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Fear and anxiety are rarely confined to specific stimuli or situations. In fear generalisation, there is a spread of fear responses elicited by physically dissimilar generalisation stimuli (GS) along a continuum between danger and safety. The current study investigated fear generalisation with a novel online task using COVID-19-relevant stimuli (i.e., busy or quiet shopping street/mall scenes) during pandemic lockdown restrictions in the United Kingdom. Participants (N = 50) first completed clinically relevant trait measures before commencing a habituation phase, where two conditioned stimuli (CSs; i.e., a busy or quiet high street/mall scene) were presented. Participants then underwent fear conditioning where one conditioned stimulus (CS+) was followed by an aversive unconditioned stimulus (US; a loud female scream accompanied by a facial photograph of a female displaying a fearful emotion) and another (CS-) was not. In a test phase, six generalisation stimuli were presented where the US was withheld, and participants provided threat expectancy and fear ratings for all stimuli. Following successful conditioning, fear generalization was observed for both threat expectancy and fear ratings. Trait worry partially predicted generalised threat expectancy and COVID-19 fear strongly predicted generalised fear. In conclusion, a generalisation gradient was evident using an online remote generalisation task with images of busy/quiet streets during the pandemic. Worry and fear of COVID-19 predicted fear generalisation., (© 2024. The Author(s).)

Low levels of estradiol in women have been associated with impaired fear extinction recall, with suggestions this may promote the return of fear and heighten the female vulnerability for anxiety disorders. A particularly important measure for the return of fear is reinstatement, but no human studies to date have examined the impact of estradiol on fear reinstatement. Forty-two healthy females completed a differential fear conditioning, extinction and reinstatement task with skin conductance response (SCR) amplitude indexing level of conditioned fear. Saliva samples were taken to measure estradiol and progesterone. To examine fear reinstatement, SCR amplitude was compared between the last trial of the late extinction phase to the first re-extinction trial following the unsignaled presentation of two aversive electric shocks. No significant effects of estradiol were found for acquisition of fear conditioning or fear extinction learning. Lower estradiol predicted a significantly larger generalized SCR amplitude at re-extinction (post-reinstatement) in women. This provides novel evidence suggesting a protective role of estradiol in potentially reducing the relapse of fear following re-exposure to aversive stimuli, although further research is necessary in clinical populations to clarify this effect., (Copyright © 2021 Elsevier Ltd. All rights reserved.)

Robustness of fear conditioning and extinction paradigms has become increasingly important for many researchers interested in improving the study of anxiety and trauma disorders. We recently illustrated the wide variability in data analysis techniques in this paradigm, which we argued may result in a lack of robustness. In the current study, we resampled data from six of our own fear acquisition and extinction data sets, with skin conductance as the outcome. In the resampled and original data sets, we found that effect sizes that were calculated using discrepant statistical strategies, sourced from a non-exhaustive search of high-impact articles, were often poorly correlated. The main contributors to poor correlations were the selection of trials from different stages of each experimental phase and the use of average compared to trial-by-trial analysis. These findings reinforce the importance of focusing on robustness in the psychophysiological measurement of fear acquisition and extinction in the laboratory and may guide prospective researchers in which decisions may most impact the robustness of their results., (© 2020 Society for Psychophysiological Research.)

The classical conditioning paradigm of fear learning has spawned a number of experimental variations for the explanation of posttraumatic stress disorder (PTSD) etiology. These paradigms include extinction learning and recall, fear inhibition, fear generalization, and conditioned avoidance. As such, each of these paradigms have significant applications for understanding the development, maintenance, treatment, and relapse of the fear-related features of PTSD. In the present review, we describe each of these conditioning-based paradigms with reference to the clinical applications, and supported by case examples from patients with severe PTSD symptoms. We also review the neurobiological models of conditioning and extinction in animals, psychiatrically healthy humans, and PTSD patients, and discuss the current balance of evidence suggesting a number of biological, behavioral, and cognitive mechanisms/moderators of the conditioning and extinction process in experimental and clinical contexts., (Copyright © 2018. Published by Elsevier Inc.)

