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\n \n\n \n \n \n \n \n \n Eating disorder symptoms and control-seeking behavior.\n \n \n \n \n\n\n \n Slanina-Davies, A.; Robinson, O. J.; and Pike, A. C.\n\n\n \n\n\n\n Brain and Behavior, 13(8): e3105. 2023.\n _eprint: https://onlinelibrary.wiley.com/doi/pdf/10.1002/brb3.3105\n\n\n\n
\n\n\n\n \n \n \"EatingPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n
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@article{slanina-davies_eating_2023,\n\ttitle = {Eating disorder symptoms and control-seeking behavior},\n\tvolume = {13},\n\tcopyright = {© 2023 The Authors. Brain and Behavior published by Wiley Periodicals LLC.},\n\tissn = {2162-3279},\n\turl = {https://onlinelibrary.wiley.com/doi/abs/10.1002/brb3.3105},\n\tdoi = {10.1002/brb3.3105},\n\tabstract = {Objective Eating disorders (EDs) are a heterogenous group of disorders characterized by disturbed eating patterns. Links have been made between ED symptoms and control-seeking behaviors, which may cause relief from distress. However, whether direct behavioral measures of control-seeking behavior correlate with ED symptoms has not been directly tested. Additionally, existing paradigms may conflate control-seeking behavior with uncertainty-reducing behavior. Method A general population sample of 183 participants completed part in an online behavioral task, in which participants rolled a die in order to obtain/avoid a set of numbers. Prior to each roll, participants could choose to change arbitrary features of the task (such as the color of their die) or view additional information (such as the current trial number). Selecting these Control Options could cost participants points or not (Cost/No-Cost conditions). Each participant completed all four conditions, each with 15 trials, followed by a series of questionnaires, including the Eating Attitudes Test-26 (EAT-26), the Intolerance of Uncertainty Scale, and the Obsessive–Compulsive Inventory—Revised (OCI-R). Results A Spearman's rank test indicated no significant correlation between total EAT-26 score and total number of Control Options selected, with only elevated scores on a measure of obsessions and compulsivity (OCI-R) correlating with the total number of Control Options selected (rs = .155, p = .036). Discussion In our novel paradigm, we find no relationship between EAT-26 score and control-seeking. However, we do find some evidence that this behavior may be present in other disorders that often coincide with ED diagnosis, which may indicate that transdiagnostic factors such as compulsivity are important to control-seeking.},\n\tlanguage = {en},\n\tnumber = {8},\n\turldate = {2024-01-10},\n\tjournal = {Brain and Behavior},\n\tauthor = {Slanina-Davies, Ashley and Robinson, Oliver J. and Pike, Alexandra C.},\n\tyear = {2023},\n\tnote = {\\_eprint: https://onlinelibrary.wiley.com/doi/pdf/10.1002/brb3.3105},\n\tkeywords = {behavioral task, control-seeking, eating disorders, intolerance of uncertainty, online},\n\tpages = {e3105},\n}\n\n
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\n Objective Eating disorders (EDs) are a heterogenous group of disorders characterized by disturbed eating patterns. Links have been made between ED symptoms and control-seeking behaviors, which may cause relief from distress. However, whether direct behavioral measures of control-seeking behavior correlate with ED symptoms has not been directly tested. Additionally, existing paradigms may conflate control-seeking behavior with uncertainty-reducing behavior. Method A general population sample of 183 participants completed part in an online behavioral task, in which participants rolled a die in order to obtain/avoid a set of numbers. Prior to each roll, participants could choose to change arbitrary features of the task (such as the color of their die) or view additional information (such as the current trial number). Selecting these Control Options could cost participants points or not (Cost/No-Cost conditions). Each participant completed all four conditions, each with 15 trials, followed by a series of questionnaires, including the Eating Attitudes Test-26 (EAT-26), the Intolerance of Uncertainty Scale, and the Obsessive–Compulsive Inventory—Revised (OCI-R). Results A Spearman's rank test indicated no significant correlation between total EAT-26 score and total number of Control Options selected, with only elevated scores on a measure of obsessions and compulsivity (OCI-R) correlating with the total number of Control Options selected (rs = .155, p = .036). Discussion In our novel paradigm, we find no relationship between EAT-26 score and control-seeking. However, we do find some evidence that this behavior may be present in other disorders that often coincide with ED diagnosis, which may indicate that transdiagnostic factors such as compulsivity are important to control-seeking.\n
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\n \n\n \n \n \n \n \n \n The influence of peer non-suicidal self-harm on young adults’ urges to self-harm: experimental study.\n \n \n \n \n\n\n \n Pitman, A.; Lowther, M.; Pike, A.; Davies, J.; Cates, A. d.; Buckman, J. E. J.; and Robinson, O.\n\n\n \n\n\n\n Acta Neuropsychiatrica,1–13. November 2023.\n Publisher: Cambridge University Press\n\n\n\n
\n\n\n\n \n \n \"ThePaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n
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@article{pitman_influence_2023,\n\ttitle = {The influence of peer non-suicidal self-harm on young adults’ urges to self-harm: experimental study},\n\tissn = {0924-2708, 1601-5215},\n\tshorttitle = {The influence of peer non-suicidal self-harm on young adults’ urges to self-harm},\n\turl = {https://www.cambridge.org/core/journals/acta-neuropsychiatrica/article/influence-of-peer-nonsuicidal-selfharm-on-young-adults-urges-to-selfharm-experimental-study/520B54D3ECB58C1725F87CCD3AFE9248},\n\tdoi = {10.1017/neu.2023.51},\n\tabstract = {Objective:To test the hypothesis that exposure to peer self-harm induces adolescents’ urges to self-harm and that this is influenced by individual suggestibility.Methods:We recruited 97 UK-based adults aged 18–25 years with a recent history of self-harm, measuring baseline suggestibility (Resistance to Peer Influence; RPI) and perceived ability to control urges to self-harm (using an adapted item from the Self-Efficacy to Resist Suicidal Action scale; SEASA) before and after two self-harm vignettes featuring named peers from the participant’s social network (to simulate exposure to peer non-suicidal self-harm) and after a wash-out exposure. We used paired t-tests to compare mean SEASA scores pre- and post-exposure, and linear regression to test for an association between RPI and change in SEASA scores pre- and post-exposure.Results:Perceived ability to control urges to self-harm was significantly reduced following exposure to peer self-harm (t(96) = 4.02, p {\\textless} 0.001, mean difference = 0.61; 95\\% CI = 0.31, 0.91), but was not significantly different from baseline after exposure to a wash-out. We found no association between suggestibility and change in urges to self-harm after exposure to peer self-harm.Conclusion:Our findings support social influences on self-harm in a sample of young adults, regardless of their individual degree of suggestibility.},\n\tlanguage = {en},\n\turldate = {2024-01-10},\n\tjournal = {Acta Neuropsychiatrica},\n\tauthor = {Pitman, Alexandra and Lowther, Millie and Pike, Alexandra and Davies, Jessica and Cates, Angharad de and Buckman, Joshua E. J. and Robinson, Oliver},\n\tmonth = nov,\n\tyear = {2023},\n\tnote = {Publisher: Cambridge University Press},\n\tkeywords = {Self-harm, adolescent, cognition, peer influence, self-injurious behaviour},\n\tpages = {1--13},\n}\n\n
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\n Objective:To test the hypothesis that exposure to peer self-harm induces adolescents’ urges to self-harm and that this is influenced by individual suggestibility.Methods:We recruited 97 UK-based adults aged 18–25 years with a recent history of self-harm, measuring baseline suggestibility (Resistance to Peer Influence; RPI) and perceived ability to control urges to self-harm (using an adapted item from the Self-Efficacy to Resist Suicidal Action scale; SEASA) before and after two self-harm vignettes featuring named peers from the participant’s social network (to simulate exposure to peer non-suicidal self-harm) and after a wash-out exposure. We used paired t-tests to compare mean SEASA scores pre- and post-exposure, and linear regression to test for an association between RPI and change in SEASA scores pre- and post-exposure.Results:Perceived ability to control urges to self-harm was significantly reduced following exposure to peer self-harm (t(96) = 4.02, p \\textless 0.001, mean difference = 0.61; 95% CI = 0.31, 0.91), but was not significantly different from baseline after exposure to a wash-out. We found no association between suggestibility and change in urges to self-harm after exposure to peer self-harm.Conclusion:Our findings support social influences on self-harm in a sample of young adults, regardless of their individual degree of suggestibility.\n
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\n \n\n \n \n \n \n \n \n Catastrophizing and Risk-Taking.\n \n \n \n \n\n\n \n Pike, A. C.; Alves Anet, Á.; Peleg, N.; and Robinson, O. J.\n\n\n \n\n\n\n Computational Psychiatry, 7(1): 1. January 2023.\n \n\n\n\n
\n\n\n\n \n \n \"CatastrophizingPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n  \n \n 1 download\n \n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{pike_catastrophizing_2023,\n\ttitle = {Catastrophizing and {Risk}-{Taking}},\n\tvolume = {7},\n\tissn = {2379-6227},\n\turl = {https://cpsyjournal.org/article/10.5334/cpsy.91/},\n\tdoi = {10.5334/cpsy.91},\n\tabstract = {Background: Catastrophizing, when an individual overestimates the probability of a severe negative outcome, is related to various aspects of mental ill-health. Here, we further characterize catastrophizing by investigating the extent to which self-reported catastrophizing is associated with risk-taking, using an online behavioural task and computational modelling.\nMethods: We performed two online studies: a pilot study (n = 69) and a main study (n = 263). In the pilot study, participants performed the Balloon Analogue Risk Task (BART), alongside two other tasks (reported in the Supplement), and completed mental health questionnaires. Based on the findings from the pilot, we explored risk-taking in more detail in the main study using two versions of the Balloon Analogue Risk task (BART), with either a high or low cost for bursting the balloon.\nResults: In the main study, there was a significant negative relationship between selfreport catastrophizing scores and risk-taking in the low (but not high) cost version of the BART. Computational modelling of the BART task revealed no relationship between any parameter and Catastrophizing scores in either version of the task.\nConclusions: We show that increased self-reported catastrophizing may be associated with reduced behavioural measures of risk-taking, but were unable to identify a computational correlate of this effect.},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2023-12-21},\n\tjournal = {Computational Psychiatry},\n\tauthor = {Pike, Alexandra C. and Alves Anet, Ágatha and Peleg, Nina and Robinson, Oliver J.},\n\tmonth = jan,\n\tyear = {2023},\n\tpages = {1},\n}\n\n
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\n Background: Catastrophizing, when an individual overestimates the probability of a severe negative outcome, is related to various aspects of mental ill-health. Here, we further characterize catastrophizing by investigating the extent to which self-reported catastrophizing is associated with risk-taking, using an online behavioural task and computational modelling. Methods: We performed two online studies: a pilot study (n = 69) and a main study (n = 263). In the pilot study, participants performed the Balloon Analogue Risk Task (BART), alongside two other tasks (reported in the Supplement), and completed mental health questionnaires. Based on the findings from the pilot, we explored risk-taking in more detail in the main study using two versions of the Balloon Analogue Risk task (BART), with either a high or low cost for bursting the balloon. Results: In the main study, there was a significant negative relationship between selfreport catastrophizing scores and risk-taking in the low (but not high) cost version of the BART. Computational modelling of the BART task revealed no relationship between any parameter and Catastrophizing scores in either version of the task. Conclusions: We show that increased self-reported catastrophizing may be associated with reduced behavioural measures of risk-taking, but were unable to identify a computational correlate of this effect.\n
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\n \n\n \n \n \n \n \n \n Emotional bias training as a treatment for anxiety and depression: evidence from experimental medicine studies in healthy and medicated samples.\n \n \n \n \n\n\n \n Suddell, S.; Müller-Glodde, M.; Lumsden, J.; Looi, C. Y.; Granger, K.; Barnett, J. H.; Robinson, O. J.; Munafò, M. R.; and Penton-Voak, I. S.\n\n\n \n\n\n\n Psychological Medicine, 53(3): 696–705. February 2023.\n \n\n\n\n
\n\n\n\n \n \n \"EmotionalPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{suddell_emotional_2023,\n\ttitle = {Emotional bias training as a treatment for anxiety and depression: evidence from experimental medicine studies in healthy and medicated samples},\n\tvolume = {53},\n\tissn = {0033-2917, 1469-8978},\n\tshorttitle = {Emotional bias training as a treatment for anxiety and depression},\n\turl = {https://www.cambridge.org/core/product/identifier/S0033291721002014/type/journal_article},\n\tdoi = {10.1017/S0033291721002014},\n\tabstract = {Background. Anxiety and depression are leading causes of disability worldwide, yet individuals are often unable to access appropriate treatment. There is a need to develop effective interventions that can be delivered remotely. Previous research has suggested that emotional processing biases are a potential target for intervention, and these may be altered through brief training programs.\nMethods. We report two experimental medicine studies of emotional bias training in two samples: individuals from the general population (n = 522) and individuals currently taking antidepressants to treat anxiety or depression (n = 212). Participants, recruited online, completed four sessions of EBT from their own home. Mental health and cognitive functioning outcomes were assessed at baseline, immediately post-training, and at 2-week follow-up.\nResults. In both studies, our intervention successfully trained participants to perceive ambiguous social information more positively. This persisted at a 2-week follow-up. There was no clear evidence that this change in emotional processing transferred to improvements in symptoms in the primary analyses. However, in both studies, there was weak evidence for improved quality of life following EBT amongst individuals with more depressive symptoms at baseline. No clear evidence of transfer effects was observed for self-reported daily stress, anhedonia or depressive symptoms. Exploratory analyses suggested that younger participants reported greater treatment gains.\nConclusions. These studies demonstrate the effectiveness of delivering a multi-session online training program to promote lasting cognitive changes. Given the inconsistent evidence for transfer effects, EBT requires further development before it can be considered as a treatment for anxiety and depression.},\n\tlanguage = {en},\n\tnumber = {3},\n\turldate = {2023-12-21},\n\tjournal = {Psychological Medicine},\n\tauthor = {Suddell, Steph and Müller-Glodde, Maren and Lumsden, Jim and Looi, Chung Yen and Granger, Kiri and Barnett, Jennifer H. and Robinson, Oliver J. and Munafò, Marcus R. and Penton-Voak, Ian S.},\n\tmonth = feb,\n\tyear = {2023},\n\tpages = {696--705},\n}\n\n
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\n Background. Anxiety and depression are leading causes of disability worldwide, yet individuals are often unable to access appropriate treatment. There is a need to develop effective interventions that can be delivered remotely. Previous research has suggested that emotional processing biases are a potential target for intervention, and these may be altered through brief training programs. Methods. We report two experimental medicine studies of emotional bias training in two samples: individuals from the general population (n = 522) and individuals currently taking antidepressants to treat anxiety or depression (n = 212). Participants, recruited online, completed four sessions of EBT from their own home. Mental health and cognitive functioning outcomes were assessed at baseline, immediately post-training, and at 2-week follow-up. Results. In both studies, our intervention successfully trained participants to perceive ambiguous social information more positively. This persisted at a 2-week follow-up. There was no clear evidence that this change in emotional processing transferred to improvements in symptoms in the primary analyses. However, in both studies, there was weak evidence for improved quality of life following EBT amongst individuals with more depressive symptoms at baseline. No clear evidence of transfer effects was observed for self-reported daily stress, anhedonia or depressive symptoms. Exploratory analyses suggested that younger participants reported greater treatment gains. Conclusions. These studies demonstrate the effectiveness of delivering a multi-session online training program to promote lasting cognitive changes. Given the inconsistent evidence for transfer effects, EBT requires further development before it can be considered as a treatment for anxiety and depression.\n
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\n \n\n \n \n \n \n \n \n Approach-avoidance reinforcement learning as a translational and computational model of anxiety-related avoidance.\n \n \n \n \n\n\n \n Yamamori, Y.; Robinson, O. J; and Roiser, J. P\n\n\n \n\n\n\n eLife, 12: RP87720. November 2023.\n \n\n\n\n
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@article{yamamori_approach-avoidance_2023,\n\ttitle = {Approach-avoidance reinforcement learning as a translational and computational model of anxiety-related avoidance},\n\tvolume = {12},\n\tissn = {2050-084X},\n\turl = {https://elifesciences.org/articles/87720},\n\tdoi = {10.7554/eLife.87720},\n\tabstract = {Although avoidance is a prevalent feature of anxiety-r­elated psychopathology, differences in the measurement of avoidance between humans and non-h­ uman animals hinder our progress in its theoretical understanding and treatment. To address this, we developed a novel translational measure of anxiety-r­elated avoidance in the form of an approach-a­ voidance reinforcement learning task, by adapting a paradigm from the non-h­ uman animal literature to study the same cognitive processes in human participants. We used computational modelling to probe the putative cognitive mechanisms underlying approach-a­ voidance behaviour in this task and investigated how they relate to subjective task-i­nduced anxiety. In a large online study (n = 372), participants who experienced greater task-i­nduced anxiety avoided choices associated with punishment, even when this resulted in lower overall reward. Computational modelling revealed that this effect was explained by greater individual sensitivities to punishment relative to rewards. We replicated these findings in an independent sample (n = 627) and we also found fair-t­o-­ excellent reliability of measures of task performance in a sub-s­ ample retested 1 week later (n = 57). Our findings demonstrate the potential of approach-a­ voidance reinforcement learning tasks as translational and computational models of anxiety-r­elated avoidance. Future studies should assess the predictive validity of this approach in clinical samples and experimental manipulations of anxiety.},\n\tlanguage = {en},\n\turldate = {2023-12-21},\n\tjournal = {eLife},\n\tauthor = {Yamamori, Yumeya and Robinson, Oliver J and Roiser, Jonathan P},\n\tmonth = nov,\n\tyear = {2023},\n\tpages = {RP87720},\n}\n\n
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\n Although avoidance is a prevalent feature of anxiety-r­elated psychopathology, differences in the measurement of avoidance between humans and non-h­ uman animals hinder our progress in its theoretical understanding and treatment. To address this, we developed a novel translational measure of anxiety-r­elated avoidance in the form of an approach-a­ voidance reinforcement learning task, by adapting a paradigm from the non-h­ uman animal literature to study the same cognitive processes in human participants. We used computational modelling to probe the putative cognitive mechanisms underlying approach-a­ voidance behaviour in this task and investigated how they relate to subjective task-i­nduced anxiety. In a large online study (n = 372), participants who experienced greater task-i­nduced anxiety avoided choices associated with punishment, even when this resulted in lower overall reward. Computational modelling revealed that this effect was explained by greater individual sensitivities to punishment relative to rewards. We replicated these findings in an independent sample (n = 627) and we also found fair-t­o-­ excellent reliability of measures of task performance in a sub-s­ ample retested 1 week later (n = 57). Our findings demonstrate the potential of approach-a­ voidance reinforcement learning tasks as translational and computational models of anxiety-r­elated avoidance. Future studies should assess the predictive validity of this approach in clinical samples and experimental manipulations of anxiety.\n
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\n \n\n \n \n \n \n \n Computational perspectives on human fear and anxiety.\n \n \n \n\n\n \n Yamamori, Y.; and Robinson, O. J.\n\n\n \n\n\n\n Neuroscience and biobehavioral reviews, 144: 104959. January 2023.\n Place: United States\n\n\n\n
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@article{yamamori_computational_2023,\n\ttitle = {Computational perspectives on human fear and anxiety.},\n\tvolume = {144},\n\tcopyright = {Copyright © 2022 The Authors. Published by Elsevier Ltd.. All rights reserved.},\n\tissn = {1873-7528 0149-7634},\n\tdoi = {10.1016/j.neubiorev.2022.104959},\n\tabstract = {Fear and anxiety are adaptive emotions that serve important defensive functions, yet in excess, they can be debilitating and lead to poor mental health.  Computational modelling of behaviour provides a mechanistic framework for  understanding the cognitive and neurobiological bases of fear and anxiety, and  has seen increasing interest in the field. In this brief review, we discuss  recent developments in the computational modelling of human fear and anxiety.  Firstly, we describe various reinforcement learning strategies that humans employ  when learning to predict or avoid threat, and how these relate to symptoms of  fear and anxiety. Secondly, we discuss initial efforts to explore, through a  computational lens, approach-avoidance conflict paradigms that are popular in  animal research to measure fear- and anxiety-relevant behaviours. Finally, we  discuss negative biases in decision-making in the face of uncertainty in anxiety.},\n\tlanguage = {eng},\n\tjournal = {Neuroscience and biobehavioral reviews},\n\tauthor = {Yamamori, Yumeya and Robinson, Oliver J.},\n\tmonth = jan,\n\tyear = {2023},\n\tpmid = {36375584},\n\tnote = {Place: United States},\n\tkeywords = {*Anxiety/psychology, *Fear/psychology, Animals, Anxiety, Anxiety Disorders/psychology, Approach-avoidance conflict, Computational modelling, Decision-making, Fear, Generative models, Humans, Psychology, Reinforcement, Reinforcement learning, Reinforcement, Psychology, Uncertainty},\n\tpages = {104959},\n}\n\n
