Conspiracy mentality, subclinical paranoia, and political conservatism are associated with perceived status threat.

Status threat (i.e., concern that one's dominant social group will be undermined by outsiders) is a significant factor in current United States politics. While demographic factors such as race (e.g., Whiteness) and political affiliation (e.g., conservatism) tend to be associated with heightened levels of status threat, its psychological facets have yet to be fully characterized. Informed by a "paranoid" model of American politics, we explored a suite of possible psychological and demographic associates of perceived status threat, including race/ethnicity, political conservatism, analytic thinking, magical ideation, subclinical paranoia, and conspiracy mentality. In a small, quota sample drawn from the United States (N = 300), we found that conspiracy mentality, subclinical paranoia, conservatism, and age were each positively (and uniquely) associated with status threat. In addition to replicating past work linking conservatism to status threat, this study identifies subclinical paranoia and conspiracy mentality as novel psychological associates of status threat. These findings pave the way for future research regarding how and why status threat concerns may become exaggerated in certain individuals, possibly to the detriment of personal and societal wellbeing.

Intrusive-like memory errors associate with positive schizotypy.

Schizophrenia is characterized by memory impairments, yet the relationships between its distinct symptom clusters (i.e., positive, negative, disorganized) and specific aspects of memory dysfunction remain poorly characterized. In the present study, we compiled a large analog sample (N = 795) to test whether positive symptoms, versus negative and disorganized symptoms, were uniquely and differentially related to false alarm versus miss errors during recognition memory. Mixed-effects beta regression analyses revealed that both positive schizotypy and paranoia were more strongly associated with false alarms than misses. Disorganized schizotypy showed a similar pattern, though to a lesser extent; negative schizotypy showed a significant relationship with neither false alarm nor miss errors. We suggest that those higher in positive schizotypy are especially prone to misattribute signal to noise stimuli during recognition memory - characteristic of an "intrusive-like" profile of memory impairment, wherein context-irrelevant stimuli trigger spurious retrieval events - and speculate on the neural processes that might give rise to this asymmetry.

Neurofeedback for obsessive compulsive disorder: A randomized, double-blind trial.

We aim to develop fMRI neurofeedback as a treatment for obsessive compulsive disorder (OCD). In prior work, we found that providing neurofeedback of activity in the anterior prefrontal cortex (aPFC) improved control over contamination anxiety in a subclinical population. Here, we present the results of a randomized, double-blind clinical trial (NCT02206945) testing this intervention in patients with OCD. We recruited patients with primary symptoms in the fear-of-harm/checking or contamination/washing domains. During neurofeedback, they viewed symptom provocative images and attempted to up- and down-regulate the aPFC during different blocks of time. The active group received two sessions of neurofeedback and the control group received yoked sham feedback. The primary outcome measure was the Yale-Brown Obsessive-Compulsive Symptom scale. The secondary outcome was control over aPFC. Thirty-six participants completed feedback training (18 active, 18 control). The active group had a slightly but significantly greater reduction of obsessive-compulsive symptoms after neurofeedback compared to the control group (p<.05) but no significant differences in control over the aPFC. These data demonstrate that neurofeedback targeting the aPFC can reduce symptoms in OCD. Future investigations should seek to optimize the training protocol to yield larger effects and to clarify the mechanism of action.

Reduced benefit of novelty detection on subsequent memory judgments in paranoia.

Novelty detection is critical to the effective employment of memory-guided behavior. While recent work has found impaired novelty detection in subclinical paranoia, other studies show different patterns. Here, we tested the hypothesis that those higher in paranoia receive less benefit from novelty in their immediate environment when making subsequent mnemonic judgments. Using a continuous recognition task (comprising Old, New, and Similar items) in a sample drawn from an online marketplace (N = 450), we found that Similar trial performance was generally enhanced by preceding judgments of "New" versus "Old"-replicating prior work. However, paranoia was associated with a reduction of this novelty-based enhancement-a novel finding. Those experiencing paranoia may thus less readily use novelty to adjudicate between the competing mnemonic processes of encoding and retrieval. We interpret this finding in light of the role of novelty detection in maintaining adaptive predictive models, suggesting that this deficit may reduce coherence between one's active predictive model and one's environment, thereby contributing to perceptions of the world as unduly uncertain and threatening. (PsycInfo Database Record (c) 2023 APA, all rights reserved).

