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Post-Traumatic Stress Disorders: HELP
Articles from USA
Based on 10,977 articles published since 2010
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These are the 10977 published articles about Stress Disorders, Post-Traumatic that originated from USA during 2010-2020.
 
+ Citations + Abstracts
Pages: 1 · 2 · 3 · 4 · 5 · 6 · 7 · 8 · 9 · 10 · 11 · 12 · 13 · 14 · 15 · 16 · 17 · 18 · 19 · 20
226 Review Stress reactivity after traumatic brain injury: implications for comorbid post-traumatic stress disorder. 2019

Hoffman, Ann N / Taylor, Anna N. ·Department of Psychology, University of California Los Angeles. · Department of Neurosurgery, Brain Injury Research Center. · Department of Psychology, Staglin Center for Brain and Behavioral Health. · Department of Neurobiology, David Geffen School of Medicine at UCLA, Los Angeles, California, USA. ·Behav Pharmacol · Pubmed #30640181.

ABSTRACT: Most people have or will experience traumatic stress at some time over the lifespan, but only a subset of traumatized individuals develop post-traumatic stress disorder (PTSD). Clinical research supports high rates of traumatic brain injury (TBI)-PTSD comorbidity and demonstrates TBI as a significant predictor of the development of PTSD. Biological factors impacted following brain injury that may contribute to increased PTSD risk are unknown. Heightened stress reactivity and dysregulated hypothalamic-pituitary-adrenal (HPA) axis function are common to both TBI and PTSD, and affect amygdalar structure and function, which is implicated in PTSD. In this review, we summarize a growing body of literature that shows HPA axis dysregulation, as well as enhanced fear and amygdalar function after TBI. We present the hypothesis that altered stress reactivity as a result of brain injury impacts the amygdala and defense systems to be vulnerable to increased fear and PTSD development from traumatic stress. Identifying biological mechanisms that underlie this vulnerability, such as dysregulated HPA axis function, may lead to better targeted treatments and preventive measures to support psychological health after TBI.

227 Review The predator odor avoidance model of post-traumatic stress disorder in rats. 2019

Albrechet-Souza, Lucas / Gilpin, Nicholas W. ·Department of Physiology, School of Medicine, Louisiana State University Health Sciences Center, New Orleans, Louisiana, USA. ·Behav Pharmacol · Pubmed #30640179.

ABSTRACT: Individuals with post-traumatic stress disorder avoid trauma-related stimuli and exhibit blunted hypothalamic-pituitary-adrenal axis response at the time of trauma. Our laboratory uses predator odor (i.e. bobcat urine) stress to divide adult Wistar rats into groups that exhibit high (avoiders) or low (nonavoiders) avoidance of a predator odor-paired context, modeling the fact that not all humans exposed to traumatic events develop psychiatric conditions. Male avoiders exhibit lower body weight gain after stress, as well as extinction-resistant avoidance that persists after a second stress exposure. These animals also show attenuated hypothalamic-pituitary-adrenal axis response to predator odor that predicts subsequent avoidance of the odor-paired context. Avoiders exhibit unique brain activation profiles relative to nonavoiders and controls (as measured by Fos immunoreactivity), and higher corticotropin-releasing factor levels in multiple brain regions. Furthermore, avoider rats exhibit escalated and compulsive-like alcohol self-administration after traumatic stress. Here, we review the predator odor avoidance model of post-traumatic stress disorder and its utility for tracking behavior and measuring biological outcomes predicted by avoidance. The major strengths of this model are (i) etiological validity with exposure to a single intense stressor, (ii) established approach distinguishing individual differences in stress reactivity, and (iii) robust behavioral and biological phenotypes during and after trauma.

228 Review Serotonin 2A receptors are a stress response system: implications for post-traumatic stress disorder. 2019

Murnane, Kevin Sean. ·Department of Pharmaceutical Sciences, Mercer University College of Pharmacy, Mercer University Health Sciences Center, Atlanta, Georgia, USA. ·Behav Pharmacol · Pubmed #30632995.

ABSTRACT: Serotonin, one of the first neurotransmitters to be identified, is an evolutionarily old molecule that is highly conserved across the animal kingdom, and widely used throughout the brain. Despite this, ascribing a specific set of functions to brain serotonin and its receptors has been difficult and controversial. The 2A subtype of serotonin receptors (5-HT2A receptor) is the major excitatory serotonin receptor in the brain and has been linked to the effects of drugs that produce profound sensory and cognitive changes. Numerous studies have shown that this receptor is upregulated by a broad variety of stressors, and have related 5-HT2A receptor function to associative learning. This review proposes that stress, particularly stress related to danger and existential threats, increases the expression and function of 5-HT2A receptors. It is argued that this is a neurobiological adaptation to promote learning and avoidance of danger in the future. Upregulation of 5-HT2A receptors during stressful events forms associations that tune the brain to environmental cues that signal danger. It is speculated that life-threatening situations may activate this system and contribute to the symptoms associated with post-traumatic stress disorder (PTSD). 3,4-Methylenedioxymethamphetamine, which activates 5-HT2A receptors, has been successful in the treatment of PTSD and has recently achieved status as a breakthrough therapy. An argument is presented that 3,4-methylenedioxymethamphetamine may paradoxically act through these same 5-HT2A receptors to ameliorate the symptoms of PTSD. The central thematic contention is that a key role of serotonin may be to function as a stress detection and response system.

229 Review A systematic review of the psychosocial impact of emotional numbing in US combat veterans. 2019

Schuman, Donna L / Bricout, John / Peterson, H Leona / Barnhart, Sheila. ·College of Social Work, University of Kentucky, Lexington, Kentucky. · School of Social Work, University of Minnesota, Minneapolis, Minnesota. · School of Social Work, University of Texas at Austin, Austin, Texas. ·J Clin Psychol · Pubmed #30597543.

