scholarly journals Endogenous salivary α-amylase does not interact with skin conductance response during fear extinction in posttraumatic stress disorder

2018 ◽  
Vol 262 ◽  
pp. 316-322 ◽  
Author(s):  
Daniel V. Zuj ◽  
Matthew A. Palmer ◽  
Gin S. Malhi ◽  
Richard A. Bryant ◽  
Kim L. Felmingham
2019 ◽  
Vol 3 ◽  
pp. 247054701984444 ◽  
Author(s):  
Rebecca Hinrichs ◽  
Sanne J. H. van Rooij ◽  
Vasiliki Michopoulos ◽  
Katharina Schultebraucks ◽  
Sterling Winters ◽  
...  

Background Exposure to a traumatic event leads to posttraumatic stress disorder in 10% to 20% of exposed individuals. Predictors of risk are needed to target early interventions to those who are most vulnerable. The objective of the study was to test whether a noninvasive mobile device that measures a physiological biomarker of autonomic nervous system activation could predict future posttraumatic stress disorder symptoms. Methods Skin conductance response was collected during a trauma interview in the emergency department within hours of exposure to trauma in 95 individuals. Trajectories of posttraumatic stress disorder symptoms over 12-month posttrauma were identified using latent growth mixture modeling. Results Skin conductance response was significantly correlated with the probability of being in the chronic posttraumatic stress disorder trajectory following trauma exposure in the emergency department (r = 0.489, p < 0.000001). Lasso regression with elastic net was performed with demographic and clinical measures obtained in the emergency department, demonstrating that skin conductance response was the most significant predictor of the chronic posttraumatic stress disorder trajectory (p < 0.00001). Conclusions This study is the first prospective study of posttraumatic stress disorder showing skin conductance response in the immediate aftermath of trauma predicts subsequent development of chronic posttraumatic stress disorder. This finding points to an easily obtained, and neurobiologically informative, biomarker in emergency departments that can be disseminated to predict the development of posttraumatic stress disorder.


2021 ◽  
Vol 53 (8S) ◽  
pp. 303-304
Author(s):  
Kevin M. Crombie ◽  
Anneliis Sartin-Tarm ◽  
Kyrie Sellnow ◽  
Rachel Ahrenholtz ◽  
Sierra Lee ◽  
...  

2011 ◽  
Vol 69 (6) ◽  
pp. 556-563 ◽  
Author(s):  
Seth D. Norrholm ◽  
Tanja Jovanovic ◽  
Ilana W. Olin ◽  
Lauren A. Sands ◽  
India Karapanou ◽  
...  

2017 ◽  
Vol 121 (5) ◽  
pp. 792-814 ◽  
Author(s):  
Auretta S. Kummar

Research in the neuroscience of mindfulness has grown rapidly in recent years. This includes empirical investigations into structural and functional changes in several brain regions—particularly, the hippocampus, the prefrontal cortex, and the amygdala—in association with the practice of mindfulness. Of interest to the current paper is that such brain regions are also implicated in empirical research focusing on fear extinction. While fear extinction has, therefore, been suggested as one of the possible mechanisms to underlie the positive effects of mindfulness, the conceptual links and research implications have lacked specific focus and detailed discussion in the literature. The purpose of this paper is, therefore, two-fold. First, this paper briefly reviews the extant literature on the neuropsychological mechanisms underlying mindfulness—particularly that, which has been found to be similarly implied in fear extinction—and hence, suggests future research directions based on its current state in the literature. Second, this paper explores the implications of this for fear-based psychopathologies, specifically for posttraumatic stress disorder (PTSD). Discussion from this paper suggests the idea of fear extinction as an underlying mechanism of mindfulness to be one that is still preliminary, yet promising; in turn, elucidating the need for further methodologically rigorous study to specifically determine fear extinction as a result of mindfulness, as well as to incorporate neuroimaging techniques in supporting the existing literature that have found preliminary support of mindfulness for PTSD.


2018 ◽  
Vol 83 (9) ◽  
pp. S21 ◽  
Author(s):  
Christine Rabinak ◽  
Craig Peters ◽  
Farrah Elrahal ◽  
Mohammed Milad ◽  
Sheila Rauch ◽  
...  