Fear reinstatement is one of several paradigms designed to measure fear return following extinction, as a laboratory model for the relapse of Posttraumatic Stress Disorder (PTSD) symptoms. Sleep is a key factor in emotional memory consolidation, and here we examined the relationship between sleep quality and fear reinstatement in PTSD, relative to trauma-exposed and non-exposed controls. The Pittsburgh Sleep Quality Index (PSQI) was used as a subjective measure of sleep quality, and skin conductance responses (SCR) and unconditioned stimulus (US)-expectancy ratings were used to index threat responses during a differential fear conditioning, extinction, and reinstatement paradigm. There were no significant between-group differences in the reinstatement of conditioned responding. Sleep disturbance and sleep onset latency were significant moderators between reinstatement of fear and PTSD symptom severity, such that there was a positive relationship between PTSD symptoms and fear reinstatement for higher levels - but not lower levels - of sleep disturbance and sleep onset latency. To our knowledge, this is the first study to investigate PTSD-specific reinstatement patterns and sleep as a boundary condition of reinstatement. Future research using polysomnographic measures of sleep-wave architecture may further clarify the relationship between fear reinstatement and sleep quality in clinical samples with PTSD relative to controls., (Copyright © 2018 Elsevier Ltd. All rights reserved.)

Posttraumatic Stress Disorder (PTSD) is associated with elevated noradrenergic signaling, which has an impact on emotional learning and memory. Fear extinction is thought to underlie the processes of exposure therapy, however the relationship between noradrenaline and extinction in PTSD is unclear. Participants with PTSD (n = 21), trauma-exposure without PTSD (TC; n = 36), and non-trauma-exposed controls (NTC; n = 27) completed a fear conditioning and extinction paradigm, and conditioned fear was indexed by skin conductance response (SCR). Salivary α-amylase (sAA) collected at baseline and immediately post-fear acquisition was used as an index of noradrenaline, and we examined whether sAA in response to fear acquisition was a moderator between fear extinction and PTSD symptoms. While there was a significant increase in sAA from baseline to post-fear acquisition, this was not modulated by group. Compared to TC and NTC, the PTSD group displayed a slower decline in SCRs during early extinction, which generalized across stimulus type, and was not moderated by sAA. These findings suggest that the relationship between fear extinction and PTSD symptoms does not change as a function of sAA levels; however previous research suggests other processes of fear learning may be associated with noradrenergic activity in PTSD., (Crown Copyright © 2018. Published by Elsevier B.V. All rights reserved.)

Background: Considerable research has revealed impaired fear extinction to be a significant predictor of PTSD. Fear extinction is also considered the primary mechanism of exposure therapy, and a critical factor in PTSD recovery. The cognitive theory of PTSD proposes that symptoms persist due to excessive negative appraisals about the trauma and its sequelae. Research has not yet examined the relationship between fear extinction and negative appraisals in PTSD., Methods: A cross-sectional sample of participants with PTSD (n =21), and trauma-exposed controls (n =33) underwent a standardized differential fear conditioning and extinction paradigm, with skin conductance response (SCR) amplitude serving as the index of conditioned responses. The Posttraumatic Cognitions Inventory (PTCI) was used to index catastrophic negative appraisals., Results: Participants with PTSD demonstrated a slower decrease in overall SCR responses during extinction and greater negative appraisals compared to the group. A moderation analysis revealed that both negative trauma-relevant appraisals and fear extinction learning were independently associated with PTSD symptoms, but there was no moderation interaction., Limitations: The current study was limited by a modest sample size, leading to the inclusion of participants with subclinical PTSD symptoms. Further, the current study only assessed fear extinction learning; including a second day extinction recall task may show alternative effects., Conclusions: These findings indicate that negative appraisals and fear extinction did not interact, but had independent relationships with PTSD symptoms. Here we show for the first time in an experimental framework that negative appraisals and fear extinction play separate roles in PTSD symptoms., (Copyright © 2017 Elsevier B.V. All rights reserved.)

Objective: Posttraumatic stress symptoms (PTSS) are commonly associated with impairments in extinguishing fear to signals previously associated with danger, and also with inhibiting fear to safety signals. Previous studies indicate that PTSS are associated with low cortisol activity, and cortisol is shown to facilitate fear extinction. Few studies have examined the influence of cortisol reactivity on fear extinction in PTSS., Method: We used a standardized fear conditioning and extinction paradigm to investigate the relationship between fear extinction and endogenous salivary cortisol activity in participants with high PTSS (n=18), trauma-exposed controls (n=33), and non-trauma-exposed controls (n=27). Skin conductance response (SCR) was used as an index of conditioned responding. Saliva samples were collected at baseline, and 20min post-fear acquisition for basal and reactive cortisol levels, respectively., Results: PTSS participants demonstrated a slower rate of extinction learning during the early extinction phase. A moderation analysis revealed that cortisol reactivity was a significant moderator between fear inhibition to the safety signal (CS-) during early extinction and PTSS, but not to the threat signal (CS+). Specifically, this interaction was significant in two ways: (1) participants with elevated cortisol reactivity showed lower PTSS as fear inhibition improved; and (2) participants with low cortisol reactivity showed higher PTSS as fear inhibition improved., Conclusion: The findings of the present study show that the relationship between fear inhibition and cortisol reactivity is complex, and suggest that cortisol reactivity shapes safety signal learning in PTSS., (Copyright © 2017 Elsevier Ltd. All rights reserved.)