ABSTRACT: CONTEXT: Previous studies have linked posttraumatic emotional numbing symptoms in US combat veterans with an adverse impact in multiple important life domains. OBJECTIVES: We updated and evaluated the evidence examining the psychosocial impact of combat-related emotional numbing, including ethnoracial and gender differences. METHOD: We reviewed 1,209 articles published betwen January 2012 and 2018 and selected 24 studies for inclusion. We assessed the overall study quality as fair using a national quality assessment tool. RESULTS: Studies found emotional numbing to wield adverse effects in the areas of symptom nonimprovement, mental health difficulties, increased service utilization, poor relationship functioning, reduced quality of life, substance use disorders, suicidality, and aggression/violence. We also found evidence of ethnoracial and gender differences in veterans' posttraumatic stress disorder-related emotional numbing symptoms. CONCLUSION: Clinicians should incorporate findings on emotional numbing into assessment, treatment planning, and monitoring, to improve treatment retention and psychosocial outcomes. Implications for ethnoracial and gender differences require further exploration.

230 Review Neuroimmune signaling in alcohol use disorder. 2019

Erickson, Emma K / Grantham, Emily K / Warden, Anna S / Harris, R A. ·Waggoner Center for Alcohol and Addiction Research, The University of Texas at Austin, Austin, TX 78712-01095, USA. Electronic address: emmaerickson@utexas.edu. · Waggoner Center for Alcohol and Addiction Research, The University of Texas at Austin, Austin, TX 78712-01095, USA. ·Pharmacol Biochem Behav · Pubmed #30590091.

ABSTRACT: Alcohol use disorder (AUD) is a widespread disease with limited treatment options. Targeting the neuroimmune system is a new avenue for developing or repurposing effective pharmacotherapies. Alcohol modulates innate immune signaling in different cell types in the brain by altering gene expression and the molecular pathways that regulate neuroinflammation. Chronic alcohol abuse may cause an imbalance in neuroimmune function, resulting in prolonged perturbations in brain function. Likewise, manipulating the neuroimmune system may change alcohol-related behaviors. Psychiatric disorders that are comorbid with AUD, such as post-traumatic stress disorder, major depressive disorder, and other substance use disorders, may also have underlying neuroimmune mechanisms; current evidence suggests that convergent immune pathways may be involved in AUD and in these comorbid disorders. In this review, we provide an overview of major neuroimmune cell-types and pathways involved in mediating alcohol behaviors, discuss potential mechanisms of alcohol-induced neuroimmune activation, and present recent clinical evidence for candidate immune-related drugs to treat AUD.

231 Review Social isolation as a promising animal model of PTSD comorbid suicide: neurosteroids and cannabinoids as possible treatment options. 2019

Locci, Andrea / Pinna, Graziano. ·The Psychiatric Institute, Department of Psychiatry, College of Medicine, University of Illinois at Chicago, 1601 W. Taylor St., Chicago, IL 60612, USA. · The Psychiatric Institute, Department of Psychiatry, College of Medicine, University of Illinois at Chicago, 1601 W. Taylor St., Chicago, IL 60612, USA. Electronic address: gpinna@uic.edu. ·Prog Neuropsychopharmacol Biol Psychiatry · Pubmed #30586627.

ABSTRACT: Post-traumatic stress disorder (PTSD) is a psychiatric condition characterized by drastic alterations in mood, emotions, social abilities and cognition. Notably, one aspect of PTSD, particularly in veterans, is its comorbidity with suicide. Elevated aggressiveness predicts high-risk to suicide in humans and despite the difficulty in reproducing a complex human suicidal behavior in rodents, aggressive behavior is a well reproducible behavioral trait of suicide. PTSD animal models are based on a peculiar phenotype, including exaggerated fear memory and impaired fear extinction associated with neurochemical dysregulations in the brain circuitry regulating emotion. The endocannabinoid and the neurosteroid systems regulate emotions and stress responses, and recent evidence shows these two systems are interrelated and critically compromised in neuropsychiatric disorders. For instance, levels of the neurosteroid, allopregnanolone, as well as those of the endocannabinoids, anandamide and its congener, palmitoylethanolamide are decreased in PTSD. Similarly, the endocannabinoid system and neurosteroid biosynthesis are altered in suicidal individuals. Selective serotonin reuptake inhibitors (SSRIs), the only FDA-approved treatments for PTSD, fail to help half of the treatment-seeking patients. This highlights the need for developing biomarker-based efficient therapies. One promising alternative to SSRIs points to stimulation of allopregnanolone biosynthesis as a treatment and a valid end-point to predict treatment response in PTSD patients. This review highlights running findings on the role of the endocannabinoid and neurosteroid systems in PTSD and suicidal behavior both in a preclinical and clinical perspective. A specific focus is given to predictive PTSD/suicide animal models. Ultimately, we discuss the idea that disruption of neurosteroid and endocannabinoid biosynthesis may offer a novel promising biomarker axis to develop new treatments for PTSD and, perhaps, suicidal behavior.

232 Review Psychiatric Care of the Post-September 11 Combat Veteran: A Review. 2019

Johnson, Justin M / Capehart, Bruce P. ·Durham VA Medical Center (J.M.J., B.P.C.), Duke University School of Medicine, Durham, NC 27705. Electronic address: Justin.m.johnson@duke.edu. · Durham VA Medical Center (J.M.J., B.P.C.), Duke University School of Medicine, Durham, NC 27705. ·Psychosomatics · Pubmed #30580807.

