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Neurobiological Trajectories of Psychological Trauma—Implications for Posttraumatic Stress Disorder (PTSD)

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A special issue of Brain Sciences (ISSN 2076-3425). This special issue belongs to the section "Systems Neuroscience".

Deadline for manuscript submissions: closed (25 January 2020) | Viewed by 31341

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Special Issue Editors

Dr. Agorastos Agorastos

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Guest Editor

1. II Department of Psychiatry, Division of Neurosciences, School of Medicine, Faculty of Medical Sciences, Aristotle University of Thessaloniki (AUTH), Thessaloniki, Greece;
2. VA Center of Excellence for Stress and Mental Health (CESAMH), San Diego, CA, USA
Interests: stress; PTSD; trauma; depression; anxiety; panic; psychoneuroendocrinology; heart rate variability; autonomic nervous system; HPA-axis; stress-related disorders; psychoneuroimmunology

Dr. Nikolaos P. Daskalakis

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Co-Guest Editor

Assistant Professor of Psychiatry, Harvard Medical School/ McLean Hospital, MA, USA
Interests: stress; PTSD; HPA-axis; systems biology; psychoneuroendocrinology; gene expression

Prof. Dr. Panagiota Pervanidou

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Co-Guest Editor

Developmental and Behavioral Pediatrics, First Department of Pediatrics, School of Medicine, National and Kapodistrian University of Athens, “Aghia Sophia” Children’s Hospital, 11527 Athens, Greece
Interests: stress; HPA-axis; autonomic nervous system; stress-related disorders; PTSD; ADHD; autism spectrum disorders; neurodevelopmental disorders; obesity; psychoneuroendocrinology
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Special Issue Information

Dear Colleagues,

Posttraumatic stress disorder (PTSD) is classified as a trauma- and stress-related disorder with distinctive symptoms following a psychologically distressing event outside the range of usual human experience. The development of acute and posttraumatic stress symptoms after a traumatic event is common and often leads to personal distress and functional impairment in trauma victims. Inadequate, excessive or prolonged stress reactions may exceed the organism’s natural adjustive capacity and permanently affect adaptive responses. Traumatic stress exposure may alter neuroendocrine responses to stress, triggering a health-related risk cascade with persistent structural and functional neuropsychobiological changes and mediate cumulative health risk leading to increased physical and mental morbidity and all-cause mortality in later life. Traumatic stress thus affects master homeostatic regulating systems at the crossroads of peripheral and central susceptibility pathways, such as the stress system and brain circuitry, and consequently circadian, immune, neuroendocrine, autonomic, metabolic and emotional (re)activity. The diverse human genetic background and the later engraved epigenetic modifications through stress-related gene expression could additionally interact with these alterations and explain inter-individual variation in vulnerability or resilience to trauma. Accordingly, many studies have reported a negative association of PTSD and traumatic stress with cardiovascular and metabolic diseases, chronic inflammatory and pain syndromes, frequency of medical consultations as well as with the number of medical diagnoses.

This Special Issue aims to highlight and review recent advances from human and animal research on the most acknowledged neurobiological allostatic trajectories exerting the enduring adverse effects of traumatic stress and PTSD in later life with special emphasis on identifying factors that explain individual variation in vulnerability or resilience. Topics of interest include, but are not limited to: HPA-axis, autonomic nervous system, genetics/epigenetics, novel biomarkers, neuroimmunology, neurocircuitry/imaging and neuroendocrinology.

Understanding the pathways susceptible to disruption following traumatic stress exposure and the effects of a dysregulated interconnection between all systems involved in PTSD could provide new insights into the pathophysiological trajectories linking traumatic stress to systems’ maladjustment and human disease.

Dr. Agorastos Agorastos
Guest Editor
Dr. Nikolaos P. Daskalakis
Dr. Panagiota Pervanidou
Co-Guest Editors

Manuscript Submission Information

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Keywords

Posttraumatic Stress Disorder (PTSD)
Stress
Trauma
Neurobiology
Hypothalamus-Pituitary-Adrenal (HPA)-axis
Autonomic Nervous System (ANS)
Epigenetics
Glucocorticoids
Brain circuitry
Fear Extinction
Arousal
Sleep
Emotion Regulation
Psychoneuroendocrinology
Psychoneuroimmunology
Memory

Published Papers (5 papers)