Background: Prior research has demonstrated that time-of-day may play an important role in the extinction of conditioned fear, with extinction better learned earlier in the day rather than later. Impaired fear extinction memory is widely considered a key mechanism of posttraumatic stress disorder (PTSD). The relationship between fear extinction and PTSD symptoms may be moderated by hours-since-waking., Method: In the present experiment, we examined whether hours-since-waking would moderate fear extinction learning ability in a clinical PTSD sample (n = 15), compared to trauma-exposed (n = 33) and nonexposed controls (n = 22). Participants completed a standardized differential fear conditioning and extinction paradigm, providing skin conductance response measures to quantify conditioned responding., Results: Mixed-model analysis of variance revealed a PTSD-specific impairment in extinction learning ability in the late extinction phase. A moderation analysis showed that hours-since-waking was a significant moderator of the relationship between impaired late extinction and PTSD symptoms. Specifically, we found that participants with higher PTSD symptoms demonstrated poorer fear extinction learning ability as they were awake for longer., Conclusions: The results of the current study add to a growing literature indicating deficits in fear extinction learning in PTSD samples, compared to trauma-exposed and nonexposed controls. These results support previous findings that fear extinction is impaired later in the day, and extends this to a clinical sample, suggesting that exposure-therapy may be optimized by scheduling sessions in the morning., (© 2016 Wiley Periodicals, Inc.)

Maladaptive avoidance of safe stimuli is a defining feature of anxiety and related disorders. Avoidance may involve physical effort or the completion of a fixed series of responses to prevent occurrence of, or cues associated with, the aversive event. Understanding the role of response effort in the acquisition and extinction of avoidance may facilitate the development of new clinical treatments for maladaptive avoidance. Despite this, little is known about the impact of response effort on extinction-resistant avoidance in humans. Here, we describe findings from two laboratory-based treatment studies designed to investigate the impact of high and low response effort on the extinction (Experiment 1) and return (Experiment 2) of avoidance. Response effort was operationalised as completion of fixed-ratio (FR) reinforcement schedules for both danger and safety cues in a multi-cue avoidance paradigm with behavioural, self-report, and physiology measures. Completion of the FR response requirements cancelled upcoming shock presentations following danger cues and had no impact on the consequences that followed safety cues. Both experiments found persistence of high response-effort avoidance across danger and safety cues and sustained (Experiment 1) and reinstated (Experiment 2) levels of fear and threat expectancy. Skin conductance responses evoked by all cues were similar across experiments. The present findings and paradigm have implications for translational research on maladaptive anxious coping and treatment development. [ABSTRACT FROM AUTHOR]

The COVID-19 pandemic continues to impact global psychological wellbeing. To investigate the sustained impact of COVID-19 on wellbeing, the current study longitudinally assessed fear of COVID-19, anxiety, depression, intolerance of uncertainty, worry, sleep quality, loneliness and alcohol use during the pandemic in the United Kingdom. Timepoint 1 (T1; N = 445) took place in February 2021 following the highest number of pandemic-related deaths in the UK. Timepoint 2 (T2, N = 198) took place in June 2021 when pandemic-related deaths had declined considerably, and many had been vaccinated. At T1, COVID-19 fear predicted elevated levels of anxiety, depression, intolerance of uncertainty, worry, sleep quality and loneliness. At T2, we observed that levels of COVID-19 fear, depression, loneliness and sleep quality decreased. However, COVID-19 fear continued to predict elevated intolerance of uncertainty, worry and impaired sleep quality. These findings demonstrate the longitudinal impact of COVID-19 fear on psychological wellbeing. [ABSTRACT FROM AUTHOR]