ABSTRACT: BACKGROUND: Post-September 11, 2001 combat veterans represent a growing cohort of patients with unique mental health needs, particularly around post-traumatic stress disorder (PTSD) and traumatic brain injury (TBI). The United States (US) remains engaged in conflicts around the globe, so this patient cohort will continue to grow in number. With around 40% of American combat veterans from Iraq and Afghanistan seeking mental health care outside of the Veterans Affairs, understanding the psychiatric needs of the post-September 11 combat veteran is an important goal for all psychiatrists. These patients are relevant to consultation-liaison (C-L) psychiatrists because of their high comorbidity of conditions such as TBI, obstructive sleep apnea, insomnia, and chronic pain. This article reviews the current literature on mental health care for the post-September 11 combat veteran, emphasizing PTSD and TBI treatment, and culling evidence-based recommendations from randomized controlled trials of combat veterans. Emphasis is also placed on the Veterans Affairs/Department of Defense Clinical Practice Guidelines. The authors also bring unique clinical expertise of having served on active duty as psychiatrists for the US Army, including in a combat zone, and both currently work in a Veterans Affairs Iraq and Afghanistan combat veteran mental health clinic. OBJECTIVE: This review outlines useful treatment approaches for PTSD and TBI and briefly covers the comorbid conditions of major depression, chronic pain, and substance use disorders. This review will prepare C-L psychiatrists to care for this challenging patient cohort.

233 Review Top-down and bottom-up control of stress-coping. 2019

de Kloet, Edo R / de Kloet, Sybren F / de Kloet, Carien S / de Kloet, Annette D. ·Division of Endocrinology, Department of Medicine, Leiden University Medical Center, Leiden, The Netherlands. · Department of Integrative Neurophysiology, Center for Neurogenomics and Cognitive Research, VU-University of Amsterdam, Amsterdam, The Netherlands. · Foundation Center '45, Arq Psychotrauma Expert Group, Leiden, The Netherlands. · Department of Physiology and Functional Genomics, University of Florida, Gainesville, Florida. ·J Neuroendocrinol · Pubmed #30578574.

ABSTRACT: In this 30th anniversary issue review, we focus on the glucocorticoid modulation of limbic-prefrontocortical circuitry during stress-coping. This action of the stress hormone is mediated by mineralocorticoid receptors (MRs) and glucocorticoid receptors (GRs) that are co-expressed abundantly in these higher brain regions. Via both receptor types, the glucocorticoids demonstrate, in various contexts, rapid nongenomic and slower genomic actions that coordinate consecutive stages of information processing. MR-mediated action optimises stress-coping, whereas, in a complementary fashion, the memory storage of the selected coping strategy is promoted via GR. We highlight the involvement of adipose tissue in the allocation of energy resources to central regulation of stress reactions, point to still poorly understood neuronal ensembles in the prefrontal cortex that underlie cognitive flexibility critical for effective coping, and evaluate the role of cortisol as a pleiotropic regulator in vulnerability to, and treatment of, trauma-related psychiatric disorders.

234 Review Cannabis and mental illness: a review. 2019

Lowe, Darby J E / Sasiadek, Julia D / Coles, Alexandria S / George, Tony P. ·Addictions Division, Centre for Addiction and Mental Health (CAMH), University of Toronto, 100 Stokes Street, BGB 3288, Toronto, ON, M6J 1H4, USA. · Institute of Medical Sciences, University of Toronto, Toronto, USA. · Addictions Division, Centre for Addiction and Mental Health (CAMH), University of Toronto, 100 Stokes Street, BGB 3288, Toronto, ON, M6J 1H4, USA. tony.george@camh.ca. · Division and Brain and Therapeutics, Department of Psychiatry, University of Toronto, Toronto, USA. tony.george@camh.ca. ·Eur Arch Psychiatry Clin Neurosci · Pubmed #30564886.

ABSTRACT: With the increasing push to legalize cannabis in Western nations, there is a need to gage the potential impact of this policy change on vulnerable populations, such as those with mental illness, including schizophrenia, mood, and anxiety disorders. This is particularly important as there are strong motives in these individuals to seek short-term reward (e.g., "getting high"). Nonetheless, data to support the beneficial effects of cannabis use in psychiatric populations are limited, and potential harms in patients with psychotic and mood disorders have been increasingly documented. This article reviews the effects of cannabis in people with mental illness. Then, we provide a reconciliation of the addiction vulnerability and allostatic hypotheses to explain co-morbidity addiction in mentally ill cannabis users, as well as to further aid in developing a rational framework for the assessment and treatment of problematic cannabis use in these patients.

235 Review Theranostic pharmacology in PTSD: Neurobiology and timing. 2019

Koek, Ralph J / Luong, Tinh N. ·Department of Psychiatry and Biobehavioral Sciences, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA; Sepulveda Ambulatory Care Center, VA Greater Los Angeles Healthcare System, North Hills, CA, USA. Electronic address: rkoek@ucla.edu. · Department of Psychiatry and Biobehavioral Sciences, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA; Olive View Medical Center, Sylmar, CA, USA. ·Prog Neuropsychopharmacol Biol Psychiatry · Pubmed #30529001.

ABSTRACT: Recent reviews and treatment guidelines regard trauma-focused cognitive-behavior therapies as the treatments of choice for chronic post-traumatic stress disorder (PTSD). However, many patients do not engage in this treatment when it is available, drop out before completion, or do not respond. Medications remain widely used, alone and in conjunction with psychotherapy, although the limitations of traditional monoamine-based pharmacotherapy are increasingly recognized. This article will review recent developments in psychopharmacology for PTSD, with a focus on current clinical data that apply putative neurobiologic mechanisms to medication use-i.e., a theranostic approach. A theranostic approach however, also requires consideration of timing, pre, peri or post trauma in conjunction with underlying dynamic processes affecting synaptic plasticity, the HPA axis, hippocampal activation, PFC-amygdala circuitry and fear memory.

236 Review DNA methylation correlates of PTSD: Recent findings and technical challenges. 2019

Morrison, Filomene G / Miller, Mark W / Logue, Mark W / Assef, Michele / Wolf, Erika J. ·National Center for PTSD, VA Boston Healthcare System, USA; Department of Psychiatry, Boston University School of Medicine, USA. Electronic address: filomene@bu.edu. · National Center for PTSD, VA Boston Healthcare System, USA; Department of Psychiatry, Boston University School of Medicine, USA. · National Center for PTSD, VA Boston Healthcare System, USA; Department of Psychiatry, Boston University School of Medicine, USA; Biomedical Genetics, Boston University School of Medicine, USA; Department of Biostatistics, Boston University School of Public Health, USA. · Boston University, College of Health & Rehabilitation Sciences: Sargent College, USA. ·Prog Neuropsychopharmacol Biol Psychiatry · Pubmed #30503303.

