Manipulating expectancy violations to strengthen the efficacy of human fear extinction.

Recent theoretical and clinical articles have emphasized a role for expectancy violations in improving the effectiveness of exposure therapy. Expectancy violations are critical to extinction learning and strengthening these violations has been suggested to improve the formation and retention of extinction memories, which should result in lasting symptom reductions after treatment. However, more detailed mechanistic insights in this process are needed to better inform clinical interventions. In two separate fear-conditioning experiments, we investigated whether stronger expectancy violations (Exp1) or fostering awareness of expectancy violations (Exp2) during extinction could reduce the subsequent return of fear. We measured fear potentiated startle (FPS) and skin conductance responses (SCR) as physiological indices of fear, and US expectancy ratings to assess our manipulations. While we successfully created stronger expectancy violations in Exp1, we found no evidence that these stronger violations reduced the return of fear at test. Interestingly, fostering awareness of violations (Exp2) reduced differential SCRs, but not FPS responses. These findings provide novel insights into the effect of US expectancies on fear extinction in the lab, but they also illustrate the complexity of capturing clinically relevant processes of change with fear-conditioning studies.

Pupil dilation and skin conductance as measures of prediction error in aversive learning.

Notwithstanding the success of CBT, it is relatively unknown how individuals can better profit from corrective learning experiences. Various theories postulate that prediction errors - the difference between what is occurring and what is expected - are the driving force of associative (re)learning. While prediction errors are typically operationalized as violations of cognitive outcome expectancies, direct physiological indices of prediction errors could capture potentially more essential automatic and emotional processes in associative learning. Although physiological responses have previously been suggested to reflect prediction errors, it remains elusive if these measures actually predict changes in subsequent conditioned responding. In three fear-conditioning experiments, we compared pupil dilation and skin conductance responses to unexpected outcomes - unconditioned stimulus (US) presentations or omissions - with expected outcomes, and tested whether outcome responses predicted actual changes in subsequent conditioned responding. We found evidence for increased physiological responses to unexpected outcomes, but the results were inconsistent across experiments. Furthermore, only pupil responses to US presentations consistently predicted an increase in conditioned responding, making it difficult to reconcile our findings with associative learning models. Both pupil dilation and skin conductance can thus index unexpected outcomes, but the relationship of these responses to future learning is not evident and requires further investigation.

Demarcating the boundary conditions of memory reconsolidation: An unsuccessful replication.

Disrupting memory reconsolidation provides an opportunity to abruptly reduce the behavioural expression of fear memories with long-lasting effects. The success of a reconsolidation intervention is, however, not guaranteed as it strongly depends on the destabilization of the memory. Identifying the necessary conditions to trigger destabilization remains one of the critical challenges in the field. We aimed to replicate a study from our lab, showing that the occurrence of a prediction error (PE) during reactivation is necessary but not sufficient for destabilization. We tested the effectiveness of a reactivation procedure consisting of a single PE, compared to two control groups receiving no or multiple PEs. All participants received propranolol immediately after reactivation and were tested for fear retention 24 h later. In contrast to the original results, we found no evidence for a reconsolidation effect in the single PE group, but a straightforward interpretation of these results is complicated by the lack of differential fear retention in the control groups. Our results corroborate other failed reconsolidation studies and exemplify the complexity of experimentally investigating this process in humans. Thorough investigation of the interaction between learning and memory reactivation is essential to understand the inconsistencies in the literature and to improve reconsolidation interventions.