A decennial review of psychotraumatology: what did we learn and where are we going?

Abstract

On 6 December 2019 we start the 10th year of the European Journal of Psychotraumatogy (EJPT), a full Open Access journal on psychotrauma. This editorial is part of a special issue/ collection celebrating the 10 years anniversary of the journal where we will acknowledge some of our most impactful articles of the past decade (also discussed below and marked with * in the reference list). In this editorial the editors present a decennial review of the field addressing a range of topics that are core to both the journal and to psychotraumatology as a discipline. These include neurobiological developments (genomics, neuroimaging and neuroendocrine research), forms of trauma exposure and impact across the lifespan, mass trauma and early interventions, work-related trauma, trauma in refugee populations, and the potential consequences of trauma such as PTSD or Complex PTSD, but also resilience. We address innovations in psychological, medication (enhanced) and technologyassisted treatments, mediators and moderators like social support and finally how new research methods help us to gain insights in symptom structures or to better predict symptom development or treatment success. We aimed to answer three questions 1. Where did we stand in 2010? 2. What did we learn in the past 10 years? 3. What are our knowledge gaps? We conclude with a number of recommendations concerning top priorities for the future direction of the field of psychotraumatology and correspondingly the journal.

Embracing data preservation, sharing, and re-use in traumatic stress research

“…With a growing international movement towards more open science (Olff et al, 2019) and making data findable and re-usable, it is time for the traumatic stress field to fully recognize the value of preservation, sharing, and re-use of data. This recognition will have implications for our current and future research practices, and will shape the choices we make now regarding the legacy of past research.…”

Neurobiological Trajectories Involving Social Isolation in PTSD: A Systematic Review

“…Withdrawal and real or expected negative responses from others relating to early experiences of bullying victimization may cultivate a vicious circle of shame and loneliness in these patients [40]. In addition, the neurobiology of social support is still poorly understood [11].…”

“…We present the results of the retrieved studies in terms of hypothalamic-pituitary-adrenal (HPA)-axis and endocannabinoid system function, immune reactions, neuroplasticity, novel pharmacological targets, and shortening of telomere length, which confirm a synergistic effect on a neurobiological level between the two entities.Brain Sci. 2020, 10, 173 2 of 15 studies have shown that trauma-related disorders are associated with the dysfunctioning of numerous biological systems, and that PTSD symptom severity exerts a cumulative effect on premature aging of the immune system and telomere length [8].Human functional imaging studies have identified an increased connectivity between the ventromedial prefrontal cortex (vmPFC), locus coeruleus (LC), hypothalamus, hippocampus, basolateral amygdala (BLA), and bed nucleus of the stria terminalis (BNST) in PTSD patients, while more subcortical areas like the periaqueductal gray area (PAG) and central amygdala (CeA) gradually become involved when the severity of a threatening stimulus becomes aggravated [9,10].Before the last decade, the predominant neurobiological model of PTSD concentrated on the pathway of fear conditioning involving mainly the amygdala system [11]. The preparations of the new DSM-5 broadened the criteria to include further emotionally dysregulated states like anger, guilt, shame, and symptoms of derealization and depersonalization, as well as altered self-and other-related conditions and deficits in social cognitions.…”

“…Such changes also gave rise to new neurobiological research challenges [12]. The emotional dysregulation in PTSD tends to be viewed as a vulnerability factor relating to genetic and developmental parameters and a response to (a) traumatic event(s) during childhood, adolescence or adulthood [11]. Neuroendocrine and neuroimmune findings in PTSD include lower basal cortisol output, increased glucocorticoid receptor (GR) function, and a proinflammatory response pre-, peri-, and post-trauma [13], whereas early trauma [14] and ongoing threat [15] are associated to similar observations.…”

“…Before the last decade, the predominant neurobiological model of PTSD concentrated on the pathway of fear conditioning involving mainly the amygdala system [11]. The preparations of the new DSM-5 broadened the criteria to include further emotionally dysregulated states like anger, guilt, shame, and symptoms of derealization and depersonalization, as well as altered self-and other-related conditions and deficits in social cognitions.…”