Peripheral and central mechanisms involved in post-traumatic stress disorder and its treatment by eye-movement desensitization & reprocessing
Although most people encounter at least one traumatic event over their lifetime, not all of them will develop post-traumatic stress disorder (PTSD). Lifetime prevalence of full-blown PTSD, known as an anxiety disorder, is in fact around 10%. In addition to accidents, aggression, grief, rape, fires, traumatic events can be caused by natural (flooding, earthquake…) or man-made stressors (war, terrorism…). With the contemporary rise in traumatic sources the World Health Organization recent reports describe PTSD as an increasing global health issue, due to its high frequency, severity, comorbidity and cost. A body of research has thus started investigating various aspects of PTSD concerned with intrusive thoughts, hypervigilance, emotional deficits, cognitive disturbances and memory issues. Similarly to other mental health problems, much remains unknown about PTSD, and similarly to other anxiety disorders it is marked by excessive fear. It comes as no surprise that the most prevalent hypothesis in PTSD is that of a fear-processing deficit. Conceptualizing PTSD as a fear disorder can be phenomenologically quite narrow. It has been nonetheless pragmatic in allowing thorough translational research from animal to bench-side and clinical studies. Most studies have suggested that central and peripheral impairments in PTSD revolve around altered neural fear processing network. These alterations involve mechanisms implicated in fear conditioning, as well as emotional and attentional processing, all of which are altered in PTSD. We address PTSD as a pathological model of altered fronto-limbic processing after traumatic exposure, bearing in mind its correlation to anxious symptomatology. The aim of our study was to investigate central and peripheral mechanisms involved in fear conditioning, emotional attending and cognitive processing of threat in PTSD and explore their correlation to symptomatology and subsequently infer on their inherited v/s. acquired characteristics of PTSD. In the absence of twin studies differing for PTSD diagnosis, we chose to do so by monitoring deficits before and after symptom removal by a validated and quick psychotherapy. Patients’ results would be compared to healthy controls and to a wait-list of PTSD patients. Stemming from the surprising lack of research investigating how different emotional and attentional components of PTSD interact, we studied altogether threat-related amygdala hyperactivity and prefrontal cortex (PFC) hypoactivity in PTSD with other aspects of anxious responding such as emotional deficits, attentional bias and self-measures of distress. We hypothesized that patients would initially have an overactive amygdala and a hypoactive PFC compared to controls, with symptoms worsened by an inadequate frontolimbic connectivity. With known roles of amygdala and PFC in fear conditioning, emotion and attention orientation, we further hypothesized that their alterations in PTSD would manifest peripherally in increased fear sensitization and delayed fear extinction, in exaggerated emotional attending and inefficient emotional suppressing and in attentional bias toward emotional cues due to a disengagement difficulty. To do so, we used an arsenal of techniques at the central and peripheral level. Tasks included classical conditioning paradigm, emotional attending and suppressing of film excerpts (inducing fear, sadness, joy and peacefulness) as well as attentional bias tasks andOur results have confirmed our hypotheses of increased amygdala and decreased prefrontal activity in PTSD alongside altered connectivity between limbic and cortical areas. PTSD also seemed characterized by an exaggerated physiological responding to fear and difficulty controlling their emotions and detaching their attention from threat cues. We have further shown that these impairments are correlated with symptom severity and are restored after symptom removal. We hereby reproduce central and peripheral alterations in PTSD and for the first time monitor them after therapy and show their intercorelation and causal dependence. We have shown these deficits remain in wait-list group and are restored after EMDR. As such this provides preliminary evidence that these could constitute acquired markers of the pathology. We also provide support to improve PTSD diagnosis using subjective scales and attentional task correlated with biological variables. Those markers should be further examined in relationship to risk of relapse. fMRI based emotional face matching.
Original Work Citation
El-Khoury, M. (2011). Peripheral and central mechanisms involved in post-traumatic stress disorder and its treatment by eye-movement desensitization & reprocessing. (Doctoral dissertation, University of Marseille). Retrieved from http://www.theses.fr/2011AIX20664/document
“Peripheral and central mechanisms involved in post-traumatic stress disorder and its treatment by eye-movement desensitization & reprocessing,” Francine Shapiro Library, accessed July 10, 2020, https://emdria.omeka.net/items/show/22295.