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\n Fear and anxiety are adaptive emotions that serve important defensive functions, yet in excess, they can be debilitating and lead to poor mental health. Computational modelling of behaviour provides a mechanistic framework for understanding the cognitive and neurobiological bases of fear and anxiety, and has seen increasing interest in the field. In this brief review, we discuss recent developments in the computational modelling of human fear and anxiety. Firstly, we describe various reinforcement learning strategies that humans employ when learning to predict or avoid threat, and how these relate to symptoms of fear and anxiety. Secondly, we discuss initial efforts to explore, through a computational lens, approach-avoidance conflict paradigms that are popular in animal research to measure fear- and anxiety-relevant behaviours. Finally, we discuss negative biases in decision-making in the face of uncertainty in anxiety.\n
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\n \n\n \n \n \n \n \n Measuring cognitive effort without difficulty.\n \n \n \n\n\n \n Fleming, H.; Robinson, O. J.; and Roiser, J. P.\n\n\n \n\n\n\n Cognitive, affective & behavioral neuroscience. February 2023.\n Place: United States\n\n\n\n
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@article{fleming_measuring_2023,\n\ttitle = {Measuring cognitive effort without difficulty.},\n\tcopyright = {© 2023. The Author(s).},\n\tissn = {1531-135X 1530-7026},\n\tdoi = {10.3758/s13415-023-01065-9},\n\tabstract = {An important finding in the cognitive effort literature has been that sensitivity to the costs of effort varies between individuals, suggesting that some people  find effort more aversive than others. It has been suggested this may explain  individual differences in other aspects of cognition; in particular that greater  effort sensitivity may underlie some of the symptoms of conditions such as  depression and schizophrenia. In this paper, we highlight a major problem with  existing measures of cognitive effort that hampers this line of research,  specifically the confounding of effort and difficulty. This means that behaviour  thought to reveal effort costs could equally be explained by cognitive capacity,  which influences the frequency of success and thereby the chance of obtaining  reward. To address this shortcoming, we introduce a new test, the Number  Switching Task (NST), specially designed such that difficulty will be unaffected  by the effort manipulation and can easily be standardised across participants. In  a large, online sample, we show that these criteria are met successfully and  reproduce classic effort discounting results with the NST. We also demonstrate  the use of Bayesian modelling with this task, producing behavioural parameters  which can be associated with other measures, and report a preliminary association  with the Need for Cognition scale.},\n\tlanguage = {eng},\n\tjournal = {Cognitive, affective \\& behavioral neuroscience},\n\tauthor = {Fleming, Hugo and Robinson, Oliver J. and Roiser, Jonathan P.},\n\tmonth = feb,\n\tyear = {2023},\n\tpmid = {36750498},\n\tnote = {Place: United States},\n\tkeywords = {Anhedonia, Cognitive effort, Computational psychiatry, Depression, Individual differences, New measures},\n}\n\n
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\n An important finding in the cognitive effort literature has been that sensitivity to the costs of effort varies between individuals, suggesting that some people find effort more aversive than others. It has been suggested this may explain individual differences in other aspects of cognition; in particular that greater effort sensitivity may underlie some of the symptoms of conditions such as depression and schizophrenia. In this paper, we highlight a major problem with existing measures of cognitive effort that hampers this line of research, specifically the confounding of effort and difficulty. This means that behaviour thought to reveal effort costs could equally be explained by cognitive capacity, which influences the frequency of success and thereby the chance of obtaining reward. To address this shortcoming, we introduce a new test, the Number Switching Task (NST), specially designed such that difficulty will be unaffected by the effort manipulation and can easily be standardised across participants. In a large, online sample, we show that these criteria are met successfully and reproduce classic effort discounting results with the NST. We also demonstrate the use of Bayesian modelling with this task, producing behavioural parameters which can be associated with other measures, and report a preliminary association with the Need for Cognition scale.\n
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\n \n\n \n \n \n \n \n \n Efficacy of attention bias modification via smartphones in a large population sample.\n \n \n \n \n\n\n \n Chelliah, A.; and Robinson, O.\n\n\n \n\n\n\n Royal Society Open Science, 9(8): 211629. August 2022.\n \n\n\n\n
\n\n\n\n \n \n \"EfficacyPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n  \n \n 1 download\n \n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{chelliah_efficacy_2022,\n\ttitle = {Efficacy of attention bias modification via smartphones in a large population sample},\n\tvolume = {9},\n\tissn = {2054-5703},\n\turl = {https://royalsocietypublishing.org/doi/10.1098/rsos.211629},\n\tdoi = {10.1098/rsos.211629},\n\tabstract = {Negative affective biases are a key feature of anxiety and depression that uphold and promote negative mood. Bias modification aims to reduce these biases using computerized training, but shows mixed success and has not been tested at scale. The aim was to determine whether bias modification delivered via smartphones can improve mood in a large sample. In total, 153 385 self-referring participants were randomly assigned to modification or sham bias training on a dot-probe or visual-search task. The primary outcome of interest was balance of mood, assessed on the Positive and Negative Affect Schedule. In total, 22 933 participants who provided at least two mood ratings were included in analyses. There was a large amount of participant attrition. In the remaining smaller sample, results supported the prediction that visual-search modification would result in improved mood (95\\%CI [0.10, 0.82];\n              p\n              = 0.01,\n              d\n              = 0.05,\n              N\n              = 2588 after two ratings; 95\\%CI [1.75,6.54];\n              p\n              = 0.001,\n              d\n              = 0.32,\n              N\n              = 118 after six ratings), which was not seen for the sham version (\n              N\n              = 4818 after two ratings;\n              N\n              = 138 after six ratings). Dot-probe modification was not associated with mood improvements (\n              p\n              = 0.52). Visual-search, but not dot-probe, bias modification slightly but significantly improved mood. Although this effect size is very small and subject to large participant drop-off, it might be worth considering an adjunct to current treatments.},\n\tlanguage = {en},\n\tnumber = {8},\n\turldate = {2023-12-21},\n\tjournal = {Royal Society Open Science},\n\tauthor = {Chelliah, Alysha and Robinson, Oliver},\n\tmonth = aug,\n\tyear = {2022},\n\tpages = {211629},\n}\n\n
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\n Negative affective biases are a key feature of anxiety and depression that uphold and promote negative mood. Bias modification aims to reduce these biases using computerized training, but shows mixed success and has not been tested at scale. The aim was to determine whether bias modification delivered via smartphones can improve mood in a large sample. In total, 153 385 self-referring participants were randomly assigned to modification or sham bias training on a dot-probe or visual-search task. The primary outcome of interest was balance of mood, assessed on the Positive and Negative Affect Schedule. In total, 22 933 participants who provided at least two mood ratings were included in analyses. There was a large amount of participant attrition. In the remaining smaller sample, results supported the prediction that visual-search modification would result in improved mood (95%CI [0.10, 0.82]; p = 0.01, d = 0.05, N = 2588 after two ratings; 95%CI [1.75,6.54]; p = 0.001, d = 0.32, N = 118 after six ratings), which was not seen for the sham version ( N = 4818 after two ratings; N = 138 after six ratings). Dot-probe modification was not associated with mood improvements ( p = 0.52). Visual-search, but not dot-probe, bias modification slightly but significantly improved mood. Although this effect size is very small and subject to large participant drop-off, it might be worth considering an adjunct to current treatments.\n
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\n \n\n \n \n \n \n \n Identifying Transdiagnostic Mechanisms in Mental Health Using Computational Factor Modeling.\n \n \n \n\n\n \n Wise, T.; Robinson, O. J.; and Gillan, C. M.\n\n\n \n\n\n\n Biological psychiatry,S0006–3223(22)01661–4. October 2022.\n Place: United States\n\n\n\n
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@article{wise_identifying_2022,\n\ttitle = {Identifying {Transdiagnostic} {Mechanisms} in {Mental} {Health} {Using} {Computational} {Factor} {Modeling}.},\n\tcopyright = {Copyright © 2022 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved.},\n\tissn = {1873-2402 0006-3223},\n\tdoi = {10.1016/j.biopsych.2022.09.034},\n\tabstract = {Most psychiatric disorders do not occur in isolation, and most psychiatric symptom dimensions are not uniquely expressed within a single diagnostic  category. Current treatments fail to work for around 25\\% to 40\\% of individuals,  perhaps due at least in part to an overreliance on diagnostic categories in  treatment development and allocation. In this review, we describe ongoing efforts  in the field to surmount these challenges and precisely characterize psychiatric  symptom dimensions using large-scale studies of unselected samples via remote,  online, and "citizen science" efforts that take a dimensional, mechanistic  approach. We discuss the importance that efforts to identify meaningful  psychiatric dimensions be coupled with careful computational modeling to formally  specify, test, and potentially falsify candidate mechanisms that underlie  transdiagnostic symptom dimensions. We refer to this approach, i.e., where  symptom dimensions are identified and validated against computationally  well-defined neurocognitive processes, as computational factor modeling. We  describe in detail some recent applications of this method to understand  transdiagnostic cognitive processes that include model-based planning,  metacognition, appetitive processing, and uncertainty estimation. In this  context, we highlight how computational factor modeling has been used to identify  specific associations between cognition and symptom dimensions and reveal  previously obscured relationships, how findings generalize to smaller in-person  clinical and nonclinical samples, and how the method is being adapted and  optimized beyond its original instantiation. Crucially, we discuss next steps for  this area of research, highlighting the value of more direct investigations of  treatment response that bridge the gap between basic research and the clinic.},\n\tlanguage = {eng},\n\tjournal = {Biological psychiatry},\n\tauthor = {Wise, Toby and Robinson, Oliver J. and Gillan, Claire M.},\n\tmonth = oct,\n\tyear = {2022},\n\tpmid = {36725393},\n\tnote = {Place: United States},\n\tkeywords = {Cognition, Computational factor modeling, Computational modeling, Factor analysis, RDoC, Transdiagnostic},\n\tpages = {S0006--3223(22)01661--4},\n}\n\n
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\n Most psychiatric disorders do not occur in isolation, and most psychiatric symptom dimensions are not uniquely expressed within a single diagnostic category. Current treatments fail to work for around 25% to 40% of individuals, perhaps due at least in part to an overreliance on diagnostic categories in treatment development and allocation. In this review, we describe ongoing efforts in the field to surmount these challenges and precisely characterize psychiatric symptom dimensions using large-scale studies of unselected samples via remote, online, and \"citizen science\" efforts that take a dimensional, mechanistic approach. We discuss the importance that efforts to identify meaningful psychiatric dimensions be coupled with careful computational modeling to formally specify, test, and potentially falsify candidate mechanisms that underlie transdiagnostic symptom dimensions. We refer to this approach, i.e., where symptom dimensions are identified and validated against computationally well-defined neurocognitive processes, as computational factor modeling. We describe in detail some recent applications of this method to understand transdiagnostic cognitive processes that include model-based planning, metacognition, appetitive processing, and uncertainty estimation. In this context, we highlight how computational factor modeling has been used to identify specific associations between cognition and symptom dimensions and reveal previously obscured relationships, how findings generalize to smaller in-person clinical and nonclinical samples, and how the method is being adapted and optimized beyond its original instantiation. Crucially, we discuss next steps for this area of research, highlighting the value of more direct investigations of treatment response that bridge the gap between basic research and the clinic.\n
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\n \n\n \n \n \n \n \n EJN stress, brain and behaviour special issue.\n \n \n \n\n\n \n Schmidt, M. V.; Robinson, O. J.; and Sandi, C.\n\n\n \n\n\n\n The European journal of neuroscience, 55(9-10): 2053–2057. May 2022.\n Place: France\n\n\n\n
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@article{schmidt_ejn_2022,\n\ttitle = {{EJN} stress, brain and behaviour special issue.},\n\tvolume = {55},\n\tcopyright = {All rights reserved},\n\tissn = {1460-9568 0953-816X},\n\tdoi = {10.1111/ejn.15718},\n\tlanguage = {eng},\n\tnumber = {9-10},\n\tjournal = {The European journal of neuroscience},\n\tauthor = {Schmidt, Mathias V. and Robinson, Oliver J. and Sandi, Carmen},\n\tmonth = may,\n\tyear = {2022},\n\tpmid = {35569819},\n\tnote = {Place: France},\n\tkeywords = {*Brain, *Head},\n\tpages = {2053--2057},\n}\n\n
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\n \n\n \n \n \n \n \n \n Reinforcement Learning in Patients With Mood and Anxiety Disorders vs Control Individuals: A Systematic Review and Meta-analysis.\n \n \n \n \n\n\n \n Pike, A. C.; and Robinson, O. J.\n\n\n \n\n\n\n JAMA Psychiatry, 79(4): 313–322. April 2022.\n \n\n\n\n
\n\n\n\n \n \n \"ReinforcementPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n  \n \n 9 downloads\n \n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n
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@article{pike_reinforcement_2022,\n\ttitle = {Reinforcement {Learning} in {Patients} {With} {Mood} and {Anxiety} {Disorders} vs {Control} {Individuals}: {A} {Systematic} {Review} and {Meta}-analysis},\n\tvolume = {79},\n\tcopyright = {All rights reserved},\n\tissn = {2168-622X},\n\tshorttitle = {Reinforcement {Learning} in {Patients} {With} {Mood} and {Anxiety} {Disorders} vs {Control} {Individuals}},\n\turl = {https://doi.org/10.1001/jamapsychiatry.2022.0051},\n\tdoi = {10.1001/jamapsychiatry.2022.0051},\n\tabstract = {Computational psychiatry studies have investigated how reinforcement learning may be different in individuals with mood and anxiety disorders compared with control individuals, but results are inconsistent.To assess whether there are consistent differences in reinforcement-learning parameters between patients with depression or anxiety and control individuals.Web of Knowledge, PubMed, Embase, and Google Scholar searches were performed between November 15, 2019, and December 6, 2019, and repeated on December 3, 2020, and February 23, 2021, with keywords (reinforcement learning) AND (computational OR model) AND (depression OR anxiety OR mood).Studies were included if they fit reinforcement-learning models to human choice data from a cognitive task with rewards or punishments, had a case-control design including participants with mood and/or anxiety disorders and healthy control individuals, and included sufficient information about all parameters in the models.Articles were assessed for inclusion according to MOOSE guidelines. Participant-level parameters were extracted from included articles, and a conventional meta-analysis was performed using a random-effects model. Subsequently, these parameters were used to simulate choice performance for each participant on benchmarking tasks in a simulation meta-analysis. Models were fitted, parameters were extracted using bayesian model averaging, and differences between patients and control individuals were examined. Overall effect sizes across analytic strategies were inspected.The primary outcomes were estimated reinforcement-learning parameters (learning rate, inverse temperature, reward learning rate, and punishment learning rate).A total of 27 articles were included (3085 participants, 1242 of whom had depression and/or anxiety). In the conventional meta-analysis, patients showed lower inverse temperature than control individuals (standardized mean difference [SMD], −0.215; 95\\% CI, −0.354 to −0.077), although no parameters were common across all studies, limiting the ability to infer differences. In the simulation meta-analysis, patients showed greater punishment learning rates (SMD, 0.107; 95\\% CI, 0.107 to 0.108) and slightly lower reward learning rates (SMD, −0.021; 95\\% CI, −0.022 to −0.020) relative to control individuals. The simulation meta-analysis showed no meaningful difference in inverse temperature between patients and control individuals (SMD, 0.003; 95\\% CI, 0.002 to 0.004).The simulation meta-analytic approach introduced in this article for inferring meta-group differences from heterogeneous computational psychiatry studies indicated elevated punishment learning rates in patients compared with control individuals. This difference may promote and uphold negative affective bias symptoms and hence constitute a potential mechanistic treatment target for mood and anxiety disorders.},\n\tnumber = {4},\n\turldate = {2022-08-02},\n\tjournal = {JAMA Psychiatry},\n\tauthor = {Pike, Alexandra C. and Robinson, Oliver J.},\n\tmonth = apr,\n\tyear = {2022},\n\tkeywords = {*Anxiety Disorders/diagnosis/therapy, *Anxiety/therapy, Affect, Bayes Theorem, Humans, Reward},\n\tpages = {313--322},\n}\n\n
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\n Computational psychiatry studies have investigated how reinforcement learning may be different in individuals with mood and anxiety disorders compared with control individuals, but results are inconsistent.To assess whether there are consistent differences in reinforcement-learning parameters between patients with depression or anxiety and control individuals.Web of Knowledge, PubMed, Embase, and Google Scholar searches were performed between November 15, 2019, and December 6, 2019, and repeated on December 3, 2020, and February 23, 2021, with keywords (reinforcement learning) AND (computational OR model) AND (depression OR anxiety OR mood).Studies were included if they fit reinforcement-learning models to human choice data from a cognitive task with rewards or punishments, had a case-control design including participants with mood and/or anxiety disorders and healthy control individuals, and included sufficient information about all parameters in the models.Articles were assessed for inclusion according to MOOSE guidelines. Participant-level parameters were extracted from included articles, and a conventional meta-analysis was performed using a random-effects model. Subsequently, these parameters were used to simulate choice performance for each participant on benchmarking tasks in a simulation meta-analysis. Models were fitted, parameters were extracted using bayesian model averaging, and differences between patients and control individuals were examined. Overall effect sizes across analytic strategies were inspected.The primary outcomes were estimated reinforcement-learning parameters (learning rate, inverse temperature, reward learning rate, and punishment learning rate).A total of 27 articles were included (3085 participants, 1242 of whom had depression and/or anxiety). In the conventional meta-analysis, patients showed lower inverse temperature than control individuals (standardized mean difference [SMD], −0.215; 95% CI, −0.354 to −0.077), although no parameters were common across all studies, limiting the ability to infer differences. In the simulation meta-analysis, patients showed greater punishment learning rates (SMD, 0.107; 95% CI, 0.107 to 0.108) and slightly lower reward learning rates (SMD, −0.021; 95% CI, −0.022 to −0.020) relative to control individuals. The simulation meta-analysis showed no meaningful difference in inverse temperature between patients and control individuals (SMD, 0.003; 95% CI, 0.002 to 0.004).The simulation meta-analytic approach introduced in this article for inferring meta-group differences from heterogeneous computational psychiatry studies indicated elevated punishment learning rates in patients compared with control individuals. This difference may promote and uphold negative affective bias symptoms and hence constitute a potential mechanistic treatment target for mood and anxiety disorders.\n
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\n \n\n \n \n \n \n \n Anxiety and amygdala connectivity during movie-watching.\n \n \n \n\n\n \n Kirk, P. A.; Robinson, O. J.; and Skipper, J. I.\n\n\n \n\n\n\n Neuropsychologia, 169: 108194. May 2022.\n \n\n\n\n