ABSTRACT: There is increasing evidence that epigenetic factors play a critical role in posttraumatic stress disorder (PTSD), by mediating the impact of environmental exposures to trauma on the regulation of gene expression. DNA methylation is one epigenetic process that has been highly studied in PTSD. This review will begin by providing an overview of DNA methylation (DNAm) methods, and will then highlight two major biological systems that have been identified in the epigenetic regulation in PTSD: (a) the immune system and (b) the stress response system. In addition to candidate gene approaches, we will review novel strategies to study epigenome-wide PTSD-related effects, including epigenome-wide algorithms that distill information from many loci into a single summary score (e.g., measures of "epigenetic age" which have been associated with PTSD). This review will also cover recent epigenome wide association studies (EWAS) of PTSD, and biological pathway models used to identify gene sets enriched in PTSD. Finally, we address technical and methodological advances and challenges to the field, and highlight exciting directions for future research.

237 Review Genomic updates in understanding PTSD. 2019

Sharma, Sumeet / Ressler, Kerry J. ·Neuroscience Program, Department of Psychiatry and Behavioral Sciences, Emory University, Atlanta, GA, United States; McLean Hospital, Division of Depression and Anxiety, Belmont, MA, United States. · McLean Hospital, Division of Depression and Anxiety, Belmont, MA, United States; Harvard Medical School, Boston, MA, United States; Neuroscience Program, Department of Psychiatry and Behavioral Sciences, Emory University, Atlanta, GA, United States. Electronic address: kressler@mclean.harvard.edu. ·Prog Neuropsychopharmacol Biol Psychiatry · Pubmed #30452941.

ABSTRACT: Twin studies as well as more recent genetics-based heritability analyses demonstrate that up to 40 to 50% of the variance in predicting PTSD following trauma is heritable. However, most of the specific gene pathways and mechanism that mediate risk vs. resilience for PTSD following trauma exposure have yet to be elucidated. This review will examine the latest results from large scale Genome-wide association studies as well as other approaches aimed at understanding mechanisms of development of and recovery from PTSD.

238 Review Insulin growth factor 2 (IGF2) as an emergent target in psychiatric and neurological disorders. Review. 2019

Pardo, M / Cheng, Y / Sitbon, Y H / Lowell, J A / Grieco, S F / Worthen, R J / Desse, S / Barreda-Diaz, A. ·University of Miami Miller School of Medicine, Department of Neurology, Miami, FL, USA. Electronic address: mpardodoc@med.miami.edu. · University of California Los Angeles, Neurology Department, Los Angeles, CA, USA. Electronic address: YCheng@mednet.ucla.edu. · University of Miami Miller School of Medicine, Department of Molecular and Cellular Pharmacology, Miami, FL, USA. Electronic address: yxs454@miami.edu. · University of Miami, Department of Psychiatry & Behavioral Sciences, Miami, FL, USA. Electronic address: jefflowell12@med.miami.edu. · University of California, Department of Anatomy and Neurobiology, Irvine, CA, USA. Electronic address: sgrieco@uci.edu. · University of Miami, Department of Psychiatry & Behavioral Sciences, Miami, FL, USA. Electronic address: rjw102@miami.edu. · University of Miami, Department of Psychiatry & Behavioral Sciences, Miami, FL, USA. Electronic address: sachidesse@msn.com. · University of Miami Miller School of Medicine, Department of Neurology, Miami, FL, USA. Electronic address: axb1748@miami.edu. ·Neurosci Res · Pubmed #30389571.

ABSTRACT: Insulin-like growth factor 2 (IGF2) is abundantly expressed in the central nervous system (CNS). Recent evidence highlights the role of IGF2 in the brain, sustained by data showing its alterations as a common feature across a variety of psychiatric and neurological disorders. Previous studies emphasize the potential role of IGF2 in psychiatric and neurological conditions as well as in memory impairments, targeting IGF2 as a pro-cognitive agent. New research on animal models supports that upcoming investigations should explore IGF2's strong promising role as a memory enhancer. The lack of effective treatments for cognitive disturbances as a result of psychiatric diseases lead to further explore IGF2 as a promising target for the development of new pharmacology for the treatment of memory dysfunctions. In this review, we aim at gathering all recent relevant studies and findings on the role of IGF2 in the development of psychiatric diseases that occur with cognitive problems.

239 Review Old Friends, immunoregulation, and stress resilience. 2019

Langgartner, Dominik / Lowry, Christopher A / Reber, Stefan O. ·Laboratory for Molecular Psychosomatics, Department of Psychosomatic Medicine and Psychotherapy, University Ulm, Albert-Einstein-Allee 23, 89081, Ulm, Germany. · Department of Integrative Physiology and Center for Neuroscience, University of Colorado Boulder, Boulder, CO, 80309, USA. · Department of Physical Medicine & Rehabilitation and Center for Neuroscience, University of Colorado Anschutz Medical Campus, Aurora, CO, 80045, USA. · Veterans Health Administration, Rocky Mountain Mental Illness Research Education and Clinical Center (MIRECC), Denver Veterans Affairs Medical Center (VAMC), Denver, CO, 80220, USA. · Military and Veteran Microbiome Consortium for Research and Education (MVM-CoRE), Denver, CO, 80220, USA. · Laboratory for Molecular Psychosomatics, Department of Psychosomatic Medicine and Psychotherapy, University Ulm, Albert-Einstein-Allee 23, 89081, Ulm, Germany. stefan.reber@uniklinik-ulm.de. ·Pflugers Arch · Pubmed #30386921.

