Neural correlates of paranoia: An ERP study of clinically anxious and healthy participants

2016 ◽  
Vol 108 ◽  
pp. 107
Author(s):  
Susan J. Thomas ◽  
Craig J. Gonsalvez ◽  
Stuart J. Johnstone
2021 ◽  
pp. 1-8
Author(s):  
Stephan Köhler ◽  
Veith Andreas Weilnhammer ◽  
Henrik Walter ◽  
Susanne Erk ◽  
Philipp Sterzer ◽  
...  

<b><i>Introduction:</i></b> Emotion regulation (ER), the ability to actively modulate one’s own emotion reactions, likely depends on the individual’s current emotional state. Here, we investigated whether negative emotions induced by an interpersonal autobiographic script affect the neuronal processes underlying ER. <b><i>Methods:</i></b> Twenty healthy participants were recruited and underwent functional magnetic resonance imaging (fMRI) during performance of distancing, a specific ER strategy, while viewing emotionally arousing pictures. Participants were instructed to either naturally experience (“permit” condition) or to actively downregulate (“regulate” condition) their emotional responses to the presented stimuli. Before each of the 4 runs in total, a neutral or negative autobiographical audio script was presented. The negative script comprised an emotionally negative event from childhood or adolescence that represented either emotional abuse or emotional neglect. The second event comprised an everyday neutral situation. We aimed at identifying the neural correlates of ER and their modulation by script-driven imagery. <b><i>Results:</i></b> fMRI analyses testing for greater responses in the “regulate” than the “permit” condition replicated previously reported neural correlates of ER in the right dorsolateral prefrontal cortex and the right inferior parietal lobule. A significant ER effect was also observed in the left orbitofrontal cortex. In the amygdala, we found greater responses in the “permit” compared to the “regulate” condition. We did not observe a significant modulation of the ER effects in any of these regions by the negative emotional state induced by autobiographical scripts. Bayesian statistics confirmed the absence of such modulations by providing marginal evidence for null effects. <b><i>Discussion:</i></b> While we replicated previously reported neural correlates of ER, we found no evidence for an effect of mood induction with individualized autobiographical scripts on the neural processes underlying ER in healthy participants.


2013 ◽  
Vol 81 (1) ◽  
pp. 57-66 ◽  
Author(s):  
Helmut Hildebrandt ◽  
Frauke Fink ◽  
Paul Eling ◽  
Heiner Stuke ◽  
Jan Klein ◽  
...  

2019 ◽  
Vol 2 ◽  
Author(s):  
Christoph Scheffel ◽  
Kersten Diers ◽  
Sabine Schönfeld ◽  
Burkhard Brocke ◽  
Alexander Strobel ◽  
...  

Abstract A common and mostly effective emotion regulation strategy is reappraisal. During reappraisal, activity in cognitive control brain regions increases and activity in brain regions associated with emotion responding (e.g., the amygdala) diminishes. Immediately after reappraisal, it has been observed that activity in the amygdala increases again, which might reflect a paradoxical aftereffect. While there is extensive empirical evidence for these neural correlates of emotion regulation, only few studies targeted the association with individual differences in personality traits. The aim of this study is to investigate these associations more thoroughly. Seventy-six healthy participants completed measures of broad personality traits (Big Five, Positive and Negative Affect) as well as of more narrow traits (habitual use of emotion regulation) and performed an experimental fMRI reappraisal task. Participants were instructed to either permit their emotions or to detach themselves from the presented negative and neutral pictures. After each picture, a relaxation period was included. Reappraisal success was determined by arousal ratings and activity in the amygdala. During reappraisal, we found activation in the prefrontal cortex and deactivation in the left amygdala. During the relaxation period, an immediate aftereffect was found in occipital regions and marginally in the amygdala. Neither personality traits nor habitual use of emotion regulation predicted reappraisal success or the magnitude of the aftereffect. We replicated typical activation and deactivation patterns during intentional emotion regulation and partially replicated the immediate aftereffect in the amygdala. However, there was no association between personality traits and emotion regulation success.


2021 ◽  
Vol 14 ◽  
Author(s):  
Arash Javanbakht ◽  
Lana Ruvolo Grasser ◽  
Shantanu Madaboosi ◽  
Asadur Chowdury ◽  
Israel Liberzon ◽  
...  