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@article{kirk_anxiety_2022,\n\ttitle = {Anxiety and amygdala connectivity during movie-watching},\n\tvolume = {169},\n\tcopyright = {All rights reserved},\n\tissn = {1873-3514},\n\tdoi = {10.1016/j.neuropsychologia.2022.108194},\n\tabstract = {Rodent and human studies have implicated an amygdala-prefrontal circuit during threat processing. One possibility is that while amygdala activity underlies core features of anxiety (e.g. detection of salient information), prefrontal cortices (i.e. dorsomedial prefrontal/anterior cingulate cortex) entrain its responsiveness. To date, this has been established in tightly controlled paradigms (predominantly using static face perception tasks) but has not been extended to more naturalistic settings. Consequently, using 'movie fMRI'-in which participants watch ecologically-rich movie stimuli rather than constrained cognitive tasks-we sought to test whether individual differences in anxiety correlate with the degree of face-dependent amygdala-prefrontal coupling in two independent samples. Analyses suggested increased face-dependent superior parietal activation and decreased speech-dependent auditory cortex activation as a function of anxiety. However, we failed to find evidence for anxiety-dependent connectivity, neither in our stimulus-dependent or -independent analyses. Our findings suggest that work using experimentally constrained tasks may not replicate in more ecologically valid settings and, moreover, highlight the importance of testing the generalizability of neuroimaging findings outside of the original context.},\n\tlanguage = {eng},\n\tjournal = {Neuropsychologia},\n\tauthor = {Kirk, Peter A. and Robinson, Oliver J. and Skipper, Jeremy I.},\n\tmonth = may,\n\tyear = {2022},\n\tpmid = {35245529},\n\tpmcid = {PMC8987737},\n\tkeywords = {*Amygdala/diagnostic imaging, *Motion Pictures, Amygdala, Anxiety, Anxiety Disorders, Anxiety/diagnostic imaging, Humans, Magnetic Resonance Imaging, Magnetic Resonance Imaging/methods, Motion Pictures, Naturalistic, Neural Pathways, Neural Pathways/diagnostic imaging, Prefrontal Cortex, fMRI},\n\tpages = {108194},\n}\n\n
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\n Rodent and human studies have implicated an amygdala-prefrontal circuit during threat processing. One possibility is that while amygdala activity underlies core features of anxiety (e.g. detection of salient information), prefrontal cortices (i.e. dorsomedial prefrontal/anterior cingulate cortex) entrain its responsiveness. To date, this has been established in tightly controlled paradigms (predominantly using static face perception tasks) but has not been extended to more naturalistic settings. Consequently, using 'movie fMRI'-in which participants watch ecologically-rich movie stimuli rather than constrained cognitive tasks-we sought to test whether individual differences in anxiety correlate with the degree of face-dependent amygdala-prefrontal coupling in two independent samples. Analyses suggested increased face-dependent superior parietal activation and decreased speech-dependent auditory cortex activation as a function of anxiety. However, we failed to find evidence for anxiety-dependent connectivity, neither in our stimulus-dependent or -independent analyses. Our findings suggest that work using experimentally constrained tasks may not replicate in more ecologically valid settings and, moreover, highlight the importance of testing the generalizability of neuroimaging findings outside of the original context.\n
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\n \n\n \n \n \n \n \n Threat vigilance and intrinsic amygdala connectivity.\n \n \n \n\n\n \n Kirk, P. A.; Holmes, A. J.; and Robinson, O. J.\n\n\n \n\n\n\n Human Brain Mapping, 43(10): 3283–3292. July 2022.\n \n\n\n\n
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@article{kirk_threat_2022,\n\ttitle = {Threat vigilance and intrinsic amygdala connectivity},\n\tvolume = {43},\n\tcopyright = {All rights reserved},\n\tissn = {1097-0193},\n\tdoi = {10.1002/hbm.25851},\n\tabstract = {A well-documented amygdala-dorsomedial prefrontal circuit is theorized to promote attention to threat ("threat vigilance"). Prior research has implicated a relationship between individual differences in trait anxiety/vigilance, engagement of this circuitry, and anxiogenic features of the environment (e.g., through threat-of-shock and movie-watching). In the present study, we predicted that-for those scoring high in self-reported anxiety and a behavioral measure of threat vigilance-this circuitry is chronically engaged, even in the absence of anxiogenic stimuli. Our analyses of resting-state fMRI data (N = 639) did not, however, provide evidence for such a relationship. Nevertheless, in our planned exploratory analyses, we saw a relationship between threat vigilance behavior (but not self-reported anxiety) and intrinsic amygdala-periaqueductal gray connectivity. Here, we suggest this subcortical circuitry may be chronically engaged in hypervigilant individuals, but that amygdala-prefrontal circuitry may only be engaged in response to anxiogenic stimuli.},\n\tlanguage = {eng},\n\tnumber = {10},\n\tjournal = {Human Brain Mapping},\n\tauthor = {Kirk, Peter A. and Holmes, Avram J. and Robinson, Oliver J.},\n\tmonth = jul,\n\tyear = {2022},\n\tpmid = {35362645},\n\tpmcid = {PMC9188965},\n\tkeywords = {*Amygdala/diagnostic imaging, *Fear/physiology, Amygdala, Anxiety, Anxiety Disorders, Anxiety/diagnostic imaging, Fear, Humans, Individuality, Magnetic Resonance Imaging, Prefrontal Cortex, Prefrontal Cortex/diagnostic imaging, amygdala, anxiety, fMRI, subcortex},\n\tpages = {3283--3292},\n}\n\n
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\n A well-documented amygdala-dorsomedial prefrontal circuit is theorized to promote attention to threat (\"threat vigilance\"). Prior research has implicated a relationship between individual differences in trait anxiety/vigilance, engagement of this circuitry, and anxiogenic features of the environment (e.g., through threat-of-shock and movie-watching). In the present study, we predicted that-for those scoring high in self-reported anxiety and a behavioral measure of threat vigilance-this circuitry is chronically engaged, even in the absence of anxiogenic stimuli. Our analyses of resting-state fMRI data (N = 639) did not, however, provide evidence for such a relationship. Nevertheless, in our planned exploratory analyses, we saw a relationship between threat vigilance behavior (but not self-reported anxiety) and intrinsic amygdala-periaqueductal gray connectivity. Here, we suggest this subcortical circuitry may be chronically engaged in hypervigilant individuals, but that amygdala-prefrontal circuitry may only be engaged in response to anxiogenic stimuli.\n
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\n \n\n \n \n \n \n \n RapidHRV: an open-source toolbox for extracting heart rate and heart rate variability.\n \n \n \n\n\n \n Kirk, P. A.; Davidson Bryan, A.; Garfinkel, S. N.; and Robinson, O. J.\n\n\n \n\n\n\n PeerJ, 10: e13147. 2022.\n Place: United States\n\n\n\n
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@article{kirk_rapidhrv_2022,\n\ttitle = {{RapidHRV}: an open-source toolbox for extracting heart rate and heart rate variability.},\n\tvolume = {10},\n\tcopyright = {© 2022 Kirk et al.},\n\tissn = {2167-8359},\n\tdoi = {10.7717/peerj.13147},\n\tabstract = {Heart rate and heart rate variability have enabled insight into a myriad of psychophysiological phenomena. There is now an influx of research attempting  using these metrics within both laboratory settings (typically derived through  electrocardiography or pulse oximetry) and ecologically-rich contexts (via  wearable photoplethysmography, i.e., smartwatches). However, these signals can be  prone to artifacts and a low signal to noise ratio, which traditionally are  detected and removed through visual inspection. Here, we developed an open-source  Python package, RapidHRV, dedicated to the preprocessing, analysis, and  visualization of heart rate and heart rate variability. Each of these modules can  be executed with one line of code and includes automated cleaning. In simulated  data, RapidHRV demonstrated excellent recovery of heart rate across most levels  of noise ({\\textgreater}=10 dB) and moderate-to-excellent recovery of heart rate variability  even at relatively low signal to noise ratios ({\\textgreater}=20 dB) and sampling rates ({\\textgreater}=20  Hz). Validation in real datasets shows good-to-excellent recovery of heart rate  and heart rate variability in electrocardiography and finger photoplethysmography  recordings. Validation in wrist photoplethysmography demonstrated RapidHRV  estimations were sensitive to heart rate and its variability under low motion  conditions, but estimates were less stable under higher movement settings.},\n\tlanguage = {eng},\n\tjournal = {PeerJ},\n\tauthor = {Kirk, Peter A. and Davidson Bryan, Alexander and Garfinkel, Sarah N. and Robinson, Oliver J.},\n\tyear = {2022},\n\tpmid = {35345583},\n\tpmcid = {PMC8957280},\n\tnote = {Place: United States},\n\tkeywords = {*Algorithms, *Electrocardiography, Heart Rate/physiology, Heart rate variability, Photoplethysmography, Python, Remote sensing, Toolbox, Wrist},\n\tpages = {e13147},\n}\n\n
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\n Heart rate and heart rate variability have enabled insight into a myriad of psychophysiological phenomena. There is now an influx of research attempting using these metrics within both laboratory settings (typically derived through electrocardiography or pulse oximetry) and ecologically-rich contexts (via wearable photoplethysmography, i.e., smartwatches). However, these signals can be prone to artifacts and a low signal to noise ratio, which traditionally are detected and removed through visual inspection. Here, we developed an open-source Python package, RapidHRV, dedicated to the preprocessing, analysis, and visualization of heart rate and heart rate variability. Each of these modules can be executed with one line of code and includes automated cleaning. In simulated data, RapidHRV demonstrated excellent recovery of heart rate across most levels of noise (\\textgreater=10 dB) and moderate-to-excellent recovery of heart rate variability even at relatively low signal to noise ratios (\\textgreater=20 dB) and sampling rates (\\textgreater=20 Hz). Validation in real datasets shows good-to-excellent recovery of heart rate and heart rate variability in electrocardiography and finger photoplethysmography recordings. Validation in wrist photoplethysmography demonstrated RapidHRV estimations were sensitive to heart rate and its variability under low motion conditions, but estimates were less stable under higher movement settings.\n
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\n \n\n \n \n \n \n \n \n Association Between a Directly Translated Cognitive Measure of Negative Bias and Self-reported Psychiatric Symptoms.\n \n \n \n \n\n\n \n Daniel-Watanabe, L.; McLaughlin, M.; Gormley, S.; and Robinson, O. J.\n\n\n \n\n\n\n Biological Psychiatry: Cognitive Neuroscience and Neuroimaging, 7(2): 201–209. February 2022.\n \n\n\n\n
\n\n\n\n \n \n \"AssociationPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n  \n \n 2 downloads\n \n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n
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@article{daniel-watanabe_association_2022,\n\ttitle = {Association {Between} a {Directly} {Translated} {Cognitive} {Measure} of {Negative} {Bias} and {Self}-reported {Psychiatric} {Symptoms}},\n\tvolume = {7},\n\tcopyright = {All rights reserved},\n\tissn = {2451-9022},\n\turl = {https://www.sciencedirect.com/science/article/pii/S2451902220300537},\n\tdoi = {10.1016/j.bpsc.2020.02.010},\n\tabstract = {Background\nNegative interpretation biases are thought to be core symptoms of mood and anxiety disorders. However, prior work using cognitive tasks to measure such biases is largely restricted to case-control group studies, which cannot be used for inference about individuals without considerable additional validation. Moreover, very few measures are fully translational (i.e., can be used across animals and humans in treatment-development pipelines). This investigation aimed to produce the first measure of negative cognitive biases that is both translational and sensitive to individual differences, and then to determine which specific self-reported psychiatric symptoms are related to bias.\nMethods\nA total of 1060 (n = 990 complete) participants performed a cognitive task of negative bias along with psychiatric symptom questionnaires. We tested the hypothesis that individual levels of mood and anxiety disorder symptomatology would covary positively with negative bias on the cognitive task using a combination of computational modeling of behavior, confirmatory factor analysis, exploratory factor analysis, and structural equation modeling.\nResults\nParticipants with higher depression symptoms (β = −0.16, p = .017) who were older (β = −0.11, p = .001) and had lower IQ (β = 0.14, p {\\textless} .001) showed greater negative bias. Confirmatory factor analysis and structural equation modeling suggested that no other psychiatric symptom (or transdiagnostic latent factor) covaried with task performance over and above the effect of depression, while exploratory factor analysis suggested combining depression/anxiety symptoms in a single latent factor. Generating groups using symptom cutoffs or latent mixture modeling recapitulated our prior case-control findings.\nConclusions\nThis measure, which uniquely spans both the clinical group-to-individual and preclinical animal-to-human generalizability gaps, can be used to measure individual differences in depression vulnerability for translational treatment-development pipelines.},\n\tlanguage = {en},\n\tnumber = {2},\n\turldate = {2022-09-01},\n\tjournal = {Biological Psychiatry: Cognitive Neuroscience and Neuroimaging},\n\tauthor = {Daniel-Watanabe, Lucie and McLaughlin, Martha and Gormley, Siobhan and Robinson, Oliver J.},\n\tmonth = feb,\n\tyear = {2022},\n\tkeywords = {*Affect, *Anxiety Disorders, Animals, Anxiety, Bias, Cognition, Computational psychiatry, Depression, Humans, Individual differences, Negative affective bias, Online testing, Self Report, Structural equation modeling},\n\tpages = {201--209},\n}\n\n
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\n Background Negative interpretation biases are thought to be core symptoms of mood and anxiety disorders. However, prior work using cognitive tasks to measure such biases is largely restricted to case-control group studies, which cannot be used for inference about individuals without considerable additional validation. Moreover, very few measures are fully translational (i.e., can be used across animals and humans in treatment-development pipelines). This investigation aimed to produce the first measure of negative cognitive biases that is both translational and sensitive to individual differences, and then to determine which specific self-reported psychiatric symptoms are related to bias. Methods A total of 1060 (n = 990 complete) participants performed a cognitive task of negative bias along with psychiatric symptom questionnaires. We tested the hypothesis that individual levels of mood and anxiety disorder symptomatology would covary positively with negative bias on the cognitive task using a combination of computational modeling of behavior, confirmatory factor analysis, exploratory factor analysis, and structural equation modeling. Results Participants with higher depression symptoms (β = −0.16, p = .017) who were older (β = −0.11, p = .001) and had lower IQ (β = 0.14, p \\textless .001) showed greater negative bias. Confirmatory factor analysis and structural equation modeling suggested that no other psychiatric symptom (or transdiagnostic latent factor) covaried with task performance over and above the effect of depression, while exploratory factor analysis suggested combining depression/anxiety symptoms in a single latent factor. Generating groups using symptom cutoffs or latent mixture modeling recapitulated our prior case-control findings. Conclusions This measure, which uniquely spans both the clinical group-to-individual and preclinical animal-to-human generalizability gaps, can be used to measure individual differences in depression vulnerability for translational treatment-development pipelines.\n
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\n \n\n \n \n \n \n \n \n Efficacy of attention bias modification via smartphones in a large population sample.\n \n \n \n \n\n\n \n Chelliah, A.; and Robinson, O.\n\n\n \n\n\n\n Royal Society Open Science, 9(8): 211629. August 2022.\n Publisher: Royal Society\n\n\n\n
\n\n\n\n \n \n \"EfficacyPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n  \n \n 1 download\n \n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n
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@article{chelliah_efficacy_2022-1,\n\ttitle = {Efficacy of attention bias modification via smartphones in a large population sample},\n\tvolume = {9},\n\tcopyright = {All rights reserved},\n\turl = {https://royalsocietypublishing.org/doi/full/10.1098/rsos.211629},\n\tdoi = {10.1098/rsos.211629},\n\tabstract = {Negative affective biases are a key feature of anxiety and depression that uphold and promote negative mood. Bias modification aims to reduce these biases using computerized training, but shows mixed success and has not been tested at scale. The aim was to determine whether bias modification delivered via smartphones can improve mood in a large sample. In total, 153 385 self-referring participants were randomly assigned to modification or sham bias training on a dot-probe or visual-search task. The primary outcome of interest was balance of mood, assessed on the Positive and Negative Affect Schedule. In total, 22 933 participants who provided at least two mood ratings were included in analyses. There was a large amount of participant attrition. In the remaining smaller sample, results supported the prediction that visual-search modification would result in improved mood (95\\%CI [0.10, 0.82]; p = 0.01, d = 0.05, N = 2588 after two ratings; 95\\%CI [1.75,6.54]; p = 0.001, d = 0.32, N = 118 after six ratings), which was not seen for the sham version (N = 4818 after two ratings; N = 138 after six ratings). Dot-probe modification was not associated with mood improvements (p = 0.52). Visual-search, but not dot-probe, bias modification slightly but significantly improved mood. Although this effect size is very small and subject to large participant drop-off, it might be worth considering an adjunct to current treatments.},\n\tnumber = {8},\n\turldate = {2023-02-17},\n\tjournal = {Royal Society Open Science},\n\tauthor = {Chelliah, Alysha and Robinson, Oliver},\n\tmonth = aug,\n\tyear = {2022},\n\tnote = {Publisher: Royal Society},\n\tkeywords = {affective bias modification, effectiveness research, mood, mood disorders, negative affective bias, prevention},\n\tpages = {211629},\n}\n\n
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\n Negative affective biases are a key feature of anxiety and depression that uphold and promote negative mood. Bias modification aims to reduce these biases using computerized training, but shows mixed success and has not been tested at scale. The aim was to determine whether bias modification delivered via smartphones can improve mood in a large sample. In total, 153 385 self-referring participants were randomly assigned to modification or sham bias training on a dot-probe or visual-search task. The primary outcome of interest was balance of mood, assessed on the Positive and Negative Affect Schedule. In total, 22 933 participants who provided at least two mood ratings were included in analyses. There was a large amount of participant attrition. In the remaining smaller sample, results supported the prediction that visual-search modification would result in improved mood (95%CI [0.10, 0.82]; p = 0.01, d = 0.05, N = 2588 after two ratings; 95%CI [1.75,6.54]; p = 0.001, d = 0.32, N = 118 after six ratings), which was not seen for the sham version (N = 4818 after two ratings; N = 138 after six ratings). Dot-probe modification was not associated with mood improvements (p = 0.52). Visual-search, but not dot-probe, bias modification slightly but significantly improved mood. Although this effect size is very small and subject to large participant drop-off, it might be worth considering an adjunct to current treatments.\n
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\n \n\n \n \n \n \n \n Threat of shock promotes passive avoidance, but not active avoidance.\n \n \n \n\n\n \n Binti Affandi, A. H.; Pike, A. C.; and Robinson, O. J.\n\n\n \n\n\n\n The European journal of neuroscience, 55(9-10): 2571–2580. May 2022.\n Place: France\n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n
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@article{binti_affandi_threat_2022,\n\ttitle = {Threat of shock promotes passive avoidance, but not active avoidance.},\n\tvolume = {55},\n\tcopyright = {© 2021 The Authors. European Journal of Neuroscience published by Federation of European Neuroscience Societies and John Wiley \\& Sons Ltd.},\n\tissn = {1460-9568 0953-816X},\n\tdoi = {10.1111/ejn.15184},\n\tabstract = {Anxiety and stress are adaptive responses to threat that promote harm avoidance. In particular, prior work has shown that anxiety induced in humans using threat  of unpredictable shock promotes behavioral inhibition in the face of harm. This  is consistent with the idea that anxiety promotes passive avoidance-that is,  withholding approach actions that could lead to harm. However, harm can also be  avoided through active avoidance, where a (withdrawal) action is taken to avoid  harm. Here, we provide the first direct within-study comparison of the effects of  threat of shock on active and passive avoidance. We operationalize passive  avoidance as withholding a button press response in the face of negative  outcomes, and active avoidance as lifting/releasing a button press in the face of  negative outcomes. We explore the impact of threat of unpredictable shock on the  learning of these behavioral responses (alongside matched responses to rewards)  within a single cognitive task. We predicted that threat of shock would promote  both active and passive avoidance, and that this would be driven by increased  reliance on Pavlovian bias, as parameterized within reinforcement-learning  models. Consistent with our predictions, we provide evidence that threat of shock  promotes passive avoidance as conceptualized by our task. However, inconsistent  with predictions, we found no evidence that threat of shock promoted active  avoidance, nor evidence of elevated Pavlovian bias in any condition. One  hypothetical framework with which to understand these findings is that anxiety  promotes passive over active harm avoidance strategies in order to conserve  energy while avoiding harm.},\n\tlanguage = {eng},\n\tnumber = {9-10},\n\tjournal = {The European journal of neuroscience},\n\tauthor = {Binti Affandi, Aida Helana and Pike, Alexandra C. and Robinson, Oliver Joe},\n\tmonth = may,\n\tyear = {2022},\n\tpmid = {33714211},\n\tnote = {Place: France},\n\tkeywords = {*Avoidance Learning/physiology, *Reinforcement, *Reinforcement, Psychology, Anxiety, Humans, Inhibition, Inhibition, Psychological, Psychological, Psychology, Reward},\n\tpages = {2571--2580},\n}\n\n