ABSTRACT: There is a considerable body of evidence indicating that chronic adverse experience, especially chronic psychosocial stress/trauma, represents a major risk factor for the development of many somatic and affective disorders, including inflammatory bowel disease (IBD) and posttraumatic stress disorder (PTSD). However, the mechanisms underlying the development of chronic stress-associated disorders are still in large part unknown, and current treatment and prevention strategies lack efficacy and reliability. A greater understanding of mechanisms involved in the development and persistence of chronic stress-induced disorders may lead to novel approaches to prevention and treatment of these disorders. In this review, we provide evidence indicating that increases in immune (re-)activity and inflammation, potentially promoted by a reduced exposure to immunoregulatory microorganisms ("Old Friends") in today's modern society, may be causal factors in mediating the vulnerability to development and persistence of stress-related pathologies. Moreover, we discuss strategies to increase immunoregulatory processes and attenuate inflammation, as for instance contact with immunoregulatory Old Friends, which appears to be a promising strategy to promote stress resilience and to prevent/treat chronic stress-related disorders.

240 Review Impaired inhibition as an intermediate phenotype for PTSD risk and treatment response. 2019

van Rooij, Sanne J H / Jovanovic, Tanja. ·Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, 49 Jesse Hill Jr Dr, Atlanta, GA, USA. · Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, 49 Jesse Hill Jr Dr, Atlanta, GA, USA; Department of Psychiatry and Behavioral Neuroscience, Wayne State University, USA. Electronic address: tjovano@emory.edu. ·Prog Neuropsychopharmacol Biol Psychiatry · Pubmed #30381236.

ABSTRACT: Inhibition of fear involves learning and then appropriately responding to safety signals, and has been shown to be impaired in PTSD patients. Response inhibition refers to cognitive control and likely uses the same prefrontal cortex circuits as fear inhibition, and has also been implicated in PTSD. Impaired inhibition can serve as an intermediate phenotype for PTSD and can be measured with neuroimaging and psychophysiological tools. We first review the neurobiological mechanisms of fear and response inhibition. Next, we summarize the functional magnetic resonance imaging (fMRI) and psychophysiological studies using fear and response inhibition paradigms in PTSD patients. Finally, we evaluate the theranostic role of impaired inhibition in PTSD risk and treatment response.

241 Review Rodent models of impaired fear extinction. 2019

Singewald, Nicolas / Holmes, Andrew. ·Department of Pharmacology and Toxicology, Institute of Pharmacy, Center for Molecular Biosciences Innsbruck, University of Innsbruck, Innsbruck, Austria. nicolas.singewald@uibk.ac.at. · Laboratory of Behavioral and Genomic Neuroscience, National Institute on Alcohol Abuse and Alcoholism, NIH, Bethesda, MD, USA. ·Psychopharmacology (Berl) · Pubmed #30377749.

ABSTRACT: The measurement of Pavlovian forms of fear extinction offers a relatively simple behavioral preparation that is nonetheless tractable, from a translational perspective, as an approach to study mechanisms of exposure therapy and biological underpinnings of anxiety and trauma-related disorders such as post-traumatic stress disorder (PTSD). Deficient fear extinction is considered a robust clinical endophenotype for these disorders and, as such, has particular significance in the current "age of RDoC (research domain criteria)." Various rodent models of impaired extinction have thus been generated with the objective of approximating this clinical, relapse prone aberrant extinction learning. These models have helped to reveal neurobiological correlates of extinction circuitry failure, gene variants, and other mechanisms underlying deficient fear extinction. In addition, they are increasingly serving as tools to investigate ways to therapeutically overcome poor extinction to support long-term retention of extinction memory and thus protection against various forms of fear relapse; modeled in the laboratory by measuring spontaneous recovery, reinstatement and renewal of fear. In the current article, we review models of impaired extinction built around (1) experimentally induced brain region and neural circuit disruptions (2) spontaneously-arising and laboratory-induced genetic modifications, or (3) exposure to environmental insults, including stress, drugs of abuse, and unhealthy diet. Collectively, these models have been instrumental in advancing in our understanding of extinction failure and underlying susceptibilities at the neural, genetic, molecular, and neurochemical levels; generating renewed interest in developing novel, targeted and effective therapeutic treatments for anxiety and trauma-related disorders.

242 Review The hypothalamic-pituitary-adrenal axis in PTSD: Pathophysiology and treatment interventions. 2019

Dunlop, Boadie W / Wong, Andrea. ·Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, GA, USA. Electronic address: bdunlop@emory.edu. · Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, GA, USA. Electronic address: andrea.wong@emory.edu. ·Prog Neuropsychopharmacol Biol Psychiatry · Pubmed #30342071.

ABSTRACT: Questions of how altered functioning of the hypothalamic pituitary adrenal (HPA) axis contribute to the development and maintenance of posttraumatic stress disorder (PTSD) have been the focus of extensive animal and human research. As a rule, results have been inconsistent across studies, likely due to a variety of confounding variables that have received inadequate attention. Important confounding factors include the effects of early life stress, biological sex, and the glucocorticoid used for interventions. In this manuscript we review: 1) the literature on identified abnormalities of HPA axis function in PTSD, both in terms of basal functioning and as part of challenge paradigms; 2) the role of HPA axis function pre- and immediately post-trauma as a risk factor for PTSD development; 3) the impact of HPA axis genes' allelic variants and epigenetic modifications on PTSD risk; 4) the contributions of HPA axis components to fear learning and extinction; and 5) therapeutic manipulations of the HPA axis to both prevent and treat PTSD, including the role of glucocorticoids as part of medication enhanced psychotherapy.

243 Review SUDEP and Grief: Overview and Current Issues. 2019

Flannery, Raymond B / Lomke, Evander. ·Harvard Medical School, Boston, MA, USA. raymond_flannery@hms.harvard.edu. · University of Massachusetts Medical School, Worcester, MA, USA. raymond_flannery@hms.harvard.edu. · Department of Psychiatry, Cambridge Health Alliance, 1493 Cambridge Street, Cambridge, MA, 02139, USA. raymond_flannery@hms.harvard.edu. · American Mental Health Foundation, 128 2nd Pl, Brooklyn, NY, 11231, USA. · AHRC of New York City, 83 Maiden Ln, New York, NY, 10038, USA. ·Psychiatr Q · Pubmed #30338420.