Extinction learning is the dominant laboratory model for exposure therapy, a treatment involving both experience of safety near the feared object, and safety instructions relayed by a therapist. While the experiential aspect of extinction learning is well researched, less is known about instructed extinction learning and its neurocircuitry. Here, in 14 healthy participants we examined the neural correlates of, and the network interactions evoked by instructed extinction learning. Following fear conditioning to two CS+ stimuli, participants were instructed about the absence of the aversive unconditioned stimulus (US) for one of the CS+s (instructed CS; CS+I) but not the second CS+ (uninstructed CS+; CS+U). Early during extinction learning, greater activation was observed for the CS+I &gt; CS+U contrast in regions including the vmPFC, dmPFC, vlPFC, and right parahippocampus. Subsequently, psychophysiological interaction (PPI) was applied to investigate functional connectivity of a seed in the vmPFC. This analyses revealed significant modulation of the dmPFC, parahippocampus, amygdala, and insula. Our findings suggest that the addition of cognitive instruction yields greater activation of emotion regulation and reappraisal networks during extinction learning. This work is a step in advancing laboratory paradigms that more accurately model exposure therapy and identifies regions which may be potential targets for neuromodulation to enhance psychotherapy effects.


2016 ◽  
Vol 11 (6) ◽  
pp. 1932-1932
Author(s):  
Salvatore Campanella ◽  
Julie Absil ◽  
Carina Carbia Sinde ◽  
Elisa Schroder ◽  
Philippe Peigneux ◽  
...  

2020 ◽  
Vol 34 (9) ◽  
pp. 969-980 ◽  
Author(s):  
Will Lawn ◽  
James Hill ◽  
Chandni Hindocha ◽  
Jocelyn Yim ◽  
Yumeya Yamamori ◽  
...  

Background: Cannabidiol has potential therapeutic benefits for people with psychiatric disorders characterised by reward function impairment. There is existing evidence that cannabidiol may influence some aspects of reward processing. However, it is unknown whether cannabidiol acutely affects brain function underpinning reward anticipation and feedback. Hypotheses: We predicted that cannabidiol would augment brain activity associated with reward anticipation and feedback. Methods: We administered a single 600 mg oral dose of cannabidiol and matched placebo to 23 healthy participants in a double-blind, placebo-controlled, repeated-measures design. We employed the monetary incentive delay task during functional magnetic resonance imaging to assay the neural correlates of reward anticipation and feedback. We conducted whole brain analyses and region-of-interest analyses in pre-specified reward-related brain regions. Results: The monetary incentive delay task elicited expected brain activity during reward anticipation and feedback, including in the insula, caudate, nucleus accumbens, anterior cingulate and orbitofrontal cortex. However, across the whole brain, we did not find any evidence that cannabidiol altered reward-related brain activity. Moreover, our Bayesian analyses showed that activity in our regions-of-interest was similar following cannabidiol and placebo. Additionally, our behavioural measures of motivation for reward did not show a significant difference between cannabidiol and placebo. Discussion: Cannabidiol did not acutely affect the neural correlates of reward anticipation and feedback in healthy participants. Future research should explore the effects of cannabidiol on different components of reward processing, employ different doses and administration regimens, and test its reward-related effects in people with psychiatric disorders.


2016 ◽  
Vol 11 (6) ◽  
pp. 1796-1811 ◽  
Author(s):  
Salvatore Campanella ◽  
Julie Absil ◽  
Carina Carbia Sinde ◽  
Elisa Schroder ◽  
Philippe Peigneux ◽  
...  

Cephalalgia ◽  
2019 ◽  
Vol 40 (1) ◽  
pp. 79-87 ◽  
Author(s):  
Maike Möller ◽  
Jan Mehnert ◽  
Arne May

Background The role of the trigeminal autonomic reflex in headache syndromes, such as cluster headache, is undisputed but sparsely investigated. The aim of the present study was therefore, to identify neural correlates that play a role in the initiation of the trigeminal autonomic reflex. We further aimed to discriminate between components of the reflex that are involved in nociceptive compared to non-nociceptive processing. Methods Kinetic Oscillation Stimulation (KOS) in the left nostril was applied in order to provoke autonomic symptoms (e.g. lacrimation) via the trigeminal autonomic reflex in 26 healthy participants using functional magnetic resonance imaging. Unpleasantness and painfulness were assessed on a visual analog scale (VAS), in order to assess the quality of the stimulus (e.g. pain or no pain). Results During non-painful activation, specific regions involved in the trigeminal autonomic reflex became activated, including several brainstem nuclei but also cerebellar and bilateral insular regions. However, when the input leading to activation of the trigeminal autonomic reflex was perceived as painful, activation of the anterior hypothalamus, the locus coeruleus (LC), the ventral posteriomedial nucleus of the thalamus (VPM), as well as an activation of ipsilateral insular regions, was observed. Conclusion Our results suggest the anterior hypothalamus, besides the thalamus and specific brain stem regions, play a significant role in networks that mediate autonomic output (e.g. lacrimation) following trigeminal input, but only if the trigeminal system is activated by a stimulus comprising a painful component.


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