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\n Anxiety and stress are adaptive responses to threat that promote harm avoidance. In particular, prior work has shown that anxiety induced in humans using threat of unpredictable shock promotes behavioral inhibition in the face of harm. This is consistent with the idea that anxiety promotes passive avoidance-that is, withholding approach actions that could lead to harm. However, harm can also be avoided through active avoidance, where a (withdrawal) action is taken to avoid harm. Here, we provide the first direct within-study comparison of the effects of threat of shock on active and passive avoidance. We operationalize passive avoidance as withholding a button press response in the face of negative outcomes, and active avoidance as lifting/releasing a button press in the face of negative outcomes. We explore the impact of threat of unpredictable shock on the learning of these behavioral responses (alongside matched responses to rewards) within a single cognitive task. We predicted that threat of shock would promote both active and passive avoidance, and that this would be driven by increased reliance on Pavlovian bias, as parameterized within reinforcement-learning models. Consistent with our predictions, we provide evidence that threat of shock promotes passive avoidance as conceptualized by our task. However, inconsistent with predictions, we found no evidence that threat of shock promoted active avoidance, nor evidence of elevated Pavlovian bias in any condition. One hypothetical framework with which to understand these findings is that anxiety promotes passive over active harm avoidance strategies in order to conserve energy while avoiding harm.\n
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\n \n\n \n \n \n \n \n Emotional bias training as a treatment for anxiety and depression: evidence from experimental medicine studies in healthy and medicated samples.\n \n \n \n\n\n \n Suddell, S.; Müller-Glodde, M.; Lumsden, J.; Looi, C. Y.; Granger, K.; Barnett, J. H.; Robinson, O. J.; Munafò, M. R.; and Penton-Voak, I. S.\n\n\n \n\n\n\n Psychological medicine,1–10. May 2021.\n Place: England\n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n  \n \n 1 download\n \n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n
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@article{suddell_emotional_2021,\n\ttitle = {Emotional bias training as a treatment for anxiety and depression: evidence from experimental medicine studies in healthy and medicated samples.},\n\tcopyright = {All rights reserved},\n\tissn = {1469-8978 0033-2917},\n\tdoi = {10.1017/S0033291721002014},\n\tabstract = {BACKGROUND: Anxiety and depression are leading causes of disability worldwide, yet individuals are often unable to access appropriate treatment. There is a need  to develop effective interventions that can be delivered remotely. Previous  research has suggested that emotional processing biases are a potential target  for intervention, and these may be altered through brief training programs.  METHODS: We report two experimental medicine studies of emotional bias training  in two samples: individuals from the general population (n = 522) and individuals  currently taking antidepressants to treat anxiety or depression (n = 212).  Participants, recruited online, completed four sessions of EBT from their own  home. Mental health and cognitive functioning outcomes were assessed at baseline,  immediately post-training, and at 2-week follow-up. RESULTS: In both studies, our  intervention successfully trained participants to perceive ambiguous social  information more positively. This persisted at a 2-week follow-up. There was no  clear evidence that this change in emotional processing transferred to  improvements in symptoms in the primary analyses. However, in both studies, there  was weak evidence for improved quality of life following EBT amongst individuals  with more depressive symptoms at baseline. No clear evidence of transfer effects  was observed for self-reported daily stress, anhedonia or depressive symptoms.  Exploratory analyses suggested that younger participants reported greater  treatment gains. CONCLUSIONS: These studies demonstrate the effectiveness of  delivering a multi-session online training program to promote lasting cognitive  changes. Given the inconsistent evidence for transfer effects, EBT requires  further development before it can be considered as a treatment for anxiety and  depression.},\n\tlanguage = {eng},\n\tjournal = {Psychological medicine},\n\tauthor = {Suddell, Steph and Müller-Glodde, Maren and Lumsden, Jim and Looi, Chung Yen and Granger, Kiri and Barnett, Jennifer H. and Robinson, Oliver J. and Munafò, Marcus R. and Penton-Voak, Ian S.},\n\tmonth = may,\n\tyear = {2021},\n\tpmid = {34057058},\n\tnote = {Place: England},\n\tkeywords = {Anxiety, cognitive training, depression, digital intervention, emotional processing},\n\tpages = {1--10},\n}\n\n
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\n BACKGROUND: Anxiety and depression are leading causes of disability worldwide, yet individuals are often unable to access appropriate treatment. There is a need to develop effective interventions that can be delivered remotely. Previous research has suggested that emotional processing biases are a potential target for intervention, and these may be altered through brief training programs. METHODS: We report two experimental medicine studies of emotional bias training in two samples: individuals from the general population (n = 522) and individuals currently taking antidepressants to treat anxiety or depression (n = 212). Participants, recruited online, completed four sessions of EBT from their own home. Mental health and cognitive functioning outcomes were assessed at baseline, immediately post-training, and at 2-week follow-up. RESULTS: In both studies, our intervention successfully trained participants to perceive ambiguous social information more positively. This persisted at a 2-week follow-up. There was no clear evidence that this change in emotional processing transferred to improvements in symptoms in the primary analyses. However, in both studies, there was weak evidence for improved quality of life following EBT amongst individuals with more depressive symptoms at baseline. No clear evidence of transfer effects was observed for self-reported daily stress, anhedonia or depressive symptoms. Exploratory analyses suggested that younger participants reported greater treatment gains. CONCLUSIONS: These studies demonstrate the effectiveness of delivering a multi-session online training program to promote lasting cognitive changes. Given the inconsistent evidence for transfer effects, EBT requires further development before it can be considered as a treatment for anxiety and depression.\n
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\n \n\n \n \n \n \n \n The development and psychometric properties of a self-report Catastrophizing Questionnaire.\n \n \n \n\n\n \n Pike, A. C.; Serfaty, J. R.; and Robinson, O. J.\n\n\n \n\n\n\n Royal Society open science, 8(1): 201362. January 2021.\n Place: England\n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n
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@article{pike_development_2021,\n\ttitle = {The development and psychometric properties of a self-report {Catastrophizing} {Questionnaire}.},\n\tvolume = {8},\n\tcopyright = {© 2021 The Authors.},\n\tissn = {2054-5703},\n\tdoi = {10.1098/rsos.201362},\n\tabstract = {Catastrophizing is a cognitive process that can be defined as predicting the worst possible outcome. It has been shown to be related to psychiatric diagnoses  such as depression and anxiety, yet there are no self-report questionnaires  specifically measuring it outside the context of pain research. Here, we  therefore develop a novel, comprehensive self-report measure of general  catastrophizing. We performed five online studies (total n = 734), in which we  created and refined a Catastrophizing Questionnaire, and used a factor analytic  approach to understand its underlying structure. We also assessed convergent and  discriminant validity, and analysed test-retest reliability. Furthermore, we  tested the ability of Catastrophizing Questionnaire scores to predict relevant  clinical variables over and above other questionnaires. Finally, we also  developed a four-item short version of this questionnaire. We found that our  questionnaire is best fit by a single underlying factor, and shows convergent and  discriminant validity. Exploratory factor analyses indicated that catastrophizing  is independent from other related constructs, including anxiety and worry.  Moreover, we demonstrate incremental validity for this questionnaire in  predicting diagnostic and medication status. Finally, we demonstrate that our  Catastrophizing Questionnaire has good test-retest reliability (intraclass  correlation coefficient = 0.77, p {\\textless} 0.001). Critically, we can now, for the first  time, obtain detailed self-report data on catastrophizing.},\n\tlanguage = {eng},\n\tnumber = {1},\n\tjournal = {Royal Society open science},\n\tauthor = {Pike, Alexandra C. and Serfaty, Jade R. and Robinson, Oliver J.},\n\tmonth = jan,\n\tyear = {2021},\n\tpmid = {33614077},\n\tpmcid = {PMC7890513},\n\tnote = {Place: England},\n\tkeywords = {anxiety disorders, catastrophizing, cognitive distortions, mood disorders, psychiatry, self-report questionnaire},\n\tpages = {201362},\n}\n\n
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\n Catastrophizing is a cognitive process that can be defined as predicting the worst possible outcome. It has been shown to be related to psychiatric diagnoses such as depression and anxiety, yet there are no self-report questionnaires specifically measuring it outside the context of pain research. Here, we therefore develop a novel, comprehensive self-report measure of general catastrophizing. We performed five online studies (total n = 734), in which we created and refined a Catastrophizing Questionnaire, and used a factor analytic approach to understand its underlying structure. We also assessed convergent and discriminant validity, and analysed test-retest reliability. Furthermore, we tested the ability of Catastrophizing Questionnaire scores to predict relevant clinical variables over and above other questionnaires. Finally, we also developed a four-item short version of this questionnaire. We found that our questionnaire is best fit by a single underlying factor, and shows convergent and discriminant validity. Exploratory factor analyses indicated that catastrophizing is independent from other related constructs, including anxiety and worry. Moreover, we demonstrate incremental validity for this questionnaire in predicting diagnostic and medication status. Finally, we demonstrate that our Catastrophizing Questionnaire has good test-retest reliability (intraclass correlation coefficient = 0.77, p \\textless 0.001). Critically, we can now, for the first time, obtain detailed self-report data on catastrophizing.\n
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\n \n\n \n \n \n \n \n \n The Importance of Common Currency Tasks in Translational Psychiatry.\n \n \n \n \n\n\n \n Pike, A. C.; Lowther, M.; and Robinson, O. J.\n\n\n \n\n\n\n Current Behavioral Neuroscience Reports, 8(1): 1–10. 2021.\n \n\n\n\n
\n\n\n\n \n \n \"ThePaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n
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@article{pike_importance_2021,\n\ttitle = {The {Importance} of {Common} {Currency} {Tasks} in {Translational} {Psychiatry}},\n\tvolume = {8},\n\tcopyright = {All rights reserved},\n\tissn = {2196-2979},\n\turl = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7904709/},\n\tdoi = {10.1007/s40473-021-00225-w},\n\tabstract = {Purpose of Review\nCommon currency tasks are tasks that investigate the same phenomenon in different species. In this review, we discuss how to ensure the translational validity of common currency tasks, summarise their benefits, present recent research in this area and offer future directions and recommendations.\n\nRecent Findings\nWe discuss the strengths and limitations of three specific examples where common currency tasks have added to our understanding of psychiatric constructs—affective bias, reversal learning and goal-based decision making.\n\nSummary\nOverall, common currency tasks offer the potential to improve drug discovery in psychiatry. We recommend that researchers prioritise construct validity above face validity when designing common currency tasks and suggest that the evidence for construct validity is summarised in papers presenting research in this area.},\n\tnumber = {1},\n\turldate = {2022-08-22},\n\tjournal = {Current Behavioral Neuroscience Reports},\n\tauthor = {Pike, Alexandra C. and Lowther, Millie and Robinson, Oliver J.},\n\tyear = {2021},\n\tpmid = {33708469},\n\tpmcid = {PMC7904709},\n\tkeywords = {Animal models, Behavioural assay, Common currency tasks, Translational psychiatry, Translational tasks, Validity},\n\tpages = {1--10},\n}\n\n
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\n Purpose of Review Common currency tasks are tasks that investigate the same phenomenon in different species. In this review, we discuss how to ensure the translational validity of common currency tasks, summarise their benefits, present recent research in this area and offer future directions and recommendations. Recent Findings We discuss the strengths and limitations of three specific examples where common currency tasks have added to our understanding of psychiatric constructs—affective bias, reversal learning and goal-based decision making. Summary Overall, common currency tasks offer the potential to improve drug discovery in psychiatry. We recommend that researchers prioritise construct validity above face validity when designing common currency tasks and suggest that the evidence for construct validity is summarised in papers presenting research in this area.\n
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\n \n\n \n \n \n \n \n Assessing the Effectiveness of Front of Pack Labels: Findings from an Online Randomised-Controlled Experiment in a Representative British Sample.\n \n \n \n\n\n \n Packer, J.; Russell, S. J.; Ridout, D.; Hope, S.; Conolly, A.; Jessop, C.; Robinson, O. J.; Stoffel, S. T.; Viner, R. M.; and Croker, H.\n\n\n \n\n\n\n Nutrients, 13(3). March 2021.\n Place: Switzerland\n\n\n\n
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@article{packer_assessing_2021,\n\ttitle = {Assessing the {Effectiveness} of {Front} of {Pack} {Labels}: {Findings} from an {Online} {Randomised}-{Controlled} {Experiment} in a {Representative} {British} {Sample}.},\n\tvolume = {13},\n\tcopyright = {All rights reserved},\n\tissn = {2072-6643},\n\tdoi = {10.3390/nu13030900},\n\tabstract = {Front of pack food labels (FOPLs) provide accessible nutritional information to guide consumer choice. Using an online experiment with a large representative  British sample, we aimed to examine whether FOPLs improve participants' ability  to identify the healthiness of foods and drinks. The primary aim was to compare  ability to rank between FOPL groups and a no label control. Adults (≥18 years),  recruited from the NatCen panel, were randomised to one of five experimental  groups (Multiple Traffic Light, MTL; Nutri-Score, N-S; Warning Label, WL;  Positive Choice tick, PC; no label control). Stratification variables were year  of recruitment to panel, sex, age, government office region, and household  income. Packaging images were created for three versions, varying in healthiness,  of six food and drink products (pizza, drinks, cakes, crisps, yoghurts, breakfast  cereals). Participants were asked to rank the three product images in order of  healthiness. Ranking was completed on a single occasion and comprised a baseline  measure (with no FOPL), and a follow-up measure including the FOPL as per each  participant's experimental group. The primary outcome was the ability to  accurately rank product healthiness (all products ranked correctly vs. any  incorrect). In 2020, 4504 participants had complete data and were included in the  analysis. The probability of correct ranking at follow-up, and improving between  baseline and follow-up, was significantly greater across all products for the  N-S, MTL and WL groups, compared to control. This was seen for only some of the  products for the PC group. The largest effects were seen for N-S, followed by  MTL. These analyses were adjusted for stratification variables, ethnicity,  education, household composition, food shopping responsibility, and current FOPL  use. Exploratory analyses showed a tendency for participants with higher compared  to lower education to rank products more accurately. Conclusions: All FOPLs were  effective at improving participants' ability to correctly rank products according  to healthiness in this large representative British sample, with the largest  effects seen for N-S, followed by MTL.},\n\tlanguage = {eng},\n\tnumber = {3},\n\tjournal = {Nutrients},\n\tauthor = {Packer, Jessica and Russell, Simon J. and Ridout, Deborah and Hope, Steven and Conolly, Anne and Jessop, Curtis and Robinson, Oliver J. and Stoffel, Sandro T. and Viner, Russell M. and Croker, Helen},\n\tmonth = mar,\n\tyear = {2021},\n\tpmid = {33802115},\n\tpmcid = {PMC7999818},\n\tnote = {Place: Switzerland},\n\tkeywords = {*Consumer Behavior, *Food Labeling, *Food Quality, *Nutritive Value, Adult, Aged, Educational Status, Female, Food, Humans, Male, Middle Aged, United Kingdom, Young Adult, comprehension, front of pack label, nutrition policy, nutritional labelling, randomised controlled experiment},\n}\n\n
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\n Front of pack food labels (FOPLs) provide accessible nutritional information to guide consumer choice. Using an online experiment with a large representative British sample, we aimed to examine whether FOPLs improve participants' ability to identify the healthiness of foods and drinks. The primary aim was to compare ability to rank between FOPL groups and a no label control. Adults (≥18 years), recruited from the NatCen panel, were randomised to one of five experimental groups (Multiple Traffic Light, MTL; Nutri-Score, N-S; Warning Label, WL; Positive Choice tick, PC; no label control). Stratification variables were year of recruitment to panel, sex, age, government office region, and household income. Packaging images were created for three versions, varying in healthiness, of six food and drink products (pizza, drinks, cakes, crisps, yoghurts, breakfast cereals). Participants were asked to rank the three product images in order of healthiness. Ranking was completed on a single occasion and comprised a baseline measure (with no FOPL), and a follow-up measure including the FOPL as per each participant's experimental group. The primary outcome was the ability to accurately rank product healthiness (all products ranked correctly vs. any incorrect). In 2020, 4504 participants had complete data and were included in the analysis. The probability of correct ranking at follow-up, and improving between baseline and follow-up, was significantly greater across all products for the N-S, MTL and WL groups, compared to control. This was seen for only some of the products for the PC group. The largest effects were seen for N-S, followed by MTL. These analyses were adjusted for stratification variables, ethnicity, education, household composition, food shopping responsibility, and current FOPL use. Exploratory analyses showed a tendency for participants with higher compared to lower education to rank products more accurately. Conclusions: All FOPLs were effective at improving participants' ability to correctly rank products according to healthiness in this large representative British sample, with the largest effects seen for N-S, followed by MTL.\n
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\n \n\n \n \n \n \n \n Affective Bias Through the Lens of Signal Detection Theory.\n \n \n \n\n\n \n Locke, S. M.; and Robinson, O. J.\n\n\n \n\n\n\n Computational psychiatry (Cambridge, Mass.), 5(1): 4–20. 2021.\n Place: England\n\n\n\n
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@article{locke_affective_2021,\n\ttitle = {Affective {Bias} {Through} the {Lens} of {Signal} {Detection} {Theory}.},\n\tvolume = {5},\n\tcopyright = {All rights reserved},\n\tissn = {2379-6227},\n\tdoi = {10.5334/cpsy.58},\n\tabstract = {Affective bias - a propensity to focus on negative information at the expense of positive information - is a core feature of many mental health problems. However,  it can be caused by wide range of possible underlying cognitive mechanisms. Here  we illustrate this by focusing on one particular behavioural signature of  affective bias - increased tendency of anxious/depressed individuals to predict  lower rewards - in the context of the Signal Detection Theory (SDT) modelling  framework. Specifically, we show how to apply this framework to measure affective  bias and compare it to the behaviour of an optimal observer. We also show how to  extend the framework to make predictions about bias when the individual holds  incorrect assumptions about the decision context. Building on this theoretical  foundation, we propose five experiments to test five hypothetical sources of this  affective bias: beliefs about prior probabilities, beliefs about performance,  subjective value of reward, learning differences, and need for accuracy  differences. We argue that greater precision about the mechanisms driving  affective bias may eventually enable us to better understand the mechanisms  underlying mood and anxiety disorders.},\n\tlanguage = {eng},\n\tnumber = {1},\n\tjournal = {Computational psychiatry (Cambridge, Mass.)},\n\tauthor = {Locke, Shannon M. and Robinson, Oliver J.},\n\tyear = {2021},\n\tpmid = {34268450},\n\tpmcid = {PMC7611246},\n\tnote = {Place: England},\n\tkeywords = {affective bias, anxiety disorders, decision-making, mood disorders, signal detection theory},\n\tpages = {4--20},\n}\n\n
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\n Affective bias - a propensity to focus on negative information at the expense of positive information - is a core feature of many mental health problems. However, it can be caused by wide range of possible underlying cognitive mechanisms. Here we illustrate this by focusing on one particular behavioural signature of affective bias - increased tendency of anxious/depressed individuals to predict lower rewards - in the context of the Signal Detection Theory (SDT) modelling framework. Specifically, we show how to apply this framework to measure affective bias and compare it to the behaviour of an optimal observer. We also show how to extend the framework to make predictions about bias when the individual holds incorrect assumptions about the decision context. Building on this theoretical foundation, we propose five experiments to test five hypothetical sources of this affective bias: beliefs about prior probabilities, beliefs about performance, subjective value of reward, learning differences, and need for accuracy differences. We argue that greater precision about the mechanisms driving affective bias may eventually enable us to better understand the mechanisms underlying mood and anxiety disorders.\n