ABSTRACT: The medical community and the general public are aware of sudden deaths in apparently healthy infants (SIDS) and in cases of cardiac arrest (SCD). However, there is a third, less-well known, form of sudden death that occurs in persons with epilepsy (SUDEP). This paper provides a detailed overview what is known about SUDEP, including the current important, unresolved issues being considered in the field (research, education, informed consent). This paper also includes an overview of the grieving process common to all three conditions. Again, the current issues being considered in the field of grieving are presented (major depression, posttraumatic stress disorder). It is written for physicians, including psychiatrists, and for the health community beyond neurologists and serves as a provider resource for persons with epilepsy, their families, and for the general public. This information about SUDEP and grief becomes also additionally important as national health care moves toward an interdisciplinary primary care model of service delivery.

244 Review A meta-analytic review of cognitive processing therapy for adults with posttraumatic stress disorder. 2019

Asmundson, Gordon J G / Thorisdottir, Audur S / Roden-Foreman, Jacob W / Baird, Scarlett O / Witcraft, Sara M / Stein, Aliza T / Smits, Jasper A J / Powers, Mark B. ·a Department of Psychology , University of Regina , Regina , Saskatchewan , Canada. · b Division of Trauma, Critical Care, Acute Care Surgery , Baylor University Medical Center at Dallas , Dallas , TX , USA. · c Department of Psychology , University of Texas at Austin , Austin , TX , USA. · d Department of Psychology , The University of Mississippi , University , MS , USA. ·Cogn Behav Ther · Pubmed #30332919.

ABSTRACT: Numerous studies have demonstrated the efficacy of cognitive processing therapy (CPT) for treating posttraumatic stress disorder (PTSD). Two prior meta-analyses of studies are available but used approaches that limit conclusions that can be drawn regarding the impact of CPT on PTSD outcomes. The current meta-analysis reviewed outcomes of trials that tested the efficacy of CPT for PTSD in adults and evaluated potential moderators of outcomes. All published trials comparing CPT against an inactive control condition (i.e. psychological placebo or wait-list) or other active treatment for PTSD in adults were included, resulting in 11 studies with a total of 1130 participants. CPT outperformed inactive control conditions on PTSD outcome measures at posttreatment (mean Hedges' g = 1.24) and follow-up (mean Hedges' g = 0.90). The average CPT-treated participant fared better than 89% of those in inactive control conditions at posttreatment and 82% at follow-up. Results also showed that CPT outperformed inactive control conditions on non-PTSD outcome measures at posttreatment and follow-up and that CPT outperformed other active treatments at posttreatment but not at follow-up. Effect sizes of CPT on PTSD symptoms were not significantly moderated by participant age, number of treatment sessions, total sample size, length of follow-up, or group versus individual treatment; but, older studies had larger effect sizes and percent female sex moderated the effect of CPT on non-PTSD outcomes. These meta-analytic findings indicate that CPT is an effective PTSD treatment with lasting benefits across a range of outcomes.

245 Review GxE effects of FKBP5 and traumatic life events on PTSD: A meta-analysis. 2019

Hawn, Sage E / Sheerin, Christina M / Lind, Mackenzie J / Hicks, Terrell A / Marraccini, Marisa E / Bountress, Kaitlin / Bacanu, Silviu-Alin / Nugent, Nicole R / Amstadter, Ananda B. ·Department of Psychiatry, Virginia Institute of Psychiatric and Behavioral Genetics, Virginia Commonwealth University, Richmond, VA, USA; Department of Psychology, Virginia Commonwealth University, Richmond, VA, USA. Electronic address: hawnse@vcu.edu. · Department of Psychiatry, Virginia Institute of Psychiatric and Behavioral Genetics, Virginia Commonwealth University, Richmond, VA, USA. · Department of Psychiatry, Virginia Institute of Psychiatric and Behavioral Genetics, Virginia Commonwealth University, Richmond, VA, USA; Department of Psychology, Virginia Commonwealth University, Richmond, VA, USA. · School of Education, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA. · Bradley-Hasbro Children's Research Center, Rhode Island Hospital, Providence, RI, USA; Departments of Psychiatry and Human Behavior and Pediatrics, Alpert Medical School of Brown University, Providence, RI, USA. · Department of Psychiatry, Virginia Institute of Psychiatric and Behavioral Genetics, Virginia Commonwealth University, Richmond, VA, USA; Department of Human and Molecular Genetics, Virginia Commonwealth University, Richmond, VA, USA. ·J Affect Disord · Pubmed #30273884.

ABSTRACT: BACKGROUND: Twin studies have demonstrated that both genetic and environmental factors influence risk for posttraumatic stress disorder (PTSD), and there is some evidence supporting the interplay of genes and environment (GxE). Many GxE studies within the PTSD literature have focused on genes implicated in the stress response system, such as FK506 binding protein 51 (FKBP5). Given inconsistencies across GxE literature as a whole, a meta-analysis to synthesize results is warranted. METHODS: Studies were identified through PubMed and PsycINFO. A meta-analysis was conducted using a random effects model in the MAc package in R. Heterogeneity of the effect size distribution was examined with Cochran's Q statistic. A Simes procedure was used to test the gene-level GxE effect for FKBP5 interacting with trauma. RESULTS: A significant gene-level GxE gene effect was demonstrated for FKBP5 when pooled across all four examined variants (rs1360780, rs3800373, rs9296158, rs9470080) when interacting with trauma exposure on PTSD. Significant large GxE effect sizes were also found for each independent variant. There was no evidence for heterogeneity of variance. LIMITATIONS: Limitations include reduced power for detecting variability across moderators, potential bias due to failure of meta-analyzed studies to account for two-way covariate x gene and covariate x environment influences, and a high false discovery rate that is characteristic of GxE analyses. CONCLUSIONS: This is the first study to quantify an overall gene-level effect of FKBP5 in a GxE analysis of PTSD, evidence which may be used to address current issues in the FKBP5 GxE literature (e.g., disparate variants, low sample sizes and power), as well as inform follow-up functional research.

