4.7 Article

Latent cause inference during extinction learning in trauma-exposed individuals with and without PTSD

期刊

PSYCHOLOGICAL MEDICINE
卷 52, 期 16, 页码 3834-3845

出版社

CAMBRIDGE UNIV PRESS
DOI: 10.1017/S0033291721000647

关键词

Causal inference; extinction learning; PTSD; generalization; computational psychiatry

资金

  1. CDC-NIOSH U01 awards [OH011473, OH010729]
  2. NARSAD Young Investigator award from the Brain and Behavior Research Foundation [28604]

向作者/读者索取更多资源

The study tested two competing hypotheses about how differences in causal inference might be related to trauma-related psychopathology, finding that individuals with more severe post-traumatic stress disorder were more likely to attribute observations from conditioning and extinction stages to a single underlying cause, suggesting a primary deficit in discriminative learning in these individuals.
Background Problems in learning that sights, sounds, or situations that were once associated with danger have become safe (extinction learning) may explain why some individuals suffer prolonged psychological distress following traumatic experiences. Although simple learning models have been unable to provide a convincing account of why this learning fails, it has recently been proposed that this may be explained by individual differences in beliefs about the causal structure of the environment. Methods Here, we tested two competing hypotheses as to how differences in causal inference might be related to trauma-related psychopathology, using extinction learning data collected from clinically well-characterised individuals with varying degrees of post-traumatic stress (N = 56). Model parameters describing individual differences in causal inference were related to multiple post-traumatic stress disorder (PTSD) and depression symptom dimensions via network analysis. Results Individuals with more severe PTSD were more likely to assign observations from conditioning and extinction stages to a single underlying cause. Specifically, greater re-experiencing symptom severity was associated with a lower likelihood of inferring that multiple causes were active in the environment. Conclusions We interpret these results as providing evidence of a primary deficit in discriminative learning in participants with more severe PTSD. Specifically, a tendency to attribute a greater diversity of stimulus configurations to the same underlying cause resulted in greater uncertainty about stimulus-outcome associations, impeding learning both that certain stimuli were safe, and that certain stimuli were no longer dangerous. In the future, better understanding of the role of causal inference in trauma-related psychopathology may help refine cognitive therapies for these disorders.

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