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\n \n\n \n \n \n \n \n Trait anxiety does not correlate with metacognitive confidence or reminder usage in a delayed intentions task.\n \n \n \n\n\n \n Kirk, P. A.; Robinson, O. J.; and Gilbert, S. J.\n\n\n \n\n\n\n Quarterly journal of experimental psychology (2006), 74(4): 634–644. April 2021.\n Place: England\n\n\n\n
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@article{kirk_trait_2021,\n\ttitle = {Trait anxiety does not correlate with metacognitive confidence or reminder usage in a delayed intentions task.},\n\tvolume = {74},\n\tcopyright = {All rights reserved},\n\tissn = {1747-0226 1747-0218},\n\tdoi = {10.1177/1747021820970156},\n\tabstract = {Setting external reminders provides a convenient way to reduce cognitive demand and ensure accurate retrieval of information for prospective tasks. Recent  experimental evidence has demonstrated that the decision to offload cognitive  information to external resources is guided by metacognitive belief, that is,  individuals' confidence in their unaided ability. Other work has also suggested a  relationship between metacognitive belief and trait anxiety. In the present study  (N = 300), we bridged these two areas by investigating whether trait anxiety  correlated with metacognitive belief and-consequently-propensity to offload  information in a delayed intentions paradigm. Participants received a financial  reward based on their ability to remember targets. However, participants could  take a reduced reward per target if they decided to use reminders. We replicated  previous findings that participants were biased to use more reminders than would  be optimal, and this bias was correlated with metacognitive judgements. However,  we show no evidence that trait anxiety held a relationship with metacognitive  belief or reminder usage. Indeed, Bayesian analyses strongly favoured the null.  Therefore, variation in self-reported trait anxiety does not necessarily  influence confidence and strategy when participants remember delayed intentions.},\n\tlanguage = {eng},\n\tnumber = {4},\n\tjournal = {Quarterly journal of experimental psychology (2006)},\n\tauthor = {Kirk, Peter A. and Robinson, Oliver J. and Gilbert, Sam J.},\n\tmonth = apr,\n\tyear = {2021},\n\tpmid = {33084484},\n\tpmcid = {PMC8044609},\n\tnote = {Place: England},\n\tkeywords = {*Memory, *Memory, Episodic, *Metacognition, Anxiety, Bayes Theorem, Episodic, Humans, Intention, Memory, Prospective Studies, anxiety, metacognition},\n\tpages = {634--644},\n}\n\n
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\n Setting external reminders provides a convenient way to reduce cognitive demand and ensure accurate retrieval of information for prospective tasks. Recent experimental evidence has demonstrated that the decision to offload cognitive information to external resources is guided by metacognitive belief, that is, individuals' confidence in their unaided ability. Other work has also suggested a relationship between metacognitive belief and trait anxiety. In the present study (N = 300), we bridged these two areas by investigating whether trait anxiety correlated with metacognitive belief and-consequently-propensity to offload information in a delayed intentions paradigm. Participants received a financial reward based on their ability to remember targets. However, participants could take a reduced reward per target if they decided to use reminders. We replicated previous findings that participants were biased to use more reminders than would be optimal, and this bias was correlated with metacognitive judgements. However, we show no evidence that trait anxiety held a relationship with metacognitive belief or reminder usage. Indeed, Bayesian analyses strongly favoured the null. Therefore, variation in self-reported trait anxiety does not necessarily influence confidence and strategy when participants remember delayed intentions.\n
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\n \n\n \n \n \n \n \n The Overlapping Neurobiology of Induced and Pathological Anxiety: A Meta-Analysis of Functional Neural Activation.\n \n \n \n\n\n \n Chavanne, A. V.; and Robinson, O. J.\n\n\n \n\n\n\n The American Journal of Psychiatry, 178(2): 156–164. February 2021.\n \n\n\n\n
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@article{chavanne_overlapping_2021,\n\ttitle = {The {Overlapping} {Neurobiology} of {Induced} and {Pathological} {Anxiety}: {A} {Meta}-{Analysis} of {Functional} {Neural} {Activation}},\n\tvolume = {178},\n\tcopyright = {All rights reserved},\n\tissn = {1535-7228},\n\tshorttitle = {The {Overlapping} {Neurobiology} of {Induced} and {Pathological} {Anxiety}},\n\tdoi = {10.1176/appi.ajp.2020.19111153},\n\tabstract = {OBJECTIVE: Although anxiety can be an adaptive response to unpredictable threats, pathological anxiety disorders occur when symptoms adversely affect daily life. Whether or not adaptive and pathological anxiety share mechanisms remains unknown, but if they do, induced (adaptive) anxiety could be used as an intermediate translational model of pathological anxiety to improve drug development pipelines. The authors therefore compared meta-analyses of functional neuroimaging studies of induced and pathological anxiety.\nMETHODS: A systematic search of the PubMed database was conducted in June 2019 for whole-brain functional MRI articles. Eligible articles contrasted either anxious patients to control subjects or an unpredictable-threat condition to a safe condition in healthy participants. Five anxiety disorders were included: posttraumatic stress disorder, social anxiety disorder, generalized anxiety disorder, panic disorder, and specific phobia. A total of 3,433 records were identified, 181 articles met selection criteria, and the largest subset of task type was emotional (N=138). Seed-based d-mapping software was used for all analyses.\nRESULTS: Induced anxiety (N=693 participants) and pathological anxiety (N=2,554 patients and 2,348 control subjects) both showed increased activation in the left and right insula (coordinates, 44, 14, -14 and -38, 20, -8; k=2,102 and k=1,305, respectively) and cingulate cortex/medial prefrontal cortex (-12, -8, 68; k=2,217). When the analyses were split by disorder, specific phobia appeared the most, and generalized anxiety disorder the least, similar to induced anxiety.\nCONCLUSIONS: This meta-analysis indicates a consistent pattern of activation across induced and pathological anxiety, supporting the proposition that some neurobiological mechanisms overlap and that the former may be used as a model for the latter. Induced anxiety might nevertheless be a better model for some anxiety disorders than others.},\n\tlanguage = {eng},\n\tnumber = {2},\n\tjournal = {The American Journal of Psychiatry},\n\tauthor = {Chavanne, Alice V. and Robinson, Oliver J.},\n\tmonth = feb,\n\tyear = {2021},\n\tpmid = {33054384},\n\tpmcid = {PMC7116679},\n\tkeywords = {*Functional Neuroimaging, Anxiety Disorders, Anxiety Disorders/etiology/*pathology/psychology, Brain, Brain/*pathology, Functional Neuroimaging, Humans, fMRI},\n\tpages = {156--164},\n}\n\n
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\n OBJECTIVE: Although anxiety can be an adaptive response to unpredictable threats, pathological anxiety disorders occur when symptoms adversely affect daily life. Whether or not adaptive and pathological anxiety share mechanisms remains unknown, but if they do, induced (adaptive) anxiety could be used as an intermediate translational model of pathological anxiety to improve drug development pipelines. The authors therefore compared meta-analyses of functional neuroimaging studies of induced and pathological anxiety. METHODS: A systematic search of the PubMed database was conducted in June 2019 for whole-brain functional MRI articles. Eligible articles contrasted either anxious patients to control subjects or an unpredictable-threat condition to a safe condition in healthy participants. Five anxiety disorders were included: posttraumatic stress disorder, social anxiety disorder, generalized anxiety disorder, panic disorder, and specific phobia. A total of 3,433 records were identified, 181 articles met selection criteria, and the largest subset of task type was emotional (N=138). Seed-based d-mapping software was used for all analyses. RESULTS: Induced anxiety (N=693 participants) and pathological anxiety (N=2,554 patients and 2,348 control subjects) both showed increased activation in the left and right insula (coordinates, 44, 14, -14 and -38, 20, -8; k=2,102 and k=1,305, respectively) and cingulate cortex/medial prefrontal cortex (-12, -8, 68; k=2,217). When the analyses were split by disorder, specific phobia appeared the most, and generalized anxiety disorder the least, similar to induced anxiety. CONCLUSIONS: This meta-analysis indicates a consistent pattern of activation across induced and pathological anxiety, supporting the proposition that some neurobiological mechanisms overlap and that the former may be used as a model for the latter. Induced anxiety might nevertheless be a better model for some anxiety disorders than others.\n
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\n \n\n \n \n \n \n \n How representative are neuroimaging samples? Large-scale evidence for trait anxiety differences between fMRI and behaviour-only research participants.\n \n \n \n\n\n \n Charpentier, C. J.; Faulkner, P.; Pool, E. R.; Ly, V.; Tollenaar, M. S.; Kluen, L. M.; Fransen, A.; Yamamori, Y.; Lally, N.; Mkrtchian, A.; Valton, V.; Huys, Q. J. M.; Sarigiannidis, I.; Morrow, K. A.; Krenz, V.; Kalbe, F.; Cremer, A.; Zerbes, G.; Kausche, F. M.; Wanke, N.; Giarrizzo, A.; Pulcu, E.; Murphy, S.; Kaltenboeck, A.; Browning, M.; Paul, L. K.; Cools, R.; Roelofs, K.; Pessoa, L.; Harmer, C. J.; Chase, H. W.; Grillon, C.; Schwabe, L.; Roiser, J. P.; Robinson, O. J.; and O'Doherty, J. P.\n\n\n \n\n\n\n Social cognitive and affective neuroscience, 16(10): 1057–1070. September 2021.\n Place: England\n\n\n\n
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@article{charpentier_how_2021,\n\ttitle = {How representative are neuroimaging samples? {Large}-scale evidence for trait anxiety differences between {fMRI} and behaviour-only research participants.},\n\tvolume = {16},\n\tcopyright = {© The Author(s) 2021. Published by Oxford University Press.},\n\tissn = {1749-5024 1749-5016},\n\tdoi = {10.1093/scan/nsab057},\n\tabstract = {Over the past three decades, functional magnetic resonance imaging (fMRI) has become crucial to study how cognitive processes are implemented in the human  brain. However, the question of whether participants recruited into fMRI studies  differ from participants recruited into other study contexts has received little  to no attention. This is particularly pertinent when effects fail to generalize  across study contexts: for example, a behavioural effect discovered in a  non-imaging context not replicating in a neuroimaging environment. Here, we  tested the hypothesis, motivated by preliminary findings (N = 272), that fMRI  participants differ from behaviour-only participants on one fundamental  individual difference variable: trait anxiety. Analysing trait anxiety scores and  possible confounding variables from healthy volunteers across multiple  institutions (N = 3317), we found robust support for lower trait anxiety in fMRI  study participants, consistent with a sampling or self-selection bias. The bias  was larger in studies that relied on phone screening (compared with full  in-person psychiatric screening), recruited at least partly from convenience  samples (compared with community samples), and in pharmacology studies. Our  findings highlight the need for surveying trait anxiety at recruitment and for  appropriate screening procedures or sampling strategies to mitigate this bias.},\n\tlanguage = {eng},\n\tnumber = {10},\n\tjournal = {Social cognitive and affective neuroscience},\n\tauthor = {Charpentier, Caroline J. and Faulkner, Paul and Pool, Eva R. and Ly, Verena and Tollenaar, Marieke S. and Kluen, Lisa M. and Fransen, Aniek and Yamamori, Yumeya and Lally, Níall and Mkrtchian, Anahit and Valton, Vincent and Huys, Quentin J. M. and Sarigiannidis, Ioannis and Morrow, Kelly A. and Krenz, Valentina and Kalbe, Felix and Cremer, Anna and Zerbes, Gundula and Kausche, Franziska M. and Wanke, Nadine and Giarrizzo, Alessio and Pulcu, Erdem and Murphy, Susannah and Kaltenboeck, Alexander and Browning, Michael and Paul, Lynn K. and Cools, Roshan and Roelofs, Karin and Pessoa, Luiz and Harmer, Catherine J. and Chase, Henry W. and Grillon, Christian and Schwabe, Lars and Roiser, Jonathan P. and Robinson, Oliver J. and O'Doherty, John P.},\n\tmonth = sep,\n\tyear = {2021},\n\tpmid = {33950220},\n\tpmcid = {PMC8483285},\n\tnote = {Place: England},\n\tkeywords = {*Anxiety Disorders, *Magnetic Resonance Imaging, Anxiety/diagnostic imaging, Attention, Humans, Neuroimaging, behaviour, neuroimaging, sampling bias, trait anxiety},\n\tpages = {1057--1070},\n}\n\n
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\n Over the past three decades, functional magnetic resonance imaging (fMRI) has become crucial to study how cognitive processes are implemented in the human brain. However, the question of whether participants recruited into fMRI studies differ from participants recruited into other study contexts has received little to no attention. This is particularly pertinent when effects fail to generalize across study contexts: for example, a behavioural effect discovered in a non-imaging context not replicating in a neuroimaging environment. Here, we tested the hypothesis, motivated by preliminary findings (N = 272), that fMRI participants differ from behaviour-only participants on one fundamental individual difference variable: trait anxiety. Analysing trait anxiety scores and possible confounding variables from healthy volunteers across multiple institutions (N = 3317), we found robust support for lower trait anxiety in fMRI study participants, consistent with a sampling or self-selection bias. The bias was larger in studies that relied on phone screening (compared with full in-person psychiatric screening), recruited at least partly from convenience samples (compared with community samples), and in pharmacology studies. Our findings highlight the need for surveying trait anxiety at recruitment and for appropriate screening procedures or sampling strategies to mitigate this bias.\n
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\n \n\n \n \n \n \n \n Does overloading cognitive resources mimic the impact of anxiety on temporal cognition?.\n \n \n \n\n\n \n Sarigiannidis, I.; Kirk, P. A.; Roiser, J. P.; and Robinson, O. J.\n\n\n \n\n\n\n Journal of experimental psychology. Learning, memory, and cognition, 46(10): 1828–1835. October 2020.\n Place: United States\n\n\n\n
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@article{sarigiannidis_does_2020,\n\ttitle = {Does overloading cognitive resources mimic the impact of anxiety on temporal cognition?},\n\tvolume = {46},\n\tcopyright = {All rights reserved},\n\tissn = {1939-1285 0278-7393},\n\tdoi = {10.1037/xlm0000845},\n\tabstract = {Anxiety alters how we perceive the world and can alter aspects of cognitive performance. Prominent theories of anxiety suggest that the effect of anxiety on  cognition is due to anxious thoughts "overloading" limited cognitive resources,  competing with other processes. If this is so, then a cognitive load manipulation  should impact performance of a task in the same way as induced anxiety. Thus, we  examined the impact of a load manipulation on a time perception task that we have  previously shown to be reliably impacted by anxiety. In contrast with our  prediction, across 3 studies we found that time perception was insensitive to our  load manipulation. Our results do not therefore support the idea that anxiety  impacts temporal cognition by overloading limited cognitive resources, at least  as induced by a commonly used load manipulation. Thus, anxiety might affect  temporal cognition in a unique way, via an evolutionary-preserved defense  survival system, as suggested by animal-inspired theories of anxiety, rather than  competing for limited attentional resources. (PsycInfo Database Record (c) 2020  APA, all rights reserved).},\n\tlanguage = {eng},\n\tnumber = {10},\n\tjournal = {Journal of experimental psychology. Learning, memory, and cognition},\n\tauthor = {Sarigiannidis, Ioannis and Kirk, Peter A. and Roiser, Jonathan P. and Robinson, Oliver J.},\n\tmonth = oct,\n\tyear = {2020},\n\tpmid = {32378938},\n\tpmcid = {PMC7872305},\n\tnote = {Place: United States},\n\tkeywords = {Adult, Anxiety/*physiopathology, Attention/*physiology, Female, Humans, Male, Memory, Memory, Short-Term/*physiology, Pattern Recognition, Pattern Recognition, Visual/*physiology, Psychomotor Performance/*physiology, Short-Term/*physiology, Time Perception/*physiology, Visual/*physiology, Young Adult},\n\tpages = {1828--1835},\n}\n\n
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\n Anxiety alters how we perceive the world and can alter aspects of cognitive performance. Prominent theories of anxiety suggest that the effect of anxiety on cognition is due to anxious thoughts \"overloading\" limited cognitive resources, competing with other processes. If this is so, then a cognitive load manipulation should impact performance of a task in the same way as induced anxiety. Thus, we examined the impact of a load manipulation on a time perception task that we have previously shown to be reliably impacted by anxiety. In contrast with our prediction, across 3 studies we found that time perception was insensitive to our load manipulation. Our results do not therefore support the idea that anxiety impacts temporal cognition by overloading limited cognitive resources, at least as induced by a commonly used load manipulation. Thus, anxiety might affect temporal cognition in a unique way, via an evolutionary-preserved defense survival system, as suggested by animal-inspired theories of anxiety, rather than competing for limited attentional resources. (PsycInfo Database Record (c) 2020 APA, all rights reserved).\n
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\n \n\n \n \n \n \n \n Anxiety makes time pass quicker while fear has no effect.\n \n \n \n\n\n \n Sarigiannidis, I.; Grillon, C.; Ernst, M.; Roiser, J. P.; and Robinson, O. J.\n\n\n \n\n\n\n Cognition, 197: 104116. April 2020.\n Place: Netherlands\n\n\n\n
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@article{sarigiannidis_anxiety_2020,\n\ttitle = {Anxiety makes time pass quicker while fear has no effect.},\n\tvolume = {197},\n\tcopyright = {Copyright © 2020 The Authors. Published by Elsevier B.V. All rights reserved.},\n\tissn = {1873-7838 0010-0277},\n\tdoi = {10.1016/j.cognition.2019.104116},\n\tabstract = {People often say that during unpleasant events, e.g. traumatic incidents such as car accidents, time slows down (i.e. time is overestimated). However aversive  events can elicit at least two dissociable subtypes of reactions: fear (transient  and relating to an imminent event) and anxiety (diffuse and relating to an  unpredictable event). We hypothesised that anxiety might have an opposite effect  on time perception compared to fear. To test this we combined a robust anxiety  manipulation (threat-of-shock) with a widely used timing task in which  participants judged whether the duration of a stimulus was long or short. In line  with our hypothesis, across three experiments (with varying stimulus timings and  shock levels), participants significantly underestimated time under inducted  anxiety, as indicated by a rightward shift of the psychophysical function  (meta-analytic effect size: d = 0.68, 95\\% confidence interval: 0.42-0.94). In two  further studies, we were unable to replicate previous findings that fear leads to  time overestimation, after adapting our temporal cognition task, which suggests a  dissociation between fear and anxiety on how they affect time perception. Our  results suggest that experimentally inducing anxiety leads to underestimating the  duration of temporal intervals, which might be a starting point in explaining  different subjective experiences of disorders related to fear (e.g.  post-traumatic stress disorder) and anxiety (e.g. generalised anxiety disorder).},\n\tlanguage = {eng},\n\tjournal = {Cognition},\n\tauthor = {Sarigiannidis, Ioannis and Grillon, Christian and Ernst, Monique and Roiser, Jonathan P. and Robinson, Oliver J.},\n\tmonth = apr,\n\tyear = {2020},\n\tpmid = {31883966},\n\tpmcid = {PMC7033556},\n\tnote = {Place: Netherlands},\n\tkeywords = {*Fear, *Time Perception, Anxiety, Anxiety Disorders, Cognition, Emotion, Fear, Humans, Threat-of-shock, Time perception},\n\tpages = {104116},\n}\n\n
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\n People often say that during unpleasant events, e.g. traumatic incidents such as car accidents, time slows down (i.e. time is overestimated). However aversive events can elicit at least two dissociable subtypes of reactions: fear (transient and relating to an imminent event) and anxiety (diffuse and relating to an unpredictable event). We hypothesised that anxiety might have an opposite effect on time perception compared to fear. To test this we combined a robust anxiety manipulation (threat-of-shock) with a widely used timing task in which participants judged whether the duration of a stimulus was long or short. In line with our hypothesis, across three experiments (with varying stimulus timings and shock levels), participants significantly underestimated time under inducted anxiety, as indicated by a rightward shift of the psychophysical function (meta-analytic effect size: d = 0.68, 95% confidence interval: 0.42-0.94). In two further studies, we were unable to replicate previous findings that fear leads to time overestimation, after adapting our temporal cognition task, which suggests a dissociation between fear and anxiety on how they affect time perception. Our results suggest that experimentally inducing anxiety leads to underestimating the duration of temporal intervals, which might be a starting point in explaining different subjective experiences of disorders related to fear (e.g. post-traumatic stress disorder) and anxiety (e.g. generalised anxiety disorder).\n
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\n \n\n \n \n \n \n \n \"Bigger\" or \"better\": the roles of magnitude and valence in \"affective bias\".\n \n \n \n\n\n \n Love, J.; and Robinson, O. J.\n\n\n \n\n\n\n Cognition & emotion, 34(4): 633–642. June 2020.\n Place: England\n\n\n\n
