Trauma exposure and post‐traumatic stress disorder in people with intellectual disabilities: A Delphi expert rating

2018 ◽  
Vol 32 (3) ◽  
pp. 558-567 ◽  
Author(s):  
Doris Rittmannsberger ◽  
Andreas Kocman ◽  
Germain Weber ◽  
Brigitte Lueger‐Schuster
2018 ◽  
Vol 24 (2) ◽  
pp. 212-232 ◽  
Author(s):  
Megan Cowles ◽  
Cathy Randle-Phillips ◽  
Andrew Medley

Trauma exposure and post-traumatic stress disorder are more prevalent in people with intellectual disabilities (PWID) than in the general population, yet the evidence base for trauma interventions in this population is sparse. Compassion-focused therapy (CFT) may be particularly well-suited to PWID for a number of reasons, including its adaptability to different developmental levels. PWID are more likely to have issues with self-relating (e.g. shame and self-criticism) and attachment than the general population, two issues that are compounded by trauma and which CFT explicitly seeks to address. Furthermore, compassion-focused approaches emphasize cultivating a sense of safeness while empowering people to make behavioural changes; this is particularly pertinent to PWID who have been traumatized and may feel unsafe and disempowered. An overview of CFT and its application to trauma are given, as well as some case studies using CFT with PWID.


2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Kunlin Zhang ◽  
Gen Li ◽  
Li Wang ◽  
Chengqi Cao ◽  
Ruojiao Fang ◽  
...  

AbstractPost-traumatic stress disorder (PTSD) is a psychiatric syndrome that occurs after trauma exposure. Neurotransmitters such as dopamine and oxytocin have been reported to be involved in neuropathology of PTSD. Previous studies indicated that the dopamine–oxytocin interaction may contribute to behavioral disorders. Thus, exploring the epistasis (gene–gene interaction) between oxytocinergic and dopaminergic systems might be useful to reveal the genetic basis of PTSD. In this study, we analyzed two functional single nucleotide polymorphisms (SNPs), rs2268498 for oxytocinergic gene OXTR and rs1801028 for dopaminergic gene DRD2 based on putative oxytocin receptor–dopamine receptor D2 (OTR–DR2) heterocomplex in a Chinese cohort exposed to the 2008 Wenchuan earthquake (156 PTSD cases and 978 controls). Statistical analyses did not find any single variant or gene–environment interaction (SNP × earthquake-related trauma exposure) associated with provisional PTSD diagnosis or symptoms. An OXTR–DRD2 interaction (rs2268498 × rs1801028) was identified to confer risk of provisional PTSD diagnosis (OR = 9.18, 95% CI = 3.07–27.46 and P = 7.37e-05) and further subset analysis indicated that rs2268498 genotypes controlled the association directions of rs1801028 and rs1801028 genotypes also controlled the association directions of rs2268498. Rs2268498 × rs1801028 is also associated with PTSD symptoms (P = 0.043). Our study uncovered a genetic and putative function-based contribution of dopaminergic–oxytocinergic system interaction to PTSD.


2021 ◽  
Vol 12 ◽  
Author(s):  
Kaitlin E. Bountress ◽  
Vladimir Vladimirov ◽  
Gowon McMichael ◽  
Z. Nathan Taylor ◽  
Gary Hardiman ◽  
...  

Background: The purpose of this study was to identify gene expression differences associated with post-traumatic stress disorder (PTSD) and trauma exposure (TE) in a three-group study design comprised of those with and without trauma exposure and PTSD.Methods: We conducted gene expression and gene network analyses in a sample (n = 45) composed of female subjects of European Ancestry (EA) with PTSD, TE without PTSD, and controls.Results: We identified 283 genes differentially expressed between PTSD-TE groups. In an independent sample of Veterans (n = 78) a small minority of these genes were also differentially expressed. We identified 7 gene network modules significantly associated with PTSD and TE (Bonferroni corrected p ≤ 0.05), which at a false discovery rate (FDR) of q ≤ 0.2, were significantly enriched for biological pathways involved in focal adhesion, neuroactive ligand receptor interaction, and immune related processes among others.Conclusions: This study uses gene network analyses to identify significant gene modules associated with PTSD, TE, and controls. On an individual gene level, we identified a large number of differentially expressed genes between PTSD-TE groups, a minority of which were also differentially expressed in the independent sample. We also demonstrate a lack of network module preservation between PTSD and TE, suggesting that the molecular signature of PTSD and trauma are likely independent of each other. Our results provide a basis for the identification of likely disease pathways and biomarkers involved in the etiology of PTSD.


Author(s):  
Arieh Y. Shalev ◽  
Anna C. Barbano ◽  
Wei Qi ◽  
Charles R. Marmar

Post-traumatic stress disorder (PTSD) follows an exposure to traumatic events and as such its onset and early development are better charted then those of most other mental disorders. It is not surprising, therefore, that major efforts have been dedicated to preventing its occurrence before, during and after trauma exposure. This chapter discusses the rationale, desirability, feasibility and outcome of interventions designed to prevent PTSD. Several efficient interventions have been documented. Barriers to their early implementations, however, greatly reduce their effectiveness and require urgent attention.


2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Christopher J. Davis ◽  
William M. Vanderheyden

Abstract Sleep disturbances are commonly found in trauma-exposed populations. Additionally, trauma exposure results in fear-associated memory impairments. Given the interactions of sleep with learning and memory, we hypothesized that increasing sleep duration following trauma exposure would restore overall function and improve trauma-induced fear-associated memory dysfunction. Here, we utilized single prolonged stress, a validated rodent model of post-traumatic stress disorder, in combination with optogenetic activation of hypothalamic melanin-concentrating hormone containing cells to increase sleep duration. The goal of this work was to ascertain if post-trauma sleep increases are sufficient to improve fear-associated memory function. In our laboratory, optogenetic stimulation after trauma exposure was sufficient to increase REM sleep duration during both the Light and Dark Phase, whereas NREM sleep duration was only increased during the Dark Phase of the circadian day. Interestingly though, animals that received optogenetic stimulation showed significantly improved fear-associated memory processing compared to non-stimulated controls. These results suggest that sleep therapeutics immediately following trauma exposure may be beneficial and that post-trauma sleep needs to be further examined in the context of the development of post-traumatic stress disorder.


Sign in / Sign up

Export Citation Format

Share Document