246 Review Posttraumatic stress disorder following the 2008 Wenchuan earthquake: A 10-year systematic review among highly exposed populations in China. 2019

Liang, Yiming / Cheng, Jin / Ruzek, Josef I / Liu, Zhengkui. ·CAS Key Laboratory of Mental Health, Institute of Psychology, Beijing, China; Department of Psychology, University of Chinese Academy of Sciences, Beijing, China. · Department of Psychiatry and Behavioral Sciences, Stanford University, Palo Alto, CA, USA. · CAS Key Laboratory of Mental Health, Institute of Psychology, Beijing, China; Department of Psychology, University of Chinese Academy of Sciences, Beijing, China. Electronic address: liuzk@psych.ac.cn. ·J Affect Disord · Pubmed #30261448.

ABSTRACT: BACKGROUND: The 2008 Wenchuan earthquake was unprecedented in Chinese history both in terms of the magnitude of the quake itself and the scale of human suffering. Following the disaster, researchers reported on a wide range of mental health outcomes, especially posttraumatic stress disorder (PTSD). In this review, we assess the cumulative body of research evidence about PTSD across the first 10 years following the earthquake. METHODS: We searched the literature in the PubMed, Web of Science, and China National Knowledge Infrastructure (CNKI) databases (from May 2008 to February 2018) using Wenchuan earthquake and PTSD as keywords. RESULTS: We selected 58 relevant studies. Published findings from the selected period suggested a substantial burden of PTSD on highly exposed survivors. Studies have found that symptoms of PTSD have been associated with a range of risk factors, including sociodemographic factors, trauma exposure characteristics, post-disaster cognitive and emotional states, and social support. Studies have explored the factor structure of PTSD in the affected Chinese population, and researchers have developed a Chinese self-report measure of PTSD symptoms. Several treatments for PTSD have been evaluated, including some indigenous intervention methods. LIMITATIONS: Only a relatively small number of the studies used longitudinal assessments, and the consistency and effectiveness of measurement tools for PTSD require further exploration. More rigorous investigations of the effectiveness of interventions for the prevention and treatment of PTSD are needed. CONCLUSION: The 10-year body of literature is important for the future deployment of disaster relief and an increased understanding of PTSD in China.

247 Review Common neurocircuitry mediating drug and fear relapse in preclinical models. 2019

Goode, Travis D / Maren, Stephen. ·Department of Psychological and Brain Sciences and Institute for Neuroscience, Texas A&M University, 301 Old Main Dr., College Station, TX, 77843-3474, USA. · Department of Psychological and Brain Sciences and Institute for Neuroscience, Texas A&M University, 301 Old Main Dr., College Station, TX, 77843-3474, USA. maren@tamu.edu. ·Psychopharmacology (Berl) · Pubmed #30255379.

ABSTRACT: BACKGROUND: Comorbidity of anxiety disorders, stressor- and trauma-related disorders, and substance use disorders is extremely common. Moreover, therapies that reduce pathological fear and anxiety on the one hand, and drug-seeking on the other, often prove short-lived and are susceptible to relapse. Considerable advances have been made in the study of the neurobiology of both aversive and appetitive extinction, and this work reveals shared neural circuits that contribute to both the suppression and relapse of conditioned responses associated with trauma or drug use. OBJECTIVES: The goal of this review is to identify common neural circuits and mechanisms underlying relapse across domains of addiction biology and aversive learning in preclinical animal models. We focus primarily on neural circuits engaged during the expression of relapse. KEY FINDINGS: After extinction, brain circuits involving the medial prefrontal cortex and hippocampus come to regulate the expression of conditioned responses by the amygdala, bed nucleus of the stria terminalis, and nucleus accumbens. During relapse, hippocampal projections to the prefrontal cortex inhibit the retrieval of extinction memories resulting in a loss of inhibitory control over fear- and drug-associated conditional responding. CONCLUSIONS: The overlapping brain systems for both fear and drug memories may explain the co-occurrence of fear and drug-seeking behaviors.

248 Review N-Methyl D-aspartate receptor subunit signaling in fear extinction. 2019

Radulovic, Jelena / Ren, Lynn Y / Gao, Can. ·Department of Psychiatry and Behavioral Sciences, Feinberg School of Medicine, Northwestern University, Chicago, IL, 60611, USA. j-radulovic@northwestern.edu. · Department of Psychiatry and Behavioral Sciences, Feinberg School of Medicine, Northwestern University, Chicago, IL, 60611, USA. · Jiangsu Key Laboratory of Anesthesiology, Xuzhou Medical University, 209 Tongshan Road, Xuzhou, 221004, Jiangsu, China. ·Psychopharmacology (Berl) · Pubmed #30238131.

ABSTRACT: N-Methyl D-aspartate receptors (NMDAR) are central mediators of glutamate actions underlying learning and memory processes including those required for extinction of fear and fear-related behaviors. Consistent with this view, in animal models, antagonists of NMDAR typically impair fear extinction, whereas partial agonists have facilitating effects. Promoting NMDAR function has thus been recognized as a promising strategy towards reduction of fear symptoms in patients suffering from anxiety disorders and post-traumatic disorder (PTSD). Nevertheless, application of these drugs in clinical trials has proved of limited utility. Here we summarize recent advances in our knowledge of NMDAR pharmacology relevant for fear extinction, focusing on molecular, cellular, and circuit aspects of NMDAR function as they relate to fear extinction at the level of behavior and cognition. We also discuss how these advances from animal models might help to understand and overcome the limitations of existing approaches in human anxiety disorders and how novel, more specific, and personalized approaches might help advance future therapeutic strategies.