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@article{love_bigger_2020,\n\ttitle = {"{Bigger}" or "better": the roles of magnitude and valence in "affective bias".},\n\tvolume = {34},\n\tcopyright = {All rights reserved},\n\tissn = {1464-0600 0269-9931},\n\tdoi = {10.1080/02699931.2019.1662373},\n\tabstract = {Negative affective biases are thought to be a key symptom driving and upholding many psychiatric disorders. When presented with ambiguous information, anxious  individuals, for example, tend to anticipate lower rewards than asymptomatic  individuals (Aylward et al., 2019. Translating a rodent measure of negative bias  into humans: the impact of induced anxiety and unmedicated mood and anxiety  disorders. Psychological Medicine). The assumption is that this is because  anxious individuals assume "worse" outcomes. However, predictions are often made  about high and low rewards, so it is not clear whether the bias is due to the  valence (the "worse" option) or just magnitude (the lower number). We therefore  explored the roles of valence and magnitude in a translational measure of  negative affective bias. We adapted a two-alternative forced choice (2AFC)  "reward-reward" task into a "punishment-punishment" paradigm, and followed up  with "high reward-high punishment" and "low reward-high punishment" variants. The  results from the "punishment-punishment" paradigm - a bias towards higher  punishments in healthy controls - suggest that it is outcome magnitude that is  important. However, this is qualified by the other variants which indicate that  both valence and magnitude are important. Overall, our results temper the  assumption that negative affective biases observed in tasks using numeric  outcomes are solely as a result of subjective outcome valence.},\n\tlanguage = {eng},\n\tnumber = {4},\n\tjournal = {Cognition \\& emotion},\n\tauthor = {Love, Jack and Robinson, Oliver J.},\n\tmonth = jun,\n\tyear = {2020},\n\tpmid = {31496360},\n\tpmcid = {PMC7446041},\n\tnote = {Place: England},\n\tkeywords = {*Affect, *Punishment/psychology, *Reward, Affective bias, Anxiety/*psychology, Bias, Healthy Volunteers/*psychology, Humans, Role, anxiety, magnitude, two-alternative forced choice, valence},\n\tpages = {633--642},\n}\n\n
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\n Negative affective biases are thought to be a key symptom driving and upholding many psychiatric disorders. When presented with ambiguous information, anxious individuals, for example, tend to anticipate lower rewards than asymptomatic individuals (Aylward et al., 2019. Translating a rodent measure of negative bias into humans: the impact of induced anxiety and unmedicated mood and anxiety disorders. Psychological Medicine). The assumption is that this is because anxious individuals assume \"worse\" outcomes. However, predictions are often made about high and low rewards, so it is not clear whether the bias is due to the valence (the \"worse\" option) or just magnitude (the lower number). We therefore explored the roles of valence and magnitude in a translational measure of negative affective bias. We adapted a two-alternative forced choice (2AFC) \"reward-reward\" task into a \"punishment-punishment\" paradigm, and followed up with \"high reward-high punishment\" and \"low reward-high punishment\" variants. The results from the \"punishment-punishment\" paradigm - a bias towards higher punishments in healthy controls - suggest that it is outcome magnitude that is important. However, this is qualified by the other variants which indicate that both valence and magnitude are important. Overall, our results temper the assumption that negative affective biases observed in tasks using numeric outcomes are solely as a result of subjective outcome valence.\n
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\n \n\n \n \n \n \n \n Translating a rodent measure of negative bias into humans: the impact of induced anxiety and unmedicated mood and anxiety disorders.\n \n \n \n\n\n \n Aylward, J.; Hales, C.; Robinson, E.; and Robinson, O. J.\n\n\n \n\n\n\n Psychological medicine, 50(2): 237–246. January 2020.\n Place: England\n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n  \n \n 1 download\n \n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n
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@article{aylward_translating_2020,\n\ttitle = {Translating a rodent measure of negative bias into humans: the impact of induced anxiety and unmedicated mood and anxiety disorders.},\n\tvolume = {50},\n\tcopyright = {All rights reserved},\n\tissn = {1469-8978 0033-2917},\n\tdoi = {10.1017/S0033291718004117},\n\tabstract = {BACKGROUND: Mood and anxiety disorders are ubiquitous but current treatment options are ineffective for many sufferers. Moreover, a number of promising  pre-clinical interventions have failed to translate into clinical efficacy in  humans. Improved treatments are unlikely without better animal-human  translational pipelines. Here, we translate a rodent measure of negative  affective bias into humans, exploring its relationship with (1) pathological mood  and anxiety symptoms and (2) transient induced anxiety. METHODS: Adult  participants (age = 29 ± 11) who met criteria for mood or anxiety disorder  symptomatology according to a face-to-face neuropsychiatric interview were  included in the symptomatic group. Study 1 included N = 77 (47 = asymptomatic  [female = 21]; 30 = symptomatic [female = 25]), study 2 included N = 47  asymptomatic participants (25 = female). Outcome measures were choice ratios,  reaction times and parameters recovered from a computational model of reaction  time - the drift diffusion model (DDM) - from a two-alternative-forced-choice  task in which ambiguous and unambiguous auditory stimuli were paired with high  and low rewards. RESULTS: Both groups showed over 93\\% accuracy on unambiguous  tones indicating intact discrimination, but symptomatic individuals demonstrated  increased negative affective bias on ambiguous tones [proportion high reward =  0.42 (s.d. = 0.14)] relative to asymptomatic individuals [0.53 (s.d. = 0.17)] as  well as a significantly reduced DDM drift rate. No significant effects were  observed for the within-subjects anxiety-induction. CONCLUSIONS: Humans with  pathological anxiety symptoms directly mimic rodents undergoing anxiogenic  manipulation. The lack of sensitivity to transient anxiety suggests the paradigm  might be more sensitive to clinically relevant symptoms. Our results establish a  direct translational pipeline (and candidate therapeutics screen) from negative  affective bias in rodents to pathological mood and anxiety symptoms in humans.},\n\tlanguage = {eng},\n\tnumber = {2},\n\tjournal = {Psychological medicine},\n\tauthor = {Aylward, Jessica and Hales, Claire and Robinson, Emma and Robinson, Oliver J.},\n\tmonth = jan,\n\tyear = {2020},\n\tpmid = {30683161},\n\tpmcid = {PMC7083556},\n\tnote = {Place: England},\n\tkeywords = {*Affect, *Reward, *Translational Research, *Translational Research, Biomedical, Adolescent, Adult, Affect, Affective bias, Animal, Animals, Anxiety Disorders, Anxiety Disorders/*physiopathology, Bias, Biomedical, Disease Models, Disease Models, Animal, Female, Humans, Male, Mood Disorders, Mood Disorders/*physiopathology, Reaction Time, Reward, Rodentia, Translational Research, Biomedical, Young Adult, anxiety, back-translation, computational psychiatry, depression, drift diffusion model},\n\tpages = {237--246},\n}\n
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\n BACKGROUND: Mood and anxiety disorders are ubiquitous but current treatment options are ineffective for many sufferers. Moreover, a number of promising pre-clinical interventions have failed to translate into clinical efficacy in humans. Improved treatments are unlikely without better animal-human translational pipelines. Here, we translate a rodent measure of negative affective bias into humans, exploring its relationship with (1) pathological mood and anxiety symptoms and (2) transient induced anxiety. METHODS: Adult participants (age = 29 ± 11) who met criteria for mood or anxiety disorder symptomatology according to a face-to-face neuropsychiatric interview were included in the symptomatic group. Study 1 included N = 77 (47 = asymptomatic [female = 21]; 30 = symptomatic [female = 25]), study 2 included N = 47 asymptomatic participants (25 = female). Outcome measures were choice ratios, reaction times and parameters recovered from a computational model of reaction time - the drift diffusion model (DDM) - from a two-alternative-forced-choice task in which ambiguous and unambiguous auditory stimuli were paired with high and low rewards. RESULTS: Both groups showed over 93% accuracy on unambiguous tones indicating intact discrimination, but symptomatic individuals demonstrated increased negative affective bias on ambiguous tones [proportion high reward = 0.42 (s.d. = 0.14)] relative to asymptomatic individuals [0.53 (s.d. = 0.17)] as well as a significantly reduced DDM drift rate. No significant effects were observed for the within-subjects anxiety-induction. CONCLUSIONS: Humans with pathological anxiety symptoms directly mimic rodents undergoing anxiogenic manipulation. The lack of sensitivity to transient anxiety suggests the paradigm might be more sensitive to clinically relevant symptoms. Our results establish a direct translational pipeline (and candidate therapeutics screen) from negative affective bias in rodents to pathological mood and anxiety symptoms in humans.\n
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\n \n\n \n \n \n \n \n The translational neural circuitry of anxiety.\n \n \n \n\n\n \n Robinson, O. J.; Pike, A. C.; Cornwell, B.; and Grillon, C.\n\n\n \n\n\n\n Journal of Neurology, Neurosurgery, and Psychiatry, 90(12): 1353–1360. December 2019.\n \n\n\n\n
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@article{robinson_translational_2019,\n\ttitle = {The translational neural circuitry of anxiety},\n\tvolume = {90},\n\tcopyright = {All rights reserved},\n\tissn = {1468-330X},\n\tdoi = {10.1136/jnnp-2019-321400},\n\tabstract = {Anxiety is an adaptive response that promotes harm avoidance, but at the same time excessive anxiety constitutes the most common psychiatric complaint. Moreover, current treatments for anxiety-both psychological and pharmacological-hover at around 50\\% recovery rates. Improving treatment outcomes is nevertheless difficult, in part because contemporary interventions were developed without an understanding of the underlying neurobiological mechanisms that they modulate. Recent advances in experimental models of anxiety in humans, such as threat of unpredictable shock, have, however, enabled us to start translating the wealth of mechanistic animal work on defensive behaviour into humans. In this article, we discuss the distinction between fear and anxiety, before reviewing translational research on the neural circuitry of anxiety in animal models and how it relates to human neuroimaging studies across both healthy and clinical populations. We highlight the roles of subcortical regions (and their subunits) such as the bed nucleus of the stria terminalis, the amgydala, and the hippocampus, as well as their connectivity to cortical regions such as dorsal medial and lateral prefrontal/cingulate cortex and insula in maintaining anxiety responding. We discuss how this circuitry might be modulated by current treatments before finally highlighting areas for future research that might ultimately improve treatment outcomes for this common and debilitating transdiagnostic symptom.},\n\tlanguage = {eng},\n\tnumber = {12},\n\tjournal = {Journal of Neurology, Neurosurgery, and Psychiatry},\n\tauthor = {Robinson, Oliver J. and Pike, Alexandra C. and Cornwell, Brian and Grillon, Christian},\n\tmonth = dec,\n\tyear = {2019},\n\tpmid = {31256001},\n\tkeywords = {Anxiety, Anxiety Disorders, Anxiety Disorders/diagnostic imaging/*physiopathology/psychology, Anxiety/diagnostic imaging/*physiopathology/psychology, Brain Mapping, Fear, Fear/psychology, Humans, Nerve Net, Nerve Net/diagnostic imaging/*physiopathology, experimental, psychiatry, psychology, psychology, experimental},\n\tpages = {1353--1360},\n}\n\n
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\n Anxiety is an adaptive response that promotes harm avoidance, but at the same time excessive anxiety constitutes the most common psychiatric complaint. Moreover, current treatments for anxiety-both psychological and pharmacological-hover at around 50% recovery rates. Improving treatment outcomes is nevertheless difficult, in part because contemporary interventions were developed without an understanding of the underlying neurobiological mechanisms that they modulate. Recent advances in experimental models of anxiety in humans, such as threat of unpredictable shock, have, however, enabled us to start translating the wealth of mechanistic animal work on defensive behaviour into humans. In this article, we discuss the distinction between fear and anxiety, before reviewing translational research on the neural circuitry of anxiety in animal models and how it relates to human neuroimaging studies across both healthy and clinical populations. We highlight the roles of subcortical regions (and their subunits) such as the bed nucleus of the stria terminalis, the amgydala, and the hippocampus, as well as their connectivity to cortical regions such as dorsal medial and lateral prefrontal/cingulate cortex and insula in maintaining anxiety responding. We discuss how this circuitry might be modulated by current treatments before finally highlighting areas for future research that might ultimately improve treatment outcomes for this common and debilitating transdiagnostic symptom.\n
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\n \n\n \n \n \n \n \n Reliability of Fronto-Amygdala Coupling during Emotional Face Processing.\n \n \n \n\n\n \n Nord, C. L.; Gray, A.; Robinson, O. J.; and Roiser, J. P.\n\n\n \n\n\n\n Brain sciences, 9(4). April 2019.\n Place: Switzerland\n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n
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@article{nord_reliability_2019,\n\ttitle = {Reliability of {Fronto}-{Amygdala} {Coupling} during {Emotional} {Face} {Processing}.},\n\tvolume = {9},\n\tcopyright = {All rights reserved},\n\tissn = {2076-3425},\n\tdoi = {10.3390/brainsci9040089},\n\tabstract = {One of the most exciting translational prospects for brain imaging research is the potential use of functional magnetic resonance imaging (fMRI) 'biomarkers' to  predict an individual's risk of developing a neuropsychiatric disorder or the  likelihood of responding to a particular intervention. This proposal depends  critically on reliable measurements at the level of the individual. Several  previous studies have reported relatively poor reliability of amygdala activation  during emotional face processing, a key putative fMRI 'biomarker'. However, the  reliability of amygdala connectivity measures is much less well understood. Here,  we assessed the reliability of task-modulated coupling between three seed regions  (left and right amygdala and the subgenual anterior cingulate cortex) and the  dorsomedial frontal/cingulate cortex (DMFC), measured using a psychophysiological  interaction analysis in 29 healthy individuals scanned approximately two weeks  apart. We performed two runs on each day of three different emotional  face-processing tasks: emotion identification, emotion matching, and gender  classification. We tested both between-day reliability and within-day  (between-run) reliability. We found good-to-excellent within-subject reliability  of amygdala-DMFC coupling, both between days (in two tasks), and within day (in  one task). This suggests that disorder-relevant regional coupling may be  sufficiently reliable to be used as a predictor of treatment response or clinical  risk in future clinical studies.},\n\tlanguage = {eng},\n\tnumber = {4},\n\tjournal = {Brain sciences},\n\tauthor = {Nord, Camilla L. and Gray, Alan and Robinson, Oliver J. and Roiser, Jonathan P.},\n\tmonth = apr,\n\tyear = {2019},\n\tpmid = {31010224},\n\tpmcid = {PMC6523743},\n\tnote = {Place: Switzerland},\n\tkeywords = {amygdala, connectivity, emotion processing, functional magnetic resonance imaging (fMRI), prefrontal cortex, reliability},\n}\n\n
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\n One of the most exciting translational prospects for brain imaging research is the potential use of functional magnetic resonance imaging (fMRI) 'biomarkers' to predict an individual's risk of developing a neuropsychiatric disorder or the likelihood of responding to a particular intervention. This proposal depends critically on reliable measurements at the level of the individual. Several previous studies have reported relatively poor reliability of amygdala activation during emotional face processing, a key putative fMRI 'biomarker'. However, the reliability of amygdala connectivity measures is much less well understood. Here, we assessed the reliability of task-modulated coupling between three seed regions (left and right amygdala and the subgenual anterior cingulate cortex) and the dorsomedial frontal/cingulate cortex (DMFC), measured using a psychophysiological interaction analysis in 29 healthy individuals scanned approximately two weeks apart. We performed two runs on each day of three different emotional face-processing tasks: emotion identification, emotion matching, and gender classification. We tested both between-day reliability and within-day (between-run) reliability. We found good-to-excellent within-subject reliability of amygdala-DMFC coupling, both between days (in two tasks), and within day (in one task). This suggests that disorder-relevant regional coupling may be sufficiently reliable to be used as a predictor of treatment response or clinical risk in future clinical studies.\n
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\n \n\n \n \n \n \n \n Modeling anxiety in healthy humans: a key intermediate bridge between basic and clinical sciences.\n \n \n \n\n\n \n Grillon, C.; Robinson, O. J.; Cornwell, B.; and Ernst, M.\n\n\n \n\n\n\n Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 44(12): 1999–2010. November 2019.\n Place: England\n\n\n\n
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@article{grillon_modeling_2019,\n\ttitle = {Modeling anxiety in healthy humans: a key intermediate bridge between basic and clinical sciences.},\n\tvolume = {44},\n\tcopyright = {All rights reserved},\n\tissn = {1740-634X 0893-133X},\n\tdoi = {10.1038/s41386-019-0445-1},\n\tabstract = {Animal models of anxiety disorders are important for elucidating neurobiological defense mechanisms. However, animal models are limited when it comes to  understanding the more complex processes of anxiety that are unique to humans  (e.g., worry) and to screen new treatments. In this review, we outline how the  Experimental Psychopathology approach, based on experimental models of anxiety in  healthy subjects, can mitigate these limitations and complement research in  animals. Experimental psychopathology can bridge basic research in animals and  clinical studies, as well as guide and constrain hypotheses about the nature of  psychopathology, treatment mechanisms, and treatment targets. This review begins  with a brief review of the strengths and limitations of animal models before  discussing the need for human models of anxiety, which are especially necessary  to probe higher-order cognitive processes. This can be accomplished by combining  anxiety-induction procedures with tasks that probe clinically relevant processes  to identify neurocircuits that are potentially altered by anxiety. The review  then discusses the validity of experimental psychopathology and introduces a  methodological approach consisting of five steps: (1) select anxiety-relevant  cognitive or behavioral operations and associated tasks, (2) identify the  underlying neurocircuits supporting these operations in healthy controls, 3)  examine the impact of experimental anxiety on the targeted operations in healthy  controls, (4) utilize findings from step 3 to generate hypotheses about  neurocircuit dysfunction in anxious patients, and 5) evaluate treatment  mechanisms and screen novel treatments. This is followed by two concrete  illustrations of this approach and suggestions for future studies.},\n\tlanguage = {eng},\n\tnumber = {12},\n\tjournal = {Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology},\n\tauthor = {Grillon, Christian and Robinson, Oliver J. and Cornwell, Brian and Ernst, Monique},\n\tmonth = nov,\n\tyear = {2019},\n\tpmid = {31226707},\n\tpmcid = {PMC6897969},\n\tnote = {Place: England},\n\tkeywords = {Animal, Animals, Anxiety Disorders/*physiopathology, Anxiety/*physiopathology, Biological, Biomedical/*methods, Disease Models, Disease Models, Animal, Humans, Models, Models, Biological, Psychopathology/*methods, Research Design, Translational Research, Translational Research, Biomedical/*methods},\n\tpages = {1999--2010},\n}\n\n
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\n Animal models of anxiety disorders are important for elucidating neurobiological defense mechanisms. However, animal models are limited when it comes to understanding the more complex processes of anxiety that are unique to humans (e.g., worry) and to screen new treatments. In this review, we outline how the Experimental Psychopathology approach, based on experimental models of anxiety in healthy subjects, can mitigate these limitations and complement research in animals. Experimental psychopathology can bridge basic research in animals and clinical studies, as well as guide and constrain hypotheses about the nature of psychopathology, treatment mechanisms, and treatment targets. This review begins with a brief review of the strengths and limitations of animal models before discussing the need for human models of anxiety, which are especially necessary to probe higher-order cognitive processes. This can be accomplished by combining anxiety-induction procedures with tasks that probe clinically relevant processes to identify neurocircuits that are potentially altered by anxiety. The review then discusses the validity of experimental psychopathology and introduces a methodological approach consisting of five steps: (1) select anxiety-relevant cognitive or behavioral operations and associated tasks, (2) identify the underlying neurocircuits supporting these operations in healthy controls, 3) examine the impact of experimental anxiety on the targeted operations in healthy controls, (4) utilize findings from step 3 to generate hypotheses about neurocircuit dysfunction in anxious patients, and 5) evaluate treatment mechanisms and screen novel treatments. This is followed by two concrete illustrations of this approach and suggestions for future studies.\n
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\n \n\n \n \n \n \n \n The impact of threat of shock-induced anxiety on the neural substrates of memory encoding and retrieval.\n \n \n \n\n\n \n Garibbo, M.; Aylward, J.; and Robinson, O. J.\n\n\n \n\n\n\n Social cognitive and affective neuroscience, 14(10): 1087–1096. October 2019.\n Place: England\n\n\n\n
