scholarly journals Hexobarbital Sleep Test for Predicting the Susceptibility or Resistance to Experimental Posttraumatic Stress Disorder

2020 ◽  
Vol 21 (16) ◽  
pp. 5900
Author(s):  
Maria Komelkova ◽  
Eugenia Manukhina ◽  
H. Fred Downey ◽  
Alexey Sarapultsev ◽  
Olga Cherkasova ◽  
...  

Hexobarbital sleep test (HST) was performed in male Wistar rats (hexobarbital 60 mg/kg, i.p.) 30 days prior to stress exposure. Based on the duration of hexobarbital-induced sleep, rats were divided into two groups, animals with high intensity (fast metabolizers (FM), sleep duration <15 min) or low intensity of hexobarbital metabolism (slow metabolizers (SM), sleep duration ≥15 min). The SM and FM groups were then divided into two subgroups: unstressed and stressed groups. The stressed subgroups were exposed to predator scent stress for 10 days followed by 15 days of rest. SM and FM rats from the unstressed group exhibited different behavioral and endocrinological patterns. SM showed greater anxiety and higher corticosterone levels. In stressed animals, anxiety-like posttraumatic stress disorder (PTSD) behavior was aggravated only in SM. Corticosterone levels in the stressed FM, PTSD-resistant rats, were lower than in unstressed SM. Thus, HST was able to predict the susceptibility or resistance to experimental PTSD, which was consistent with the changes in glucocorticoid metabolism.

2018 ◽  
Vol 2 ◽  
pp. 247054701880713 ◽  
Author(s):  
Carissa N. Weis ◽  
Emily L. Belleau ◽  
Walker S. Pedersen ◽  
Tara A. Miskovich ◽  
Christine L. Larson

Posttraumatic stress disorder is a heterogeneous disorder with disturbances in hyperarousal or avoidance behaviors and intrusive or reexperiencing thoughts. The uncinate fasciculus and cingulum bundle are white matter pathways implicated in stress and trauma pathophysiology, yet their structural integrity related to posttraumatic stress disorder symptom domains is yet to be understood. Forty-four trauma-exposed young adults underwent structural and diffusion-weighted magnetic resonance imaging. Stress and trauma exposure indices and severity of posttraumatic stress disorder symptoms were collected and used to predict current integrity of the uncinate fasciculus and cingulum bundle. Severity of reexperiencing posttraumatic stress disorder symptoms was significantly related to increased fractional anisotropy ( r = .469 p < .001) and decreased mean diffusivity ( r =  −.373, p = .013) of the right posterior cingulum bundle. No other findings emerged with respect to stress exposure or of hyperarousal ( p’s > 0.05) or avoidance ( p’s > 0.2) posttraumatic stress disorder symptoms. The posterior cingulum connects medial temporal lobe structures with visual areas in the occipital lobe and has been implicated in visual memory and self-referential thought. Increased structural connectivity along this pathway may therefore explain the emergence of reexperiencing posttraumatic stress disorder symptoms. This along with the lack of results with respect to stress exposure suggests that structural aberrations in white matter pathways are more strongly linked with the actual experience of stress-related psychological symptoms than just exposure to stress.


CNS Spectrums ◽  
1998 ◽  
Vol 3 (S2) ◽  
pp. 22-29 ◽  
Author(s):  
Rachel Yehuda

In 1980, the diagnosis of posttraumatic stress disorder (PTSD) was established to recognize that exposure to events such as rape, physical assault, torture, or combat can leave long-lasting psychological scars in persons who undergo these experiences. The intention of the diagnosis was to acknowledge that exposure to a traumatic event was a sufficient explanation for the occurrence of longterm psychological problems. Prior to this formulation, stressful events were thought to precipitate symptoms that would resolve over time. The symptoms manifested by persons following adverse events were characterized as transient adjustment reactions. Longerterm symptoms were considered to be a reflection of underlying neurosis, rather than stress exposure per se.The diagnosis of PTSD provided a paradigm for acknowledging that exposure to devastating trauma can produce symptoms that can be quite severe and chronic in nature. Although many of the symptoms of PTSD were similar to those that occur in other anxiety or mood disorders, the hallmark of PTSD appeared to be a preoccupation with the traumatic event and a resultant set of behavioral changes that occurred because of attempts to avoid reminders of the event.


SLEEP ◽  
2019 ◽  
Vol 43 (4) ◽  
Author(s):  
Mackenzie J Lind ◽  
Leslie A Brick ◽  
Philip R Gehrman ◽  
Laramie E Duncan ◽  
Bizu Gelaye ◽  
...  

Abstract Study Objectives Sleep problems are common, serving as both a predictor and symptom of posttraumatic stress disorder (PTSD), with these bidirectional relationships well established in the literature. While both sleep phenotypes and PTSD are moderately heritable, there has been a paucity of investigation into potential genetic overlap between sleep and PTSD. Here, we estimate genetic correlations between multiple sleep phenotypes (including insomnia symptoms, sleep duration, daytime sleepiness, and chronotype) and PTSD, using results from the largest genome-wide association study (GWAS) to date of PTSD, as well as publicly available GWAS results for sleep phenotypes within UK Biobank data (23 variations, encompassing four main phenotypes). Methods Genetic correlations were estimated utilizing linkage disequilibrium score regression (LDSC), an approach that uses GWAS summary statistics to compute genetic correlations across traits, and Mendelian randomization (MR) analyses were conducted to follow up on significant correlations. Results Significant, moderate genetic correlations were found between insomnia symptoms (rg range 0.36–0.49), oversleeping (rg range 0.32–0.44), undersleeping (rg range 0.48–0.49), and PTSD. In contrast, there were mixed results for continuous sleep duration and daytime sleepiness phenotypes, and chronotype was not correlated with PTSD. MR analyses did not provide evidence for casual effects of sleep phenotypes on PTSD. Conclusion Sleep phenotypes, particularly insomnia symptoms and extremes of sleep duration, have shared genetic etiology with PTSD, but causal relationships were not identified. This highlights the importance of further investigation into the overlapping influences on these phenotypes as sample sizes increase and new methods to investigate directionality and causality become available.


2015 ◽  
Vol 26 (1) ◽  
pp. 35-50 ◽  
Author(s):  
Sara C. Schroeder ◽  
Ronald M. Ruff ◽  
Lutz Jäncke

The aim of this study was to examine the effect of posttraumatic stress disorder (PTSD) on (a) neuropsychological test performance and (b) self-reported emotional complaints within individuals suffering from postconcussional disorder (PCD) after a mild traumatic brain injury (MTBI). A two-group comparative research design was employed. Two MTBI samples with and without PTSD were assessed with a neuropsychological test battery and the Ruff Neurobehavioral Inventory (RNBI). On the neurocognitive test performances no significant between group differences were found, but the MTBI group with PTSD endorsed a significantly greater number of emotional complaints, especially in the RNBI subscales of anxiety and depression. The patients with PTSD also endorsed a significantly greater number of premorbid sequelae in the RNBI emotional composite scale as well as the RNBI premorbid subscales of pain, anxiety and abuse. In sum, PTSD has a negative impact on emotional but not cognitive functioning within individuals suffering from PCD after a mild TBI.


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