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Research

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13 pages, 291 KiB

Open AccessArticle

Genetic and Environmental Predictors of Adolescent PTSD Symptom Trajectories Following a Natural Disaster

by Christina M. Sheerin, Laurel V. Kovalchick, Cassie Overstreet, Lance M. Rappaport, Vernell Williamson, Vladimir Vladimirov, Kenneth J. Ruggiero and Ananda B. Amstadter

Brain Sci. 2019, 9(6), 146; https://doi.org/10.3390/brainsci9060146 - 20 Jun 2019

Cited by 8 | Viewed by 4696

Abstract

Genes, environmental factors, and their interplay affect posttrauma symptoms. Although environmental predictors of the longitudinal course of posttraumatic stress disorder (PTSD) symptoms are documented, there remains a need to incorporate genetic risk into these models, especially in youth who are underrepresented in genetic studies. In an epidemiologic sample tornado-exposed adolescents (n = 707, 51% female, M_age = 14.54 years), trajectories of PTSD symptoms were examined at baseline and at 4-months and 12-months following baseline. This study aimed to determine if rare genetic variation in genes previously found in the sample to be related to PTSD diagnosis at baseline (MPHOSPH9, LGALS13, SLC2A2), environmental factors (disaster severity, social support), or their interplay were associated with symptom trajectories. A series of mixed effects models were conducted. Symptoms decreased over the three time points. Elevated tornado severity was associated with elevated baseline symptoms. Elevated recreational support was associated with lower baseline symptoms and attenuated improvement over time. Greater LGLAS13 variants attenuated symptom improvement over time. An interaction between MPHOSPH9 variants and tornado severity was associated with elevated baseline symptoms, but not change over time. Findings suggest the importance of rare genetic variation and environmental factors on the longitudinal course of PTSD symptoms following natural disaster trauma exposure. Full article

(This article belongs to the Special Issue Neurobiological Trajectories of Psychological Trauma—Implications for Posttraumatic Stress Disorder (PTSD))

13 pages, 1069 KiB

Open AccessArticle

Victims of War: Dehydroepiandrosterone Concentrations in Hair and Their Associations with Trauma Sequelae in Palestinian Adolescents Living in the West Bank

by Lena Schindler, Mohammed Shaheen, Rotem Saar-Ashkenazy, Kifah Bani Odeh, Sophia-Helen Sass, Alon Friedman and Clemens Kirschbaum

Brain Sci. 2019, 9(2), 20; https://doi.org/10.3390/brainsci9020020 - 23 Jan 2019

Cited by 10 | Viewed by 4481

Abstract

Due to its anti-glucocorticoid properties, the steroid hormone dehydroepiandrosterone (DHEA) might play a role for coping with traumatic stress and posttraumatic stress disorder (PTSD). The majority of studies report elevated DHEA secretion and decreased cortisol/DHEA ratio associated with traumatic stress, however, contrasting results have also been published. One reason for this heterogeneity might be that in past studies, DHEA has been measured in plasma or saliva samples reflecting acute hormone levels. In comparison, the current study assessed the hair levels of DHEA and cortisol as long-term markers along with self-reported data on psychopathology and coping in 92 female adolescents aged 11–16 from the West Bank affected by the Israeli–Palestinian conflict. Results showed that trauma-exposed individuals had significantly higher DHEA levels (p = 0.013) and lower cortisol/DHEA ratios (p = 0.036) than participants from the non-trauma group. Furthermore, DHEA and cortisol/DHEA ratio emerged as associated with trauma load and timing, but not with coping. By applying the novel method of DHEA analysis from hair samples, this study adds to the growing literature on the interplay of DHEA, cortisol, traumatic stress and coping, and provides valuable starting points for further research. Full article

(This article belongs to the Special Issue Neurobiological Trajectories of Psychological Trauma—Implications for Posttraumatic Stress Disorder (PTSD))

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Review

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28 pages, 1887 KiB

Open AccessReview

Oxidative Dysregulation in Early Life Stress and Posttraumatic Stress Disorder: A Comprehensive Review

by Evangelos Karanikas, Nikolaos P. Daskalakis and Agorastos Agorastos

Brain Sci. 2021, 11(6), 723; https://doi.org/10.3390/brainsci11060723 - 29 May 2021