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@article{garibbo_impact_2019,\n\ttitle = {The impact of threat of shock-induced anxiety on the neural substrates of memory encoding and retrieval.},\n\tvolume = {14},\n\tcopyright = {© The Author(s) 2019. Published by Oxford University Press.},\n\tissn = {1749-5024 1749-5016},\n\tdoi = {10.1093/scan/nsz080},\n\tabstract = {Dysfunctional memory processes are widely reported in anxiety disorders, but the underlying neurocognitive mechanisms are unclear. Recent work shows that the  impact of anxiety on memory depends on the context and memory modality. For  instance, threat of shock, a translational within-subject anxiety induction, has  been shown to impair the encoding of facial stimuli, while improving spatial  working memory (WM) accuracy. The present study aimed to delineate the neural  circuitry regulating these opposing behavioural effects. Thirty-three healthy  volunteers performed the previously assessed facial recognition and a spatial WM  tasks inside an fMRI scanner, under alternating within-subject conditions of  threat or safe from shock across encoding and retrieval. Facial recognition  impairments were replicated when threat was selectively induced at encoding.  Neuroimaging results suggest that this effect was driven by increased competition  for attentional resources within the anterior cingulate cortex, in which  activation correlated positively with stress levels. The impact of threat on  spatial WM performance did not, however, replicate in the fMRI environment.  Nevertheless, state-dependent hippocampal activation was observed in both tasks.  These findings suggest a neurocognitive mechanism by which anxiety impairs facial  recognition as well as a state-dependent hippocampal activation pattern, which  may putatively underline retrieval of negative experiences in anxiety.},\n\tlanguage = {eng},\n\tnumber = {10},\n\tjournal = {Social cognitive and affective neuroscience},\n\tauthor = {Garibbo, Michele and Aylward, Jessica and Robinson, Oliver J.},\n\tmonth = oct,\n\tyear = {2019},\n\tpmid = {31680142},\n\tpmcid = {PMC6970151},\n\tnote = {Place: England},\n\tkeywords = {ACC, Adult, Anxiety Disorders, Anxiety/*physiopathology/*psychology, Attention/physiology, Female, Gyrus Cinguli/physiopathology, Hippocampus/physiopathology, Humans, Magnetic Resonance Imaging, Male, Memory/*physiology, Psychology/physiology, Recognition, Recognition, Psychology/physiology, Spatial Memory/physiology, Temporal Lobe/physiopathology, Young Adult, anxiety, fMRI, memory, threat of shock},\n\tpages = {1087--1096},\n}\n\n
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\n Dysfunctional memory processes are widely reported in anxiety disorders, but the underlying neurocognitive mechanisms are unclear. Recent work shows that the impact of anxiety on memory depends on the context and memory modality. For instance, threat of shock, a translational within-subject anxiety induction, has been shown to impair the encoding of facial stimuli, while improving spatial working memory (WM) accuracy. The present study aimed to delineate the neural circuitry regulating these opposing behavioural effects. Thirty-three healthy volunteers performed the previously assessed facial recognition and a spatial WM tasks inside an fMRI scanner, under alternating within-subject conditions of threat or safe from shock across encoding and retrieval. Facial recognition impairments were replicated when threat was selectively induced at encoding. Neuroimaging results suggest that this effect was driven by increased competition for attentional resources within the anterior cingulate cortex, in which activation correlated positively with stress levels. The impact of threat on spatial WM performance did not, however, replicate in the fMRI environment. Nevertheless, state-dependent hippocampal activation was observed in both tasks. These findings suggest a neurocognitive mechanism by which anxiety impairs facial recognition as well as a state-dependent hippocampal activation pattern, which may putatively underline retrieval of negative experiences in anxiety.\n
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\n \n\n \n \n \n \n \n When Expectancies Are Violated: A Functional Magnetic Resonance Imaging Study.\n \n \n \n\n\n \n Colloca, L.; Schenk, L. A.; Nathan, D. E.; Robinson, O. J.; and Grillon, C.\n\n\n \n\n\n\n Clinical pharmacology and therapeutics, 106(6): 1246–1252. December 2019.\n Place: United States\n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n  \n \n 2 downloads\n \n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n
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@article{colloca_when_2019,\n\ttitle = {When {Expectancies} {Are} {Violated}: {A} {Functional} {Magnetic} {Resonance} {Imaging} {Study}.},\n\tvolume = {106},\n\tcopyright = {© 2019 The Authors Clinical Pharmacology \\& Therapeutics © 2019 American Society for Clinical Pharmacology and Therapeutics. This article has been contributed to  by US Government employees and their work is in the public domain in the USA.},\n\tissn = {1532-6535 0009-9236},\n\tdoi = {10.1002/cpt.1587},\n\tabstract = {Positive and negative expectancies drive behavioral and neurobiological placebo and nocebo effects, which in turn can have profound effects on patient  improvement or worsening. However, expectations of events and outcomes are often  not met in daily life and clinical practice. It is currently unknown how this  affects placebo and nocebo effects. We have demonstrated that the violation of  expectancies, such as when there is a discrepancy between what is expected and  what is actually presented, reduces both placebo and nocebo effects while causing  an extinction of placebo effects. The reduction of placebo and nocebo effects was  paralleled by an activation of the left inferior parietal cortex, a brain region  that redirects attention when discrepancies between sensory and cognitive events  occur. Our findings highlight the importance of expectancy violation in shaping  placebo and nocebo effects and open up new avenues for managing positive and  negative expectations in clinical trials and practices.},\n\tlanguage = {eng},\n\tnumber = {6},\n\tjournal = {Clinical pharmacology and therapeutics},\n\tauthor = {Colloca, Luana and Schenk, Lieven A. and Nathan, Dominic E. and Robinson, Oliver J. and Grillon, Christian},\n\tmonth = dec,\n\tyear = {2019},\n\tpmid = {31350784},\n\tpmcid = {PMC6851406},\n\tnote = {Place: United States},\n\tkeywords = {*Cues, *Magnetic Resonance Imaging, *Placebo Effect, *Randomized Controlled Trials as Topic, *Research Design, Adult, Female, Humans, Male, Nocebo Effect, Pain Perception, Pain Threshold, Pain/*diagnostic imaging/physiopathology/psychology, Parietal Lobe/*diagnostic imaging/physiopathology, Predictive Value of Tests, Visual Perception, Young Adult},\n\tpages = {1246--1252},\n}\n\n
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\n Positive and negative expectancies drive behavioral and neurobiological placebo and nocebo effects, which in turn can have profound effects on patient improvement or worsening. However, expectations of events and outcomes are often not met in daily life and clinical practice. It is currently unknown how this affects placebo and nocebo effects. We have demonstrated that the violation of expectancies, such as when there is a discrepancy between what is expected and what is actually presented, reduces both placebo and nocebo effects while causing an extinction of placebo effects. The reduction of placebo and nocebo effects was paralleled by an activation of the left inferior parietal cortex, a brain region that redirects attention when discrepancies between sensory and cognitive events occur. Our findings highlight the importance of expectancy violation in shaping placebo and nocebo effects and open up new avenues for managing positive and negative expectations in clinical trials and practices.\n
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\n \n\n \n \n \n \n \n Altered learning under uncertainty in unmedicated mood and anxiety disorders.\n \n \n \n\n\n \n Aylward, J.; Valton, V.; Ahn, W.; Bond, R. L.; Dayan, P.; Roiser, J. P.; and Robinson, O. J.\n\n\n \n\n\n\n Nature Human Behaviour, 3(10): 1116–1123. October 2019.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n  \n \n 1 download\n \n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n
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@article{aylward_altered_2019,\n\ttitle = {Altered learning under uncertainty in unmedicated mood and anxiety disorders},\n\tvolume = {3},\n\tcopyright = {All rights reserved},\n\tissn = {2397-3374},\n\tdoi = {10.1038/s41562-019-0628-0},\n\tabstract = {Anxiety is characterized by altered responses under uncertain conditions, but the precise mechanism by which uncertainty changes the behaviour of anxious individuals is unclear. Here we probe the computational basis of learning under uncertainty in healthy individuals and individuals suffering from a mix of mood and anxiety disorders. Participants were asked to choose between four competing slot machines with fluctuating reward and punishment outcomes during safety and stress. We predicted that anxious individuals under stress would learn faster about punishments and exhibit choices that were more affected by those punishments, thus formalizing our predictions as parameters in reinforcement learning accounts of behaviour. Overall, the data suggest that anxious individuals are quicker to update their behaviour in response to negative outcomes (increased punishment learning rates). When treating anxiety, it may therefore be more fruitful to encourage anxious individuals to integrate information over longer horizons when bad things happen, rather than try to blunt their responses to negative outcomes.},\n\tlanguage = {eng},\n\tnumber = {10},\n\tjournal = {Nature Human Behaviour},\n\tauthor = {Aylward, Jessica and Valton, Vincent and Ahn, Woo-Young and Bond, Rebecca L. and Dayan, Peter and Roiser, Jonathan P. and Robinson, Oliver J.},\n\tmonth = oct,\n\tyear = {2019},\n\tpmid = {31209369},\n\tpmcid = {PMC6790140},\n\tkeywords = {*Uncertainty, Adolescent, Adult, Anxiety Disorders, Anxiety Disorders/physiopathology/*psychology, Case-Control Studies, Depressive Disorder, Depressive Disorder, Major, Depressive Disorder, Major/physiopathology/*psychology, Female, Humans, Learning, Learning/*physiology, Major/physiopathology/*psychology, Male, Mood Disorders, Mood Disorders/physiopathology/psychology, Panic Disorder, Panic Disorder/physiopathology/psychology, Psychological/physiopathology/*psychology, Punishment, Reward, Stress, Stress, Psychological, Stress, Psychological/physiopathology/*psychology, Uncertainty, Young Adult},\n\tpages = {1116--1123},\n}\n\n
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\n Anxiety is characterized by altered responses under uncertain conditions, but the precise mechanism by which uncertainty changes the behaviour of anxious individuals is unclear. Here we probe the computational basis of learning under uncertainty in healthy individuals and individuals suffering from a mix of mood and anxiety disorders. Participants were asked to choose between four competing slot machines with fluctuating reward and punishment outcomes during safety and stress. We predicted that anxious individuals under stress would learn faster about punishments and exhibit choices that were more affected by those punishments, thus formalizing our predictions as parameters in reinforcement learning accounts of behaviour. Overall, the data suggest that anxious individuals are quicker to update their behaviour in response to negative outcomes (increased punishment learning rates). When treating anxiety, it may therefore be more fruitful to encourage anxious individuals to integrate information over longer horizons when bad things happen, rather than try to blunt their responses to negative outcomes.\n
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\n  \n 2018\n \n \n (1)\n \n \n
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\n \n\n \n \n \n \n \n The role of prefrontal-subcortical circuitry in negative bias in anxiety: Translational, developmental and treatment perspectives.\n \n \n \n\n\n \n Carlisi, C. O.; and Robinson, O. J.\n\n\n \n\n\n\n Brain and Neuroscience Advances, 2: 2398212818774223. January 2018.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n \n \n \n \n\n\n\n
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@article{carlisi_role_2018,\n\ttitle = {The role of prefrontal-subcortical circuitry in negative bias in anxiety: {Translational}, developmental and treatment perspectives},\n\tvolume = {2},\n\tcopyright = {All rights reserved},\n\tissn = {2398-2128},\n\tshorttitle = {The role of prefrontal-subcortical circuitry in negative bias in anxiety},\n\tdoi = {10.1177/2398212818774223},\n\tabstract = {Anxiety disorders are the most common cause of mental ill health in the developed world, but our understanding of symptoms and treatments is not presently grounded in knowledge of the underlying neurobiological mechanisms. In this review, we discuss accumulating work that points to a role for prefrontal-subcortical brain circuitry in driving a core psychological symptom of anxiety disorders - negative affective bias. Specifically, we point to converging work across humans and animal models, suggesting a reciprocal relationship between dorsal and ventral prefrontal-amygdala circuits in promoting and inhibiting negative bias, respectively. We discuss how the developmental trajectory of these circuits may lead to the onset of anxiety during adolescence and, moreover, how effective pharmacological and psychological treatments may serve to shift the balance of activity within this circuitry to ameliorate negative bias symptoms. Together, these findings may bring us closer to a mechanistic, neurobiological understanding of anxiety disorders and their treatment.},\n\tlanguage = {eng},\n\tjournal = {Brain and Neuroscience Advances},\n\tauthor = {Carlisi, Christina O. and Robinson, Oliver J.},\n\tmonth = jan,\n\tyear = {2018},\n\tpmid = {30167466},\n\tpmcid = {PMC6097108},\n\tkeywords = {Anxiety, circuit, negative bias, prefrontal cortex},\n\tpages = {2398212818774223},\n}\n\n
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\n Anxiety disorders are the most common cause of mental ill health in the developed world, but our understanding of symptoms and treatments is not presently grounded in knowledge of the underlying neurobiological mechanisms. In this review, we discuss accumulating work that points to a role for prefrontal-subcortical brain circuitry in driving a core psychological symptom of anxiety disorders - negative affective bias. Specifically, we point to converging work across humans and animal models, suggesting a reciprocal relationship between dorsal and ventral prefrontal-amygdala circuits in promoting and inhibiting negative bias, respectively. We discuss how the developmental trajectory of these circuits may lead to the onset of anxiety during adolescence and, moreover, how effective pharmacological and psychological treatments may serve to shift the balance of activity within this circuitry to ameliorate negative bias symptoms. Together, these findings may bring us closer to a mechanistic, neurobiological understanding of anxiety disorders and their treatment.\n
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\n  \n 2017\n \n \n (11)\n \n \n
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\n \n\n \n \n \n \n \n Learning and Choice in Mood Disorders: Searching for the Computational Parameters of Anhedonia.\n \n \n \n\n\n \n Robinson, O. J.; and Chase, H. W.\n\n\n \n\n\n\n Computational psychiatry (Cambridge, Mass.), 1(1): 208–233. 2017.\n Place: England\n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n
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@article{robinson_learning_2017,\n\ttitle = {Learning and {Choice} in {Mood} {Disorders}: {Searching} for the {Computational} {Parameters} of {Anhedonia}.},\n\tvolume = {1},\n\tcopyright = {All rights reserved},\n\tissn = {2379-6227},\n\tdoi = {10.1162/CPSY_a_00009},\n\tabstract = {Computational approaches are increasingly being used to model behavioral and neural processes in mood and anxiety disorders. Here we explore the extent to  which the parameters of popular learning and decision-making models are  implicated in anhedonic symptoms of major depression. We first highlight the  parameters of reinforcement learning that have been implicated in anhedonia,  focusing, in particular, on the role that choice variability (i.e.,  "temperature") may play in explaining heterogeneity across previous findings. We  then turn to neuroimaging findings implicating attenuated ventral striatum  response in anhedonic responses and discuss possible causes of the heterogeneity  in the literature. Taken together, the reviewed findings highlight the potential  of the computational approach in teasing apart the observed heterogeneity in both  behavioral and functional imaging results. Nevertheless, considerable challenges  remain, and we conclude with five unresolved questions that seek to address  issues highlighted by the reviewed data.},\n\tlanguage = {eng},\n\tnumber = {1},\n\tjournal = {Computational psychiatry (Cambridge, Mass.)},\n\tauthor = {Robinson, Oliver J. and Chase, Henry W.},\n\tyear = {2017},\n\tpmid = {29400358},\n\tpmcid = {PMC5796642},\n\tnote = {Place: England},\n\tkeywords = {anxiety, computational psychiatry, decision making, mood disorders, reinforcement learning},\n\tpages = {208--233},\n}\n\n
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\n Computational approaches are increasingly being used to model behavioral and neural processes in mood and anxiety disorders. Here we explore the extent to which the parameters of popular learning and decision-making models are implicated in anhedonic symptoms of major depression. We first highlight the parameters of reinforcement learning that have been implicated in anhedonia, focusing, in particular, on the role that choice variability (i.e., \"temperature\") may play in explaining heterogeneity across previous findings. We then turn to neuroimaging findings implicating attenuated ventral striatum response in anhedonic responses and discuss possible causes of the heterogeneity in the literature. Taken together, the reviewed findings highlight the potential of the computational approach in teasing apart the observed heterogeneity in both behavioral and functional imaging results. Nevertheless, considerable challenges remain, and we conclude with five unresolved questions that seek to address issues highlighted by the reviewed data.\n
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\n \n\n \n \n \n \n \n Cognitive bias modification for facial interpretation: a randomized controlled trial of transfer to self-report and cognitive measures in a healthy sample.\n \n \n \n\n\n \n Peters, S. E.; Lumsden, J.; Peh, O. H.; Penton-Voak, I. S.; Munafò, M. R.; and Robinson, O. J.\n\n\n \n\n\n\n Royal Society open science, 4(12): 170681. December 2017.\n Place: England\n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n \n \n \n \n\n\n\n
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@article{peters_cognitive_2017,\n\ttitle = {Cognitive bias modification for facial interpretation: a randomized controlled trial of transfer to self-report and cognitive measures in a healthy sample.},\n\tvolume = {4},\n\tcopyright = {All rights reserved},\n\tissn = {2054-5703},\n\tdoi = {10.1098/rsos.170681},\n\tabstract = {Cognitive bias modification is a potential low-intensity intervention for mood disorders, but previous studies have shown mixed success. This study explored  whether facial interpretation bias modification (FIBM), a similar paradigm  designed to shift emotional interpretation (and/or perception) of faces would  transfer to: (i) self-reported symptoms and (ii) a battery of cognitive tasks. In  a preregistered, double-blind randomized controlled trial, healthy participants  received eight online sessions of FIBM (N = 52) or eight sham sessions (N = 52).  While we replicate that FIBM successfully shifts ambiguous facial expression  interpretation in the intervention group, this failed to transfer to the majority  of self-report or cognitive measures. There was, however, weak, inconclusive  evidence of transfer to a self-report measure of stress, a cognitive measure of  anhedonia, and evidence that results were moderated by trait anxiety (whereby  transference was greatest in those with higher baseline symptoms). We discuss the  need for work in both larger and clinical samples, while urging caution that  these FIBM training effects may not transfer to clinically relevant domains.},\n\tlanguage = {eng},\n\tnumber = {12},\n\tjournal = {Royal Society open science},\n\tauthor = {Peters, S. E. and Lumsden, J. and Peh, O. H. and Penton-Voak, I. S. and Munafò, M. R. and Robinson, O. J.},\n\tmonth = dec,\n\tyear = {2017},\n\tpmid = {29308221},\n\tpmcid = {PMC5749989},\n\tnote = {Place: England},\n\tkeywords = {cognitive bias modification, facial interpretation, randomized controlled trial, translational research},\n\tpages = {170681},\n}\n\n
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\n Cognitive bias modification is a potential low-intensity intervention for mood disorders, but previous studies have shown mixed success. This study explored whether facial interpretation bias modification (FIBM), a similar paradigm designed to shift emotional interpretation (and/or perception) of faces would transfer to: (i) self-reported symptoms and (ii) a battery of cognitive tasks. In a preregistered, double-blind randomized controlled trial, healthy participants received eight online sessions of FIBM (N = 52) or eight sham sessions (N = 52). While we replicate that FIBM successfully shifts ambiguous facial expression interpretation in the intervention group, this failed to transfer to the majority of self-report or cognitive measures. There was, however, weak, inconclusive evidence of transfer to a self-report measure of stress, a cognitive measure of anhedonia, and evidence that results were moderated by trait anxiety (whereby transference was greatest in those with higher baseline symptoms). We discuss the need for work in both larger and clinical samples, while urging caution that these FIBM training effects may not transfer to clinically relevant domains.\n
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\n \n\n \n \n \n \n \n Unreliability of putative fMRI biomarkers during emotional face processing.\n \n \n \n\n\n \n Nord, C. L.; Gray, A.; Charpentier, C. J.; Robinson, O. J.; and Roiser, J. P.\n\n\n \n\n\n\n NeuroImage, 156: 119–127. August 2017.\n Place: United States\n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n