249 Review Blast-induced "PTSD": Evidence from an animal model. 2019

Perez-Garcia, Georgina / Gama Sosa, Miguel A / De Gasperi, Rita / Tschiffely, Anna E / McCarron, Richard M / Hof, Patrick R / Gandy, Sam / Ahlers, Stephen T / Elder, Gregory A. ·Research and Development Service, James J. Peters Department of Veterans Affairs Medical Center, 130 West Kingsbridge Road, Bronx, NY 10468, USA; Department of Neurology, Icahn School of Medicine at Mount Sinai, One Gustave Levy Place, New York, NY 10029, USA. · General Medical Research Service, James J. Peters Department of Veterans Affairs Medical Center, Bronx, NY 10468, USA; Department of Psychiatry, Icahn School of Medicine at Mount Sinai, One Gustave Levy Place, New York, NY 10029, USA. · Research and Development Service, James J. Peters Department of Veterans Affairs Medical Center, 130 West Kingsbridge Road, Bronx, NY 10468, USA; Department of Psychiatry, Icahn School of Medicine at Mount Sinai, One Gustave Levy Place, New York, NY 10029, USA. · Department of Neurotrauma, Naval Medical Research Center, 503 Robert Grant Avenue, Silver Spring, MD 20910, USA. · Department of Neurotrauma, Naval Medical Research Center, 503 Robert Grant Avenue, Silver Spring, MD 20910, USA; Department of Surgery, Uniformed Services University of the Health Sciences, Bethesda, MD 20914, USA. · Fishberg Department of Neuroscience, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA; Department of Geriatrics and Palliative Care, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA; Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA; Mount Sinai Alzheimer's Disease Research Center and the Ronald M. Loeb Center for Alzheimer's Disease, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA. · Research and Development Service, James J. Peters Department of Veterans Affairs Medical Center, 130 West Kingsbridge Road, Bronx, NY 10468, USA; Department of Neurology, Icahn School of Medicine at Mount Sinai, One Gustave Levy Place, New York, NY 10029, USA; Department of Psychiatry, Icahn School of Medicine at Mount Sinai, One Gustave Levy Place, New York, NY 10029, USA; Mount Sinai Alzheimer's Disease Research Center and the Ronald M. Loeb Center for Alzheimer's Disease, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA; NFL Neurological Care Center, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA. · Department of Neurology, Icahn School of Medicine at Mount Sinai, One Gustave Levy Place, New York, NY 10029, USA; Department of Psychiatry, Icahn School of Medicine at Mount Sinai, One Gustave Levy Place, New York, NY 10029, USA; Mount Sinai Alzheimer's Disease Research Center and the Ronald M. Loeb Center for Alzheimer's Disease, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA; Neurology Service, James J. Peters Department of Veterans Affairs Medical Center, 130 West Kingsbridge Road, Bronx, NY 10468, USA. Electronic address: gregory.elder@va.gov. ·Neuropharmacology · Pubmed #30227150.

ABSTRACT: A striking observation among veterans returning from the recent conflicts in Iraq and Afghanistan has been the co-occurrence of blast-related mild traumatic brain injury (mTBI) and post-traumatic stress disorder (PTSD). PTSD and mTBI might coexist due to additive effects of independent psychological and physical traumas experienced in a war zone. Alternatively blast injury might induce PTSD-related traits or damage brain structures that mediate responses to psychological stressors, increasing the likelihood that PTSD will develop following a subsequent psychological stressor. Rats exposed to repetitive low-level blasts consisting of three 74.5 kPa exposures delivered once daily for three consecutive days develop a variety of anxiety and PTSD-related behavioral traits that are present for at least 9 months after blast exposure. A single predator scent challenge delivered 8 months after the last blast exposure induces additional anxiety-related changes that are still present 45 days later. Because the blast injuries occur under general anesthesia, it appears that blast exposure in the absence of a psychological stressor can induce chronic PTSD-related traits. The reaction to a predator scent challenge delivered many months after blast exposure suggests that blast exposure in addition sensitizes the brain to react abnormally to subsequent psychological stressors. The development of PTSD-related behavioral traits in the absence of a psychological stressor suggests the existence of blast-induced "PTSD". Findings that PTSD-related behavioral traits can be reversed by BCI-838, a group II metabotropic glutamate receptor antagonist offers insight into pathogenesis and possible treatment options for blast-related brain injury. This article is part of the Special Issue entitled "Novel Treatments for Traumatic Brain Injury".

250 Review Role of social cognition in post-traumatic stress disorder: A review and meta-analysis. 2019

Stevens, Jennifer S / Jovanovic, Tanja. ·Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, Georgia. ·Genes Brain Behav · Pubmed #30221467.

ABSTRACT: Social functioning is a key component of recovery after a potentially traumatic experience, and the buffering role of the social support in trauma resilience and recovery has been very well documented. Factors contributing to resilience and recovery are notable because although most people will experience a traumatic event during their lifetimes, only 6% to 10% are diagnosed with post-traumatic stress disorder (PTSD). The relationship between an individual and their social environment is determined both by the quality of the social environment itself, and by the individual's perception and understanding of information conveyed by the other people around them. However, little research has considered the contribution of these internal social cognitive processes to PTSD risk or resilience. The current review draws on the existing literature on social cognitive functioning in trauma exposure and PTSD, identifying key questions and themes for future research. We utilized a meta-analytic approach to assess the evidence for alterations in social cognition in PTSD, finding a consistent large deficit in social cognitive performance in PTSD groups relative to trauma-exposed and healthy controls. We then reviewed the literature on the interaction of genes and the social environment, supporting the hypothesis that social cognitive deficits are a preexisting risk factor for PTSD. Finally, we reviewed relevant neuroimaging findings, which suggest that alterations in social cognition affect the perception of threat cues in PTSD. Overall, research on social cognition and PTSD is still emerging, but existing findings suggest this is an important and understudied area for the understanding of PTSD.

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