scholarly journals Post-traumatic stress disorder symptoms form a traumatic and non-traumatic stress response dimension

2013 ◽  
Vol 47 (6) ◽  
pp. 569-577 ◽  
Author(s):  
Roger Mulder ◽  
David Fergusson ◽  
John Horwood
2020 ◽  
Author(s):  
Ravi Philip Rajkumar

There is preliminary evidence that some patients recovering from novel coronavirus disease (COVID-19) may experience ongoing symptoms such as myalgia, fatigue and headache. Such symptoms have been observed as persistent sequelae of the earlier outbreak of severe acute respiratory syndrome (SARS). In this paper, evidence is presented that novel coronavirus infections may be associated with hypocortisolism which may persist for weeks or months, and that this may be a risk factor for both post-viral symptoms and post-traumatic stress disorder in patients recovering from COVID-19. The mechanisms underlying this phenomenon may involve reversible inflammation or dysfunction at the level of the pituitary gland, or a dysregulated host immune or stress response. The implications of these findings for the assessment and management of patients recovering from the acute phase of COVID-19 are discussed.


Author(s):  
Elizabeth C. Perkins ◽  
Shaun P. Brothers ◽  
Charles B. Nemeroff

Animal models of post-traumatic stress disorder (PTSD) provide a wellspring of biological information about this complex condition by providing the opportunity to manipulate trauma exposure and measure biological outcomes in a systematic manner that is not possible in clinical studies. Symptoms of PTSD may be induced in animals by physical (immobilization, foot shock, underwater stress) and psychological stressors (exposure to predator, social defeat, early life trauma) or a combination of both. In addition, genetic, epigenetic and transgenic models have been created by breeding animals with a behavioral propensity for maladaptive stress response or by directly manipulating genes that have been implicated in PTSD. The effect of stressors in animals is measured by a variety of means, including observation of behavior, measurement of structural alterations in the brain and of physiological markers such as HPA axis activity and altered gene expression of central nervous system neurotransmitter system components including receptors. By comparing changes observed in stress exposed animals to humans with PTSD and by comparing animal response to treatments that are effective in humans, we can determine the validity of PTSD animal models. The identification of a reliable physiological marker of maladaptive stress response in animals as well as standard use of behavioral cutoff criteria are critical to the development of a valid animal model of PTSD.


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