Intolerance of uncertainty (IU), the tendency to find uncertainty aversive, is an important transdiagnostic dimension in mental health disorders. Over the last decade, there has been a surge of research on the role of IU in classical threat conditioning procedures, which serve as analogues to the development, treatment, and relapse of anxiety, obsessive-compulsive, and trauma- and stressor-related disorders. This review provides an overview of the existing literature on IU in classical threat conditioning procedures. The review integrates findings based on the shared or discrete parameters of uncertainty embedded within classical threat conditioning procedures. Under periods of unexpected uncertainty, where threat and safety contingencies change, high IU, over other self-reported measures of anxiety, is specifically associated with poorer threat extinction learning and retention, as well as overgeneralisation. Under periods of estimation and expected uncertainty, where the parameters of uncertainty are being learned or have been learned, such as threat acquisition training and avoidance learning, the findings are mixed for IU. These findings provide evidence that individual differences in IU play a significant role in maintaining learned fear and anxiety, particularly under volatile environments. Recommendations for future research are outlined, with discussion focusing on how parameters of uncertainty can be better defined to capture how IU is involved in the maintenance of learned fear and anxiety. Such work will be crucial for understanding the role of IU in neurobiological models of uncertainty-based maintenance of fear and anxiety and inform translational work aiming to improve the diagnosis and treatment of relevant psychopathology. • We provide a review on the role of IU in classical threat conditioning procedures. • Parameters of uncertainty determine the association of IU with learning indexes. • IU is related to specific learning indexes under periods of unexpected uncertainty. • These observations can guide future research on IU and threat conditioning. [ABSTRACT FROM AUTHOR]

The low expression Met allele of the BDNF Val66Met polymorphism is associated with impaired fear extinction in healthy controls, and poorer response to exposure therapy in patients with Posttraumatic Stress Disorder (PTSD). Given that fear extinction underlies exposure therapy, this raises the question of the impact of BDNFVal66Met polymorphism on fear extinction in PTSD, yet this question has not yet been examined. One hundred and six participants (22 PTSD, 46 trauma-exposed controls (TC) and 38 non-trauma exposed controls (NTC)) completed a fear conditioning and extinction task and saliva samples were taken for DNA extraction and genotyped for the BDNF Val66Met polymorphism. Moderation analyses using PROCESS examined whether BDNF genotype (Val–Val vs Met carriers) moderated the relationship between PTSD symptom severity (and diagnostic status) and skin conductance response (SCR) amplitude during fear extinction. The PTSD group displayed significantly slower fear extinction learning compared to TC and NTC in the early extinction phase. The BDNF Val66Met polymorphism moderated the relationship between PTSD and fear extinction learning, such that poorer fear extinction learning was associated with greater PTSD symptom severity (and PTSD diagnostic status) in individuals with the low-expression Met allele, but no relationship was demonstrated in individuals with the Val–Val allele. This study reveals that impaired fear extinction learning is particularly evident in individuals with PTSD who carry the low-expression BDNF Met allele and importantly not in those with the Val–Val allele. This provides novel evidence of a link between BDNF and impaired fear extinction learning in PTSD, which may contribute to poorer response to exposure therapy. [ABSTRACT FROM AUTHOR]

Recent prospective studies in emergency services have identified impaired fear extinction learning and memory to be a significant predictor of Posttraumatic Stress Disorder (PTSD), complementing a wealth of cross-sectional evidence of extinction deficits associated with the disorder. Additional fields of research show specific risk factors and biomarkers of the disorder, including candidate genotypes, stress and sex hormones, cognitive factors, and sleep disturbances. Studies in mostly nonclinical populations also reveal that the aforementioned factors are involved in fear extinction learning and memory. Here, we provide a comprehensive narrative review of the literature linking PTSD to these risk factors, and linking these risk factors to impaired fear extinction. On balance, the evidence suggests that fear extinction may play a role in the relationship between risk factors and PTSD. Should this notion hold true, this review carries important implications for the improvement of exposure-based treatments, as well as strategies for the implementation of treatment. [ABSTRACT FROM AUTHOR]

Avoidance is an adaptive response to actual or perceived threat. However, persistent avoidance despite low likelihood of threat can become maladaptive and prevent effective psychological treatment. To examine behavioural avoidance, in-person, lab-based threat learning paradigms are typically used with relatively small sample sizes. However, such methods pose issues when in-person testing is difficult. The aim of the current study was therefore to adapt a validated lab-based threat and avoidance conditioning paradigm into an online avoidance learning task to investigate threat expectancy and avoidance remotely during the COVID-19 pandemic. An online fear and avoidance learning task was developed and administered to 119 participants who differed in the opportunity to avoid a safe stimulus. Fear and avoidance conditioning were successful and the opportunity to avoid a known safe stimulus increased threat expectancy and fear for the experimental group, relative to the control group. Such remote delivery paradigms may therefore be useful when evaluating changes in fear and avoidance • Avoidance increases threat expectancy for a previously benign stimulus. • Online delivery of an avoidance learning task. • Threat learning was dissimilar across groups in key stages. • The presence of an avoidance cue increased threat-relevance. [ABSTRACT FROM AUTHOR]