Cited by 31 | Viewed by 5856

Abstract

Traumatic stress may chronically affect master homeostatic systems at the crossroads of peripheral and central susceptibility pathways and lead to the biological embedment of trauma-related allostatic trajectories through neurobiological alterations even decades later. Lately, there has been an exponential knowledge growth concerning the effect of traumatic stress on oxidative components and redox-state homeostasis. This extensive review encompasses a detailed description of the oxidative cascade components along with their physiological and pathophysiological functions and a systematic presentation of both preclinical and clinical, genetic and epigenetic human findings on trauma-related oxidative stress (OXS), followed by a substantial synthesis of the involved oxidative cascades into specific and functional, trauma-related pathways. The bulk of the evidence suggests an imbalance of pro-/anti-oxidative mechanisms under conditions of traumatic stress, respectively leading to a systemic oxidative dysregulation accompanied by toxic oxidation byproducts. Yet, there is substantial heterogeneity in findings probably relative to confounding, trauma-related parameters, as well as to the equivocal directionality of not only the involved oxidative mechanisms but other homeostatic ones. Accordingly, we also discuss the trauma-related OXS findings within the broader spectrum of systemic interactions with other major influencing systems, such as inflammation, the hypothalamic-pituitary-adrenal axis, and the circadian system. We intend to demonstrate the inherent complexity of all the systems involved, but also put forth associated caveats in the implementation and interpretation of OXS findings in trauma-related research and promote their comprehension within a broader context. Full article

(This article belongs to the Special Issue Neurobiological Trajectories of Psychological Trauma—Implications for Posttraumatic Stress Disorder (PTSD))

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15 pages, 373 KiB

Open AccessReview

Neurobiological Trajectories Involving Social Isolation in PTSD: A Systematic Review

by Ilias I Vlachos, Charalambos Papageorgiou and Maria Margariti

Brain Sci. 2020, 10(3), 173; https://doi.org/10.3390/brainsci10030173 - 18 Mar 2020

Cited by 18 | Viewed by 7655

Abstract

Social isolation (SI) stress has been recognized as a major risk factor of morbidity in humans and animals, exerting damaging effects at the physical and mental health levels. Posttraumatic stress disorder (PTSD), on the other hand, occurs as a result of experiencing serious, life-threatening, traumatic events and involves involuntary re-experiencing trauma (intrusion), avoidance symptoms, and distortions of cognition and emotional arousal. The literature shows that PTSD is affected by genetic predisposition and triggers a large neurocircuitry involving the amygdala, insula, hippocampus, anterior cingulate- and prefrontal-cortex, and affects the function of the neuroendocrine and immune systems. Social isolation seems to influence the predisposition, onset and outcome of PTSD in humans, whereas it constitutes a valid model of the disorder in animals. According to the PRISMA (preferred reporting items for systematic reviews and meta-analyses) protocol, we systematically reviewed all original studies involving the neurobiological trajectories between SI and PTSD published till July 2019 (database: PubMed/Medline). Out of 274 studies, 10 met the inclusion criteria. 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. Full article

(This article belongs to the Special Issue Neurobiological Trajectories of Psychological Trauma—Implications for Posttraumatic Stress Disorder (PTSD))

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16 pages, 648 KiB

Open AccessFeature PaperReview

Early Life Stress and Pediatric Posttraumatic Stress Disorder

by Panagiota Pervanidou, Gerasimos Makris, George Chrousos and Agorastos Agorastos

Brain Sci. 2020, 10(3), 169; https://doi.org/10.3390/brainsci10030169 - 14 Mar 2020

Cited by 24 | Viewed by 7427

Abstract

Traumatic stress exposure during critical periods of development may have essential and long-lasting effects on the physical and mental health of individuals. Two thirds of youth are exposed to potentially traumatic experiences by the age of 17, and approximately 5% of adolescents meet lifetime criteria for posttraumatic stress disorder (PTSD). The role of the stress system is the maintenance of homeostasis in the presence of real/perceived and acute/chronic stressors. Early-life stress (ELS) has an impact on neuronal brain networks involved in stress reactions, and could exert a programming effect on glucocorticoid signaling. Studies on pediatric PTSD reveal diverse neuroendocrine responses to adverse events and related long-term neuroendocrine and epigenetic alterations. Neuroendocrine, neuroimaging, and genetic studies in children with PTSD and ELS experiences are crucial in understanding risk and resilience factors, and also the natural history of PTSD. Full article

(This article belongs to the Special Issue Neurobiological Trajectories of Psychological Trauma—Implications for Posttraumatic Stress Disorder (PTSD))

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