [5 ]Department of Psychiatry, James J. Peters Veterans Affairs Medical Center, The Bronx, NY, USA
                Author notes
                [* ] Ruth A. Lanius, Department of Psychiatry, The University of Western Ontario, 339 Windermere Road, London, ON N6A 5A5, Canada. Email: ruth.lanius@ 123456lhsc.on.ca
                Article
                EJPT-1-5467
                10.3402/ejpt.v1i0.5467
                3401986
                22893793
                9d5dad42-33a6-481e-8f92-1cf0c9f209e0
                © 2010 Ruth A. Lanius et al.

                This is an Open Access article distributed under the terms of the Creative Commons Attribution-Noncommercial 3.0 Unported License, permitting all non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 15 July 2010
                : 18 November 2010
                : 20 November 2010
                Categories
                Invited Review Article

                Clinical Psychology & Psychiatry
                attachment,amygdale,emotion,hpa-axis,infant,development,medial prefrontal cortex,dsm-v,anterior cingulate cortex

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