Cortisol suppression by dexamethasone reduces exaggerated fear responses in posttraumatic stress disorder

Emory University School of Medicine, Department of Psychiatry and Behavioral Sciences, Atlanta, GA 30303, United States.
Psychoneuroendocrinology (Impact Factor: 4.94). 05/2011; 36(10):1540-52. DOI: 10.1016/j.psyneuen.2011.04.008
Source: PubMed


PTSD symptoms are associated with heightened fear responses in laboratory fear conditioning paradigms. This study examined the effects of dexamethasone administration on hypothalamic-pituitary-adrenal (HPA) function and fear-potentiated startle (FPS) in trauma-exposed individuals with and without PTSD. We used an established fear discrimination procedure, in which one visual stimulus (CS+, danger cue) was paired with aversive airblasts to the throat (unconditioned stimulus, US), and another stimulus (CS-, safety cue) was presented without airblasts. In addition to FPS, the dexamethasone suppression test (DST) was performed. The study sample (N=100) was recruited from a highly traumatized civilian population in Atlanta, GA. Half of the subjects (n=54, 16 PTSD, 38 controls) underwent conditioning at baseline and the other half (n=46, 17 PTSD, 29 controls) after DST, in a cross-sectional design. We found a significant interaction effect of diagnostic group and dexamethasone treatment. Under baseline conditions, subjects with PTSD showed more than twice as much fear-potentiated startle to the danger cue compared to traumatized controls, F(1,53)=8.08, p=0.006. However, there was no group difference in subjects tested after dexamethasone suppression. Furthermore, there was a significant treatment effect in PTSD subjects but not in controls, with dexamethasone reducing fear-potentiated startle to the CS+, F(1,32)=4.00, p=0.05. There was also a positive correlation between PTSD subjects' FPS and cortisol levels, r=0.46, p=0.01. These results suggest that transient suppression of HPA function via dexamethasone suppression may reduce exaggerated fear in patients with PTSD.

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Available from: Kerry Ressler, Sep 16, 2014
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    • "Inconsistency in measurement of cortisol (e.g., diurnal vs. baseline vs. reactivity, plasma vs. saliva, etc.) may account for variability in sex-related findings (Olff, Langeland, Draijer, & Gersons, 2007). Cortisol itself may have an effect on fear learning, with different patterns for males and females (Jovanovic et al., 2011; Van Ast, Vervliet, & Kindt, 2012). Thus, it would seem that both biological propensities and social constructions maintain this gender disparity. "
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    ABSTRACT: Posttraumatic stress (PTSS) and generalized anxiety symptoms (GAS) may ensue following trauma. While they are now thought to represent different psychopathological entities, it is not clear whether both GAS and PTSS show a dose-response to trauma exposure. The current study aimed to address this gap in knowledge and to investigate the moderating role of subjects' demographics in the exposure-outcome associations. The sample included 249 civilian adults, assessed during the 2014 Israel-Gaza military conflict. The survey probed demographic information, trauma exposure, and symptoms. PTSS but not GAS was associated with exposure severity. Women were at higher risk for both PTSS and GAS than men. In addition, several demographic variables were only associated with PTSS levels. PTSS dose-response effect was moderated by education. These findings are in line with emerging neurobiological and cognitive research, suggesting that although PTSS and GAS have shared risk factors they represent two different psychopathological entities. Clinical and theoretical implications are discussed.
    08/2015; 35. DOI:10.1016/j.janxdis.2015.08.001
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    • "Besides the already mentioned causal link to SAM hyperdrive, a larger startle response was found to be positively associated with cortisol levels and negatively associated with the steroid hormone dehydroepiandrosterone (DHEA-S) [81]. Interestingly, cortisol suppression by dexamethasone reduces exaggerated startle responses in PTSD patients [82]. "
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    Disease markers 07/2013; 35(1):43-54. DOI:10.1155/2013/835876 · 1.56 Impact Factor
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    • "In healthy individuals, prefrontal cortex activity is associated with deep semantic encoding that supports improved recall of emotional memories (Ritchey et al., 2011), as well as suppression of aversive memories that reduces recall (Depue et al., 2007). However, less is known regarding the extent to which patients with PTSD can engage critical prefrontal cortex regions to influence the memorability of emotional stimuli. "
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    ABSTRACT: Posttraumatic stress disorder (PTSD) is a psychiatric syndrome that develops after exposure to terrifying and life-threatening events including warfare, motor-vehicle accidents, and physical and sexual assault. The emotional experience of psychological trauma can have long-term cognitive effects. The hallmark symptoms of PTSD involve alterations to cognitive processes such as memory, attention, planning, and problem solving, underscoring the detrimental impact that negative emotionality has on cognitive functioning. As such, an important challenge for PTSD researchers and treatment providers is to understand the dynamic interplay between emotion and cognition. Contemporary cognitive models of PTSD theorize that a preponderance of information processing resources are allocated toward threat detection and interpretation of innocuous stimuli as threatening, narrowing one's attentional focus at the expense of other cognitive operations. Decades of research have shown support for these cognitive models of PTSD using a variety of tasks and methodological approaches. The primary goal of this review is to summarize the latest neurocognitive and neuroimaging research of emotion-cognition interactions in PTSD. To directly assess the influence of emotion on cognition and vice versa, the studies reviewed employed challenge tasks that included both cognitive and emotional components. The findings provide evidence for memory and attention deficits in PTSD that are often associated with changes in functional brain activity. The results are reviewed to provide future directions for research that may direct better and more effective treatments for PTSD.
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