Amygdala downregulation training using fMRI neurofeedback in post-traumatic stress disorder: a randomized, double-blind trial.

Hyperactivation of amygdala is a neural marker for post-traumatic stress disorder (PTSD) and improvement in control over amygdala activity has been associated with treatment success in PTSD. In this randomized, double-blind clinical trial we evaluated the efficacy of a real-time fMRI neurofeedback intervention designed to train control over amygdala activity following trauma recall. Twenty-five patients with PTSD completed three sessions of neurofeedback training in which they attempted to downregulate the feedback signal after exposure to personalized trauma scripts. For subjects in the active experimental group (N = 14), the feedback signal was from a functionally localized region of their amygdala associated with trauma recall. For subjects in the control group (N = 11), yoked-sham feedback was provided. Changes in control over the amygdala and PTSD symptoms served as the primary and secondary outcome measurements, respectively. We found significantly greater improvements in control over amygdala activity in the active group than in the control group 30-days following the intervention. Both groups showed improvements in symptom scores, however the symptom reduction in the active group was not significantly greater than in the control group. Our finding of greater improvement in amygdala control suggests potential clinical application of neurofeedback in PTSD treatment. Thus, further development of amygdala neurofeedback training in PTSD treatment, including evaluation in larger samples, is warranted.

Aberrant memory and delusional ideation: A pernicious partnership?

Delusions can be conceptualized as beliefs that are both at odds with consensus reality and espoused with high conviction. While delusions represent a cardinal symptom of schizophrenia, delusion-like beliefs can be found in the general population. Do similar cognitive mechanisms support delusionality across this spectrum? If so, what are they? Here, we examine evidence for a mechanistic role of the (associative) memory system in the formation and maintenance of delusions and delusion-like beliefs. While general neurocognitive metrics do not tend to associate with delusionality, our scoping review of the clinical and subclinical literature reveals several subdomains of memory function that do. These include a propensity to commit errors of commission (i.e., false alarms and intrusions), source memory biases, and metamemory impairment. We discuss how several of these effects may stem from aberrant associative memory function and offer recommendations for future research. Further, we propose a state/trait interaction model in which underlying traits (i.e., impaired associative and metamemory function) may become coupled with delusionality during states of acute psychosis, when memory function is particularly challenged by aberrant salience attribution and noisy perceptual input. According to this model, delusions may arise as explanations to high-salience (but low-source) mnemonic content that is endorsed with high confidence.

Paranoia is associated with impaired novelty detection and overconfidence in recognition memory judgments.

False recognition, or the mis-categorization of a "new" stimulus as "old," might support fixed false beliefs by blocking new learning or otherwise contributing to internal representations of the world that are at odds with reality. However, the mechanisms through which false recognition is facilitated among paranoid individuals remain unclear. We examined 2 phenomena that may contribute to this effect: an overreliance on fluency-based processes during recognition, manifesting as a lower threshold for judging items as recently studied, and a propensity to require less information to come to a highly confident judgment. The former would be expected to be particularly pronounced among items that are generally familiar, as opposed to completely novel. Here, we manipulated familiarity in a recognition memory paradigm by using stimuli that varied in their rate of extraexperimental exposure (i.e., real words vs. pseudowords). Further, to determine whether paranoia was associated with a tendency to differentially misallocate confidence to errors, we calculated a hierarchical Bayesian estimate of metacognitive sensitivity (meta-d') in addition to the more classic d'. In line with our hypotheses, paranoia was associated with an increased rate of false alarm errors, differentially so for familiar versus unfamiliar stimuli, suggesting that a context-agnostic, familiarity-based memory system might underlie observed memory distortions. What's more, paranoia was associated with heightened confidence on error trials and reduced metacognitive sensitivity. These findings highlight 2 distinct deficits-in both novelty detection and metacognitive monitoring-that contribute to false recognition judgments, offering targets for cognitive interventions to reduce memory distortion among paranoid individuals. (PsycInfo Database Record (c) 2021 APA, all rights reserved).