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@article{nord_unreliability_2017,\n\ttitle = {Unreliability of putative {fMRI} biomarkers during emotional face processing.},\n\tvolume = {156},\n\tcopyright = {Copyright © 2017 The Authors. Published by Elsevier Inc. All rights reserved.},\n\tissn = {1095-9572 1053-8119},\n\tdoi = {10.1016/j.neuroimage.2017.05.024},\n\tabstract = {There is considerable need to develop tailored approaches to psychiatric treatment. Numerous researchers have proposed using functional magnetic resonance  imaging (fMRI) biomarkers to predict therapeutic response, in particular by  measuring task-evoked subgenual anterior cingulate (sgACC) and amygdala  activation in mood and anxiety disorders. Translating this to the clinic relies  on the assumption that blood-oxygen-level dependent (BOLD) responses in these  regions are stable within individuals. To test this assumption, we scanned a  group of 29 volunteers twice (mean test-retest interval=14.3 days) and calculated  the within-subject reliability of the amplitude of the amygdalae and sgACC BOLD  responses to emotional faces using three paradigms: emotion identification;  emotion matching; and gender classification. We also calculated the reliability  of activation in a control region, the right fusiform face area (FFA). All three  tasks elicited robust group activations in the amygdalae and sgACC (which changed  little on average over scanning sessions), but within-subject reliability was  surprisingly low, despite excellent reliability in the control right FFA region.  Our findings demonstrate low statistical reliability of two important putative  treatment biomarkers in mood and anxiety disorders.},\n\tlanguage = {eng},\n\tjournal = {NeuroImage},\n\tauthor = {Nord, C. L. and Gray, A. and Charpentier, C. J. and Robinson, O. J. and Roiser, J. P.},\n\tmonth = aug,\n\tyear = {2017},\n\tpmid = {28506872},\n\tpmcid = {PMC5553850},\n\tnote = {Place: United States},\n\tkeywords = {Adult, Amygdala, Biomarker, Brain Mapping/*methods, Brain/*diagnostic imaging, Emotion, Emotions/physiology, Facial Recognition/*physiology, Female, Humans, Magnetic Resonance Imaging/*methods, Male, Mental Disorders/diagnosis, Psychiatry, Reproducibility of Results, Subgenual cingulate, Young Adult, fMRI},\n\tpages = {119--127},\n}\n\n
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\n There is considerable need to develop tailored approaches to psychiatric treatment. Numerous researchers have proposed using functional magnetic resonance imaging (fMRI) biomarkers to predict therapeutic response, in particular by measuring task-evoked subgenual anterior cingulate (sgACC) and amygdala activation in mood and anxiety disorders. Translating this to the clinic relies on the assumption that blood-oxygen-level dependent (BOLD) responses in these regions are stable within individuals. To test this assumption, we scanned a group of 29 volunteers twice (mean test-retest interval=14.3 days) and calculated the within-subject reliability of the amplitude of the amygdalae and sgACC BOLD responses to emotional faces using three paradigms: emotion identification; emotion matching; and gender classification. We also calculated the reliability of activation in a control region, the right fusiform face area (FFA). All three tasks elicited robust group activations in the amygdalae and sgACC (which changed little on average over scanning sessions), but within-subject reliability was surprisingly low, despite excellent reliability in the control right FFA region. Our findings demonstrate low statistical reliability of two important putative treatment biomarkers in mood and anxiety disorders.\n
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\n \n\n \n \n \n \n \n Threat of shock and aversive inhibition: Induced anxiety modulates Pavlovian-instrumental interactions.\n \n \n \n\n\n \n Mkrtchian, A.; Roiser, J. P.; and Robinson, O. J.\n\n\n \n\n\n\n Journal of experimental psychology. General, 146(12): 1694–1704. December 2017.\n Place: United States\n\n\n\n
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@article{mkrtchian_threat_2017,\n\ttitle = {Threat of shock and aversive inhibition: {Induced} anxiety modulates {Pavlovian}-instrumental interactions.},\n\tvolume = {146},\n\tcopyright = {(c) 2017 APA, all rights reserved).},\n\tissn = {1939-2222 0096-3445 0022-1015},\n\tdoi = {10.1037/xge0000363},\n\tabstract = {Anxiety can be an adaptive response to potentially threatening situations. However, if experienced in inappropriate contexts, it can also lead to  pathological and maladaptive anxiety disorders. Experimentally, anxiety can be  induced in healthy individuals using the threat of shock (ToS) paradigm.  Accumulating work with this paradigm suggests that anxiety promotes harm-avoidant  mechanisms through enhanced inhibitory control. However, the specific cognitive  mechanisms underlying anxiety-linked inhibitory control are unclear. Critically,  behavioral inhibition can arise from at least 2 interacting valuation systems:  instrumental (a goal-directed system) and Pavlovian (a "hardwired" reflexive  system). The present study (N = 62) replicated a study showing improved response  inhibition under ToS in healthy participants, and additionally examined the  impact of ToS on aversive and appetitive Pavlovian-instrumental interactions in a  reinforced go/no-go task. When Pavlovian and instrumental systems were in  conflict, ToS increased inhibition to aversive events, while leaving appetitive  interactions unperturbed. We argue that anxiety promotes avoidant behavior in  potentially harmful situations by potentiating aversive Pavlovian reactions  (i.e., promoting avoidance in the face of threats). Critically, such a mechanism  would drive adaptive harm-avoidant behavior in threatening situations where  Pavlovian and instrumental processes are aligned, but at the same time, result in  maladaptive behaviors when misaligned and where instrumental control would be  advantageous. This has important implications for our understanding of the  mechanisms that underlie pathological anxiety. (PsycINFO Database Record},\n\tlanguage = {eng},\n\tnumber = {12},\n\tjournal = {Journal of experimental psychology. General},\n\tauthor = {Mkrtchian, Anahit and Roiser, Jonathan P. and Robinson, Oliver J.},\n\tmonth = dec,\n\tyear = {2017},\n\tpmid = {28910125},\n\tpmcid = {PMC5733814},\n\tnote = {Place: United States},\n\tkeywords = {*Inhibition, *Inhibition, Psychological, *Reinforcement, *Reinforcement, Psychology, Adolescent, Adult, Anxiety/*physiopathology, Avoidance Learning/*physiology, Classical/*physiology, Conditioning, Conditioning, Classical/*physiology, Female, Humans, Male, Middle Aged, Psychological, Psychology, Young Adult},\n\tpages = {1694--1704},\n}\n\n
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\n Anxiety can be an adaptive response to potentially threatening situations. However, if experienced in inappropriate contexts, it can also lead to pathological and maladaptive anxiety disorders. Experimentally, anxiety can be induced in healthy individuals using the threat of shock (ToS) paradigm. Accumulating work with this paradigm suggests that anxiety promotes harm-avoidant mechanisms through enhanced inhibitory control. However, the specific cognitive mechanisms underlying anxiety-linked inhibitory control are unclear. Critically, behavioral inhibition can arise from at least 2 interacting valuation systems: instrumental (a goal-directed system) and Pavlovian (a \"hardwired\" reflexive system). The present study (N = 62) replicated a study showing improved response inhibition under ToS in healthy participants, and additionally examined the impact of ToS on aversive and appetitive Pavlovian-instrumental interactions in a reinforced go/no-go task. When Pavlovian and instrumental systems were in conflict, ToS increased inhibition to aversive events, while leaving appetitive interactions unperturbed. We argue that anxiety promotes avoidant behavior in potentially harmful situations by potentiating aversive Pavlovian reactions (i.e., promoting avoidance in the face of threats). Critically, such a mechanism would drive adaptive harm-avoidant behavior in threatening situations where Pavlovian and instrumental processes are aligned, but at the same time, result in maladaptive behaviors when misaligned and where instrumental control would be advantageous. This has important implications for our understanding of the mechanisms that underlie pathological anxiety. (PsycINFO Database Record\n
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\n \n\n \n \n \n \n \n \n Modeling Avoidance in Mood and Anxiety Disorders Using Reinforcement Learning.\n \n \n \n \n\n\n \n Mkrtchian, A.; Aylward, J.; Dayan, P.; Roiser, J. P.; and Robinson, O. J.\n\n\n \n\n\n\n Biological Psychiatry, 82(7): 532–539. October 2017.\n \n\n\n\n
\n\n\n\n \n \n \"ModelingPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n  \n \n 1 download\n \n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n
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@article{mkrtchian_modeling_2017,\n\tseries = {Stress: {Mechanisms} in {Gut} and {Brain}},\n\ttitle = {Modeling {Avoidance} in {Mood} and {Anxiety} {Disorders} {Using} {Reinforcement} {Learning}},\n\tvolume = {82},\n\tcopyright = {All rights reserved},\n\tissn = {0006-3223},\n\turl = {https://www.sciencedirect.com/science/article/pii/S0006322317300914},\n\tdoi = {10.1016/j.biopsych.2017.01.017},\n\tabstract = {Background\nSerious and debilitating symptoms of anxiety are the most common mental health problem worldwide, accounting for around 5\\% of all adult years lived with disability in the developed world. Avoidance behavior—avoiding social situations for fear of embarrassment, for instance—is a core feature of such anxiety. However, as for many other psychiatric symptoms the biological mechanisms underlying avoidance remain unclear.\nMethods\nReinforcement learning models provide formal and testable characterizations of the mechanisms of decision making; here, we examine avoidance in these terms. A total of 101 healthy participants and individuals with mood and anxiety disorders completed an approach-avoidance go/no-go task under stress induced by threat of unpredictable shock.\nResults\nWe show an increased reliance in the mood and anxiety group on a parameter of our reinforcement learning model that characterizes a prepotent (pavlovian) bias to withhold responding in the face of negative outcomes. This was particularly the case when the mood and anxiety group was under stress.\nConclusions\nThis formal description of avoidance within the reinforcement learning framework provides a new means of linking clinical symptoms with biophysically plausible models of neural circuitry and, as such, takes us closer to a mechanistic understanding of mood and anxiety disorders.},\n\tlanguage = {en},\n\tnumber = {7},\n\turldate = {2022-08-22},\n\tjournal = {Biological Psychiatry},\n\tauthor = {Mkrtchian, Anahit and Aylward, Jessica and Dayan, Peter and Roiser, Jonathan P. and Robinson, Oliver J.},\n\tmonth = oct,\n\tyear = {2017},\n\tkeywords = {*Reinforcement, *Reinforcement, Psychology, Adolescent, Adult, Anxiety, Anxiety/*psychology, Avoidance, Avoidance Learning/*physiology, Bayes Theorem, Decision Making/physiology, Diathesis–stress, Female, Humans, Male, Middle Aged, Models, Models, Psychological, Mood Disorders/*psychology/rehabilitation, Pavlovian bias, Psychiatric Status Rating Scales, Psychological, Psychology, Reinforcement learning, Threat of shock, Young Adult},\n\tpages = {532--539},\n}\n\n
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\n Background Serious and debilitating symptoms of anxiety are the most common mental health problem worldwide, accounting for around 5% of all adult years lived with disability in the developed world. Avoidance behavior—avoiding social situations for fear of embarrassment, for instance—is a core feature of such anxiety. However, as for many other psychiatric symptoms the biological mechanisms underlying avoidance remain unclear. Methods Reinforcement learning models provide formal and testable characterizations of the mechanisms of decision making; here, we examine avoidance in these terms. A total of 101 healthy participants and individuals with mood and anxiety disorders completed an approach-avoidance go/no-go task under stress induced by threat of unpredictable shock. Results We show an increased reliance in the mood and anxiety group on a parameter of our reinforcement learning model that characterizes a prepotent (pavlovian) bias to withhold responding in the face of negative outcomes. This was particularly the case when the mood and anxiety group was under stress. Conclusions This formal description of avoidance within the reinforcement learning framework provides a new means of linking clinical symptoms with biophysically plausible models of neural circuitry and, as such, takes us closer to a mechanistic understanding of mood and anxiety disorders.\n
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\n \n\n \n \n \n \n \n Anxiety-mediated facilitation of behavioral inhibition: Threat processing and defensive reactivity during a go/no-go task.\n \n \n \n\n\n \n Grillon, C.; Robinson, O. J.; Krimsky, M.; O'Connell, K.; Alvarez, G.; and Ernst, M.\n\n\n \n\n\n\n Emotion (Washington, D.C.), 17(2): 259–266. March 2017.\n Place: United States\n\n\n\n
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@article{grillon_anxiety-mediated_2017,\n\ttitle = {Anxiety-mediated facilitation of behavioral inhibition: {Threat} processing and defensive reactivity during a go/no-go task.},\n\tvolume = {17},\n\tcopyright = {(c) 2017 APA, all rights reserved).},\n\tissn = {1931-1516 1528-3542},\n\tdoi = {10.1037/emo0000214},\n\tabstract = {Anxiety can be broken down into multiple facets including behavioral components, such as defensive reactivity, and cognitive components, such as distracting  anxious thoughts. In a previous study, we showed that anticipation of  unpredictable shocks facilitated response inhibition to infrequent no-go trials  during a go/no-go task. The present study extends this work to examine the  distinct contribution of defensive reactivity, measures with fear-potentiated  startle, and anxious thought, assessed with thought probes, on go and no-go  performance. Consistent with our prior findings, shock anticipation facilitated  response inhibition (i.e., reduced errors of commission) on the no-go trials.  Regression analyses showed that (a) no-go accuracy was positively associated with  fear-potentiated startle and negatively associated with  threat-related/task-unrelated thoughts and (b) go accuracy correlated negatively  with fear-potentiated startle. Thus, while the present findings confirm the  influence of anxiety on response inhibition, they also show that such influence  reflects the balance between the positive effect of defensive reactivity and the  negative effect of distracting anxious thoughts. (PsycINFO Database Record},\n\tlanguage = {eng},\n\tnumber = {2},\n\tjournal = {Emotion (Washington, D.C.)},\n\tauthor = {Grillon, Christian and Robinson, Oliver J. and Krimsky, Marissa and O'Connell, Katherine and Alvarez, Gabriella and Ernst, Monique},\n\tmonth = mar,\n\tyear = {2017},\n\tpmid = {27642657},\n\tpmcid = {PMC5328922},\n\tnote = {Place: United States},\n\tkeywords = {*Inhibition, *Inhibition, Psychological, Adult, Anxiety/*psychology, Fear/*psychology, Female, Humans, Male, Neuropsychological Tests, Psychological, Reflex, Reflex, Startle/*physiology, Startle/*physiology, Young Adult},\n\tpages = {259--266},\n}\n\n
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\n Anxiety can be broken down into multiple facets including behavioral components, such as defensive reactivity, and cognitive components, such as distracting anxious thoughts. In a previous study, we showed that anticipation of unpredictable shocks facilitated response inhibition to infrequent no-go trials during a go/no-go task. The present study extends this work to examine the distinct contribution of defensive reactivity, measures with fear-potentiated startle, and anxious thought, assessed with thought probes, on go and no-go performance. Consistent with our prior findings, shock anticipation facilitated response inhibition (i.e., reduced errors of commission) on the no-go trials. Regression analyses showed that (a) no-go accuracy was positively associated with fear-potentiated startle and negatively associated with threat-related/task-unrelated thoughts and (b) go accuracy correlated negatively with fear-potentiated startle. Thus, while the present findings confirm the influence of anxiety on response inhibition, they also show that such influence reflects the balance between the positive effect of defensive reactivity and the negative effect of distracting anxious thoughts. (PsycINFO Database Record\n
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\n \n\n \n \n \n \n \n Clinical anxiety promotes excessive response inhibition.\n \n \n \n\n\n \n Grillon, C.; Robinson, O. J.; O'Connell, K.; Davis, A.; Alvarez, G.; Pine, D. S.; and Ernst, M.\n\n\n \n\n\n\n Psychological medicine, 47(3): 484–494. February 2017.\n Place: England\n\n\n\n
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@article{grillon_clinical_2017,\n\ttitle = {Clinical anxiety promotes excessive response inhibition.},\n\tvolume = {47},\n\tcopyright = {All rights reserved},\n\tissn = {1469-8978 0033-2917},\n\tdoi = {10.1017/S0033291716002555},\n\tabstract = {BACKGROUND: Laboratory tasks to delineate anxiety disorder features are used to refine classification and inform our understanding of etiological mechanisms. The  present study examines laboratory measures of response inhibition, specifically  the inhibition of a pre-potent motor response, in clinical anxiety. Data on  associations between anxiety and response inhibition remain inconsistent, perhaps  because of dissociable effects of clinical anxiety and experimentally manipulated  state anxiety. Few studies directly assess the independent and interacting  effects of these two anxiety types (state v. disorder) on response inhibition.  The current study accomplished this goal, by manipulating state anxiety in  healthy and clinically anxious individuals while they complete a response  inhibition task. METHOD: The study employs the threat-of-shock paradigm, one of  the best-established manipulations for robustly increasing state anxiety.  Participants included 82 adults (41 healthy; 41 patients with an anxiety  disorder). A go/nogo task with highly frequent go trials was administered during  alternating periods of safety and shock threat. Signal detection theory was used  to quantify response bias and signal-detection sensitivity. RESULTS: There were  independent effects of anxiety and clinical anxiety on response inhibition. In  both groups, heightened anxiety facilitated response inhibition, leading to  reduced nogo commission errors. Compared with the healthy group, clinical anxiety  was associated with excessive response inhibition and increased go omission  errors in both the safe and threat conditions. CONCLUSIONS: Response inhibition  and its impact on go omission errors appear to be a promising behavioral marker  of clinical anxiety. These results have implications for a dimensional view of  clinical anxiety.},\n\tlanguage = {eng},\n\tnumber = {3},\n\tjournal = {Psychological medicine},\n\tauthor = {Grillon, C. and Robinson, O. J. and O'Connell, K. and Davis, A. and Alvarez, G. and Pine, D. S. and Ernst, M.},\n\tmonth = feb,\n\tyear = {2017},\n\tpmid = {27776562},\n\tpmcid = {PMC6100803},\n\tnote = {Place: England},\n\tkeywords = {*Inhibition, *Inhibition, Psychological, Adult, Anxiety, Anxiety Disorders/*physiopathology, Biomarkers, Fear/*physiology, Female, Humans, Male, Psychological, Psychological/*physiology, Psychomotor Performance/*physiology, Signal Detection, Signal Detection, Psychological/*physiology, Young Adult, anxiety disorders, behavioral inhibition, go/nogo, threat of shock},\n\tpages = {484--494},\n}\n\n
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\n BACKGROUND: Laboratory tasks to delineate anxiety disorder features are used to refine classification and inform our understanding of etiological mechanisms. The present study examines laboratory measures of response inhibition, specifically the inhibition of a pre-potent motor response, in clinical anxiety. Data on associations between anxiety and response inhibition remain inconsistent, perhaps because of dissociable effects of clinical anxiety and experimentally manipulated state anxiety. Few studies directly assess the independent and interacting effects of these two anxiety types (state v. disorder) on response inhibition. The current study accomplished this goal, by manipulating state anxiety in healthy and clinically anxious individuals while they complete a response inhibition task. METHOD: The study employs the threat-of-shock paradigm, one of the best-established manipulations for robustly increasing state anxiety. Participants included 82 adults (41 healthy; 41 patients with an anxiety disorder). A go/nogo task with highly frequent go trials was administered during alternating periods of safety and shock threat. Signal detection theory was used to quantify response bias and signal-detection sensitivity. RESULTS: There were independent effects of anxiety and clinical anxiety on response inhibition. In both groups, heightened anxiety facilitated response inhibition, leading to reduced nogo commission errors. Compared with the healthy group, clinical anxiety was associated with excessive response inhibition and increased go omission errors in both the safe and threat conditions. CONCLUSIONS: Response inhibition and its impact on go omission errors appear to be a promising behavioral marker of clinical anxiety. These results have implications for a dimensional view of clinical anxiety.\n
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\n \n\n \n \n \n \n \n Enhanced Risk Aversion, But Not Loss Aversion, in Unmedicated Pathological Anxiety.\n \n \n \n\n\n \n Charpentier, C. J.; Aylward, J.; Roiser, J. P.; and Robinson, O. J.\n\n\n \n\n\n\n Biological psychiatry, 81(12): 1014–1022. June 2017.\n Place: United States\n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n  \n \n 1 download\n \n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n
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@article{charpentier_enhanced_2017,\n\ttitle = {Enhanced {Risk} {Aversion}, {But} {Not} {Loss} {Aversion}, in {Unmedicated} {Pathological} {Anxiety}.},\n\tvolume = {81},\n\tcopyright = {Copyright © 2017 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved.},\n\tissn = {1873-2402 0006-3223},\n\tdoi = {10.1016/j.biopsych.2016.12.010},\n\tabstract = {BACKGROUND: Anxiety disorders are associated with disruptions in both emotional processing and decision making. As a result, anxious individuals often make  decisions that favor harm avoidance. However, this bias could be driven by  enhanced aversion to uncertainty about the decision outcome (e.g., risk) or  aversion to negative outcomes (e.g., loss). Distinguishing between these  possibilities may provide a better cognitive understanding of anxiety disorders  and hence inform treatment strategies. METHODS: To address this question,  unmedicated individuals with pathological anxiety (n = 25) and matched healthy  control subjects (n = 23) completed a gambling task featuring a decision between  a gamble and a safe (certain) option on every trial. Choices on one type of  gamble-involving weighing a potential win against a potential loss (mixed)-could  be driven by both loss and risk aversion, whereas choices on the other  type-featuring only wins (gain only)-were exclusively driven by risk aversion. By  fitting a computational prospect theory model to participants' choices, we were  able to reliably estimate risk and loss aversion and their respective  contribution to gambling decisions. RESULTS: Relative to healthy control  subjects, pathologically anxious participants exhibited enhanced risk aversion  but equivalent levels of loss aversion. CONCLUSIONS: Individuals with  pathological anxiety