Daniel V. Zuj

Registered Replication Report

Trying to remember something now typically improves your ability to remember it later. However, after watching a video of a simulated bank robbery, participants who verbally described the robber were 25% worse at identifying the robber in a lineup than were participants who instead listed U.S. states and capitals—this has been termed the “verbal overshadowing” effect (Schooler & Engstler-Schooler, 1990). More recent studies suggested that this effect might be substantially smaller than first reported. Given uncertainty about the effect size, the influence of this finding in the memory literature, and its practical importance for police procedures, we conducted two collections of preregistered direct replications (RRR1 and RRR2) that differed only in the order of the description task and a filler task. In RRR1, when the description task immediately followed the robbery, participants who provided a description were 4% less likely to select the robber than were those in the control condition. In RRR2, when the description was delayed by 20 min, they were 16% less likely to select the robber. These findings reveal a robust verbal overshadowing effect that is strongly influenced by the relative timing of the tasks. The discussion considers further implications of these replications for our understanding of verbal overshadowing.

The centrality of fear extinction in linking risk factors to PTSD: A narrative review.

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.

IMPAIRED FEAR EXTINCTION ASSOCIATED WITH PTSD INCREASES WITH HOURS-SINCE-WAKING.

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.

Endogenous cortisol reactivity moderates the relationship between fear inhibition to safety signals and posttraumatic stress disorder symptoms

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.

Negative appraisals and fear extinction are independently related to PTSD symptoms

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.

The BDNF Val66Met polymorphism moderates the relationship between Posttraumatic Stress Disorder and fear extinction learning

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.

Endogenous salivary α-amylase does not interact with skin conductance response during fear extinction in posttraumatic stress disorder

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.

Cigarette cravings impair mock jurors' recall of trial evidence

Prior research has demonstrated that cravings for substances, such as cigarettes and food, impair performance on basic cognitive tasks. This experiment examined whether these effects translate to impaired cognition on an important task in an applied setting: jury duty. Forty-six smokers were randomly allocated to a high-craving or control condition of an in vivo procedure designed to invoke cigarette cravings. Participants were then asked to act as mock jurors and read a written legal transcript based on evidence presented in an actual civil case. Later, participants were tested on their recall and recognition of information from the transcript. Participants in the high-craving condition recalled fewer correct facts from the transcript than participants in the control condition, but cravings did not significantly affect the recognition of trial information. These results are consistent with cognitive models of cravings, highlight the importance of providing jurors with sufficient breaks, and suggest that cravings may impair cognition in a variety of important applied settings.

Neural activity and emotional processing following military deployment: Effects of mild traumatic brain injury and posttraumatic stress disorder

HIGHLIGHTSPTSD and mTBI groups show distinct neural patterns in emotional face processing.Soldiers from OEF/OIF provided EEG responses prior to, and following deployment.PTSD symptoms associated with increased P1 and P2 amplitudes to threatening faces.mTBI group show reduced N170 amplitude to all facial expressions. ABSTRACT Posttraumatic Stress Disorder (PTSD) and mild traumatic brain injury (mTBI) are common comorbidities during military deployment that affect emotional brain processing, yet few studies have examined the independent effects of mTBI and PTSD. The purpose of this study was to examine distinct differences in neural responses to emotional faces in mTBI and PTSD. Twenty‐one soldiers reporting high PTSD symptoms were compared to 21 soldiers with low symptoms, and 16 soldiers who reported mTBI‐consistent injury and symptoms were compared with 16 soldiers who did not sustain an mTBI. Participants viewed emotional face expressions while their neural activity was recorded (via event‐related potentials) prior to and following deployment. The high‐PTSD group displayed increased P1 and P2 amplitudes to threatening faces at post‐deployment compared to the low‐PTSD group. In contrast, the mTBI group displayed reduced face‐specific processing (N170 amplitude) to all facial expressions compared to the no‐mTBI group. Here, we identified distinctive neural patterns of emotional face processing, with attentional biases towards threatening faces in PTSD, and reduced emotional face processing in mTBI.

The clinical applications and practical relevance of human conditioning paradigms for posttraumatic stress disorder

Abstract 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. HighlightsClassical conditioning paradigm of fear learning are discussed in terms of their relevance to the etiology and treatment of Posttraumatic Stress Disorder (PTSD)Clinically relevant paradigms include extinction learning and recall, fear inhibition, fear generalization, and conditioned avoidanceEach of these conditioning‐based paradigms is discussed with reference to clinical applications and case examples from patients with severe PTSD symptoms