Randomized, Sham-Controlled Trial of Real-Time Functional Magnetic Resonance Imaging Neurofeedback for Tics in Adolescents With Tourette Syndrome.

BACKGROUND: Activity in the supplementary motor area (SMA) has been associated with tics in Tourette syndrome (TS). The aim of this study was to test a novel intervention-real-time functional magnetic resonance imaging neurofeedback from the SMA-for reduction of tics in adolescents with TS. METHODS: Twenty-one adolescents with TS were enrolled in a double-blind, randomized, sham-controlled, crossover study involving two sessions of neurofeedback from their SMA. The primary outcome measure of tic severity was the Yale Global Tic Severity Scale administered by an independent evaluator before and after each arm. The secondary outcome was control over the SMA assessed in neuroimaging scans, in which subjects were cued to increase/decrease activity in SMA without receiving feedback. RESULTS: All 21 subjects completed both arms of the study and all assessments. Participants had significantly greater reduction of tics on the Yale Global Tic Severity Scale after real neurofeedback as compared with the sham control (p < .05). Mean Yale Global Tic Severity Scale Total Tic score decreased from 25.2 ± 4.6 at baseline to 19.9 ± 5.7 at end point in the neurofeedback condition and from 24.8 ± 8.1 to 23.3 ± 8.5 in the sham control condition. The 3.8-point difference is clinically meaningful and corresponds to an effect size of 0.59. However, there were no differences in changes on the secondary measure of control over the SMA. CONCLUSIONS: This first randomized controlled trial of real-time functional magnetic resonance imaging neurofeedback in adolescents with TS suggests that this neurofeedback intervention may be helpful for improving tic symptoms. However, no effects were found in terms of change in control over the SMA, the hypothesized mechanism of action.

Developing image sets for inducing obsessive-compulsive checking symptoms.

Visual stimuli are often used for obsessive-compulsive (OC) symptom provocation in research studies. We tested the induction of anxiety and OC checking symptoms across different types of checking provocation stimuli in three populations: individuals with obsessive compulsive disorder (OCD), individuals with checking symptoms but without a diagnosis of OCD, and control individuals with neither checking symptoms nor a clinical diagnosis. One set of provocative images depicted objects that are commonly associated with checking anxiety. Another set ('enhanced provocative images') depicted similar objects but also included contextual cues suggesting a specific harmful scenario that could occur. As expected, the enhanced provocative images were more effective at inducing anxiety and OC symptoms than the standard provocative images. Future studies requiring checking symptom provocation should therefore consider incorporating similarly suggestive images. Individuals with clinical OCD reported the greatest provocation in response to these images, followed by those with nonclinical checking, followed by control individuals. Thus, these stimuli are able to provoke OC checking symptoms and anxiety differentially across groups, with the intensity of provocation reflecting diagnostic status. All groups demonstrated a similar qualitative pattern of provocation across images. Finally, in all groups, reported anxiety closely tracked intrusive thoughts and checking urges.

Time course of clinical change following neurofeedback.

Neurofeedback - learning to modulate brain function through real-time monitoring of current brain state - is both a powerful method to perturb and probe brain function and an exciting potential clinical tool. For neurofeedback effects to be useful clinically, they must persist. Here we examine the time course of symptom change following neurofeedback in two clinical populations, combining data from two ongoing neurofeedback studies. This analysis reveals a shared pattern of symptom change, in which symptoms continue to improve for weeks after neurofeedback. This time course has several implications for future neurofeedback studies. Most neurofeedback studies are not designed to test an intervention with this temporal pattern of response. We recommend that new studies incorporate regular follow-up of subjects for weeks or months after the intervention to ensure that the time point of greatest effect is sampled. Furthermore, this time course of continuing clinical change has implications for crossover designs, which may attribute long-term, ongoing effects of real neurofeedback to the control intervention that follows. Finally, interleaving neurofeedback sessions with assessments and examining when clinical improvement peaks may not be an appropriate approach to determine the optimal number of sessions for an application.