scholarly journals Corrigendum to “Preventing the return of fear in humans using reconsolidation update mechanisms: A verification report of Schiller et al. (2010)” [Cortex 129 (2020) 510–525]

Cortex ◽  
2021 ◽  
Author(s):  
Anastasia Chalkia ◽  
Lukas Van Oudenhove ◽  
Tom Beckers
Keyword(s):  
Return Of Fear

Induced mood, phobic responding and the return of fear

1994 ◽  
Vol 32 (4) ◽  
pp. 439-445 ◽  
Author(s):  
Paul Salkovskis ◽  
Irene Mills
Keyword(s):  
Return Of Fear ◽  
Induced Mood

Treatment context and return of fear in spider phobia

2002 ◽  
Vol 33 (3) ◽  
pp. 399-416 ◽  
Author(s):  
Jayson L. Mystkowski ◽  
Michelle G. Craske ◽  
Aileen M. Echiverri
Keyword(s):  
Spider Phobia ◽  
Return Of Fear ◽  
Treatment Context

EXPRESS: Limitations of occasional reinforced extinction to alleviate spontaneous recovery and reinstatement effects: Evidence for a trial signalling mechanism

2021 ◽  
pp. 174702182110434
Author(s):  
María José Quintero ◽  
Amanda Flores ◽  
María Teresa Gutiérrez-Huerta ◽  
Patricia Molina-Guerrero ◽  
Francisco J López ◽  
...  
Keyword(s):  
Spontaneous Recovery ◽  
Fear Memory ◽  
Clinical Settings ◽  
Conditioning Procedure ◽  
Psychological Conditions ◽  
Return Of Fear ◽  
Promising Strategy ◽  
Potential Benefits ◽  
Theoretical Standpoint ◽  
Extinction Treatment

Fear extinction is not permanent but is instead more vulnerable than the original fear memory, as traditionally shown by the return of fear phenomena. Because of this, techniques to mitigate the return of fear are needed in the clinical treatment of related psychological conditions. One promising strategy is the occasional reinforced extinction treatment, introducing a gradual and sparse number of CS-US pairings within the extinction treatment. We present the results of three experiments in which we used a threat conditioning procedure in humans. Our main aim was to evaluate whether occasional reinforced extinction could reduce two different forms of relapse: spontaneous recovery (Experiments 1 and 2) and reinstatement (Experiment 3). Contrary to our predictions and previous literature, the results indicate that an occasional reinforcement treatment did not mitigate relapse compared with standard extinction. From a theoretical standpoint, these results are more consistent with the idea that extinction entails the acquisition of new knowledge than with the idea that there are conditions in which extinction leads to a weakening of the original fear memory. These findings also question the generality of the potential benefits of using occasional reinforced extinction in clinical settings.

Immediate extinction promotes the return of fear

2016 ◽  
Vol 131 ◽  
pp. 109-116 ◽  
Author(s):  
Christian J. Merz ◽  
Tanja C. Hamacher-Dang ◽  
Oliver T. Wolf
Keyword(s):  
Return Of Fear

scholarly journals Feature Specific Attention and Return of Fear after Extinction

2016 ◽  
Vol 8 (1) ◽  
pp. 76-87 ◽  
Author(s):  
Tom J. Barry ◽  
Bram Vervliet ◽  
Dirk Hermans
Keyword(s):  
Individual Differences ◽  
Attentional Control ◽  
Self Report ◽  
Common Condition ◽  
Similar Stimulus ◽  
Return Of Fear ◽  
The Common ◽  
Fear Potentiated Startle ◽  
Report Measure ◽  
Unique Condition

Anxiety disorders are often treated by repeatedly presenting stimuli that are perceptually similar to original stimuli to which fear was originally acquired. Fear can return after it is extinguished because of the differences between these stimuli. It may possible to attenuate return of fear by manipulating attention to the commonalities between feared stimuli and extinction stimuli. After acquiring fear for an animal-like stimulus by pairing with an electro-cutaneous shock, fear was extinguished by repeatedly presenting a similar stimulus. During extinction participants were asked questions that instructed them to attend towards the features in common between the acquisition and extinction stimulus or towards the unique features of the extinction stimulus. Return of fear was assessed by presenting a second perceptually similar stimulus after extinction. Participants showed a return in skin conductance responding after extinction in the unique condition, and not in the common condition. Both groups showed a return in self-report ratings of US expectancy. Neither group showed a return in fear potentiated startle, but there was evidence that this may have been due to individual differences in emotional attentional control. Our conclusions are limited by the use of a self-report measure of emotional attentional control and the absence of limits on the length of time participants could take to answer the extinction questions. It may be possible to enhance extinction and prevent a return of the physiological aspects of fear by manipulating attention during extinction. However, this does not appear to influence explicit expectancy of aversive outcomes. Individual differences in attentional control may influence this process.

scholarly journals Propranolol-induced inhibition of unconditioned stimulus-reactivated fear memory prevents the return of fear in humans

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Jiahui Deng ◽  
Le Shi ◽  
Kai Yuan ◽  
Ping Yao ◽  
Sijing Chen ◽  
...  
Keyword(s):  
Unconditioned Stimulus ◽  
Memory Retrieval ◽  
Adrenergic Receptor ◽  
Fear Memory ◽  
Fear Response ◽  
Return Of Fear ◽  
The Us ◽  
Propranolol Administration ◽  
Retrieval Interference ◽  
Oral Propranolol

Abstract Fear memories can be reactivated by a fear-associated conditioned stimulus (CS) or unconditioned stimulus (US) and then undergo reconsolidation. Propranolol administration during CS retrieval-induced reconsolidation can impair fear memory that is specific to the reactivated CS. However, from a practical perspective, the US is often associated with multiple CSs, and each CS can induce a fear response. The present study sought to develop and test a US-based memory retrieval interference procedure with propranolol to disrupt the original fear memory and eliminate all CS-associated fear responses in humans. We recruited 127 young healthy volunteers and conducted three experiments. All of the subjects acquired fear conditioning, after which they received the β-adrenergic receptor antagonist propranolol (40 mg) or placebo (vitamin C) and were exposed to the US or CS to reactivate the original fear memory. Fear responses were measured. Oral propranolol administration 1 h before US retrieval significantly decreased subsequent fear responses and disrupted associations between all CSs and the US. However, propranolol administration before CS retrieval only inhibited the fear memory that was related to the reactivated CS. Moreover, the propranolol-induced inhibition of fear memory reconsolidation that was retrieved by the US had a relatively long-lasting effect (at least 2 weeks) and was also effective for remote fear memory. These findings indicate that the US-based memory retrieval interference procedure with propranolol can permanently decrease the fear response and prevent the return of fear for all CSs in humans. This procedure may open new avenues for treating fear-related disorders.

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