Causal attribution, coping strategies, and combat‐related post‐traumatic stress disorder

1989 ◽  
Vol 3 (4) ◽  
pp. 269-284 ◽  
Author(s):  
Mario Mikulincer ◽  
Zahava Solomon

The present study assesses the intervening role of ways of coping in mediating the effects of causal attribution for negative events on combat‐related post‐traumatic stress disorder (PTSD). The sample consisted of Israeli soldiers who suffered a combat stress reaction episode during the 1982 Lebanon War and were followed 2 and 3 years after their participation in combat. The results showed that an attribution of negative events to stable and uncontrollable causes was associated with both a more frequent use of emotion‐focused coping and a less frequent use of problem‐focused coping. It was also found that emotion‐focused coping and problem‐focused coping were more direct antecedents of combat‐related PTSD than causal attribution. Finally, it was found that the association between causal attribution and combat‐related PTSD was mediated by variations in emotion‐focused coping. The discussion attempts to integrate theoretical notions derived from attributional models and Lazarus and Folkman's stress‐coping model.

Author(s):  
Susanne Fischer ◽  
Tabea Schumacher ◽  
Christine Knaevelsrud ◽  
Ulrike Ehlert ◽  
Sarah Schumacher

Abstract Background Less than half of all individuals with post-traumatic stress disorder (PTSD) remit spontaneously and a large proportion of those seeking treatment do not respond sufficiently. This suggests that there may be subgroups of individuals who are in need of augmentative or alternative treatments. One of the most frequent pathophysiological findings in PTSD is alterations in the hypothalamic–pituitary–adrenal (HPA) axis, including enhanced negative feedback sensitivity and attenuated peripheral cortisol. Given the role of the HPA axis in cognition, this pattern may contribute to PTSD symptoms and interfere with key processes of standard first-line treatments, such as trauma-focused cognitive behavioural therapy (TF-CBT). Methods This review provides a comprehensive summary of the current state of research regarding the role of HPA axis functioning in PTSD symptoms and treatment. Results Overall, there is preliminary evidence that hypocortisolaemia contributes to symptom manifestation in PTSD; that it predicts non-responses to TF-CBT; and that it is subject to change in parallel with positive treatment trajectories. Moreover, there is evidence that genetic and epigenetic alterations within the genes NR3C1 and FKBP5 are associated with this hypocortisolaemic pattern and that some of these alterations change as symptoms improve over the course of treatment. Conclusions Future research priorities include investigations into the role of the HPA axis in day-to-day symptom variation, the time scale in which biological changes in response to treatment occur, and the effects of sex. Furthermore, before conceiving augmentative or alternative treatments that target the described mechanisms, multilevel studies are warranted.


2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Z. Ardi ◽  
A. Richter-Levin ◽  
L. Xu ◽  
X. Cao ◽  
H. Volkmer ◽  
...  

Abstract Pre-pubertal stress increases post-traumatic stress disorder (PTSD) susceptibility. We have previously demonstrated that enriched environment (EE) intervention immediately after pre-pubertal stress protects from the effects of trauma in adulthood. Here, we examined whether exposure to EE would also be beneficial if applied after exposure to trauma in adulthood. We have recently shown that exposure to juvenile stress and under-water trauma (UWT) is associated with increased expression of GABAA receptor subunit α1 in the ventral hippocampus. However, differentiating between affected and unaffected individuals, this increased expression was confined to stress-exposed, behaviorally unaffected individuals, suggesting upregulation of α1 expression as a potential mechanism of resilience. We now examined whether EE-induced resilience renders increased expression of α1 in the ventral hippocampus redundant when facing a trauma later in life. Adult rats were exposed to UWT, with pre-exposure to juvenile stress, and tested in the open field and elevated plus maze paradigms four weeks later. EE exposure during juvenility prevented pre-pubertal stress-induced vulnerability, but not if performed following UWT in adulthood. Furthermore, juvenile EE exposure prevented the trauma-associated increase in α1 expression levels. Our findings emphasize the importance of early interventions in order to reduce the likelihood of developing psychopathologies in adulthood.


Sign in / Sign up

Export Citation Format

Share Document