2018 ◽  
Vol 19 (12) ◽  
pp. 3848 ◽  
Author(s):  
Sheng-Chiang Wang ◽  
Chen-Cheng Lin ◽  
Chun-Chuan Chen ◽  
Nian-Sheng Tzeng ◽  
Yia-Ping Liu

Posttraumatic stress disorder (PTSD) is a trauma-induced mental disorder characterized by fear extinction abnormalities, which involve biological dysfunctions among fear circuit areas in the brain. Oxytocin (OXT) is a neuropeptide that regulates sexual reproduction and social interaction and has recently earned specific attention due to its role in adjusting neurobiological and behavioral correlates of PTSD; however, the mechanism by which this is achieved remains unclear. The present study aimed to examine whether the effects of OXT on traumatic stress-induced abnormalities of fear extinction (specifically induced by single prolonged stress (SPS), an animal model of PTSD) are associated with pro-inflammatory cytokines. Seven days after SPS, rats received intranasal OXT 40 min before a cue-dependent Pavlovian fear conditioning-extinction test in which rats’ freezing degree was used to reflect the outcome of fear extinction. We also measured mRNA expression of IL-1β, IFN-γ, and TNF-α in the medial prefrontal cortex (mPFC), hippocampus, and amygdala at the end of the study, together with plasma oxytocin, corticosterone, IL-1β, IFN-γ, and TNF-α, to reflect the central and peripheral changes of stress-related hormones and cytokines after SPS. Our results suggested that intranasal OXT effectively amends the SPS-impaired behavior of fear extinction retrieval. Moreover, it neurochemically reverses the SPS increase in pro-inflammatory cytokines; thus, IL-1β and IFN-γ can be further blocked by the OXT antagonist atosiban (ASB) in the hippocampus. Peripheral profiles revealed a similar response pattern to SPS of OXT and corticosterone (CORT), and the SPS-induced increase in plasma levels of IL-1β and TNF-α could be reduced by OXT. The present study suggests potential therapeutic effects of OXT in both behavioral and neuroinflammatory profiles of PTSD.


2016 ◽  
Vol 136 ◽  
pp. 116-126 ◽  
Author(s):  
Manon Wicking ◽  
Frauke Steiger ◽  
Frauke Nees ◽  
Slawomira J. Diener ◽  
Oliver Grimm ◽  
...  

2019 ◽  
Vol 3 ◽  
pp. 247054701985016 ◽  
Author(s):  
Lynn D. Selemon ◽  
Keith A. Young ◽  
Dianne A. Cruz ◽  
Douglas E. Williamson

Symptoms of posttraumatic stress disorder include hyperarousal, avoidance of trauma-related stimuli, re-experiencing of trauma, and mood changes. This review focuses on the frontal cortical areas that form crucial links in circuitry pertinent to posttraumatic stress disorder symptomatology: (1) the conditioned fear extinction circuit, (2) the salience circuit, and (3) the mood circuit. These frontal areas include the ventromedial prefrontal cortex (conditioned fear extinction), the dorsal anterior cingulate and insular cortices (salience), and the lateral orbitofrontal and subgenual cingulate cortices (mood). Frontal lobe structural abnormalities in posttraumatic stress disorder, including volumetric reductions in the cingulate cortices, impact all three circuits. Functional analyses of frontal cortices in posttraumatic stress disorder show abnormal activation in all three according to task demand and emotional valence. Network analyses reveal altered amygdalo-frontal connectivity and failure to suppress the default mode network during cognitive engagement. Spine shape alterations also have been detected in the medial orbitofrontal cortex in posttraumatic stress disorder postmortem brains, suggesting reduced synaptic plasticity. Importantly, frontal lobe abnormalities in posttraumatic stress disorder extend beyond emotion-related circuits to include the lateral prefrontal cortices that mediate executive functions. In conclusion, widespread frontal lobe dysfunction in posttraumatic stress disorder provides a neurobiologic basis for the core symptomatology of the disorder, as well as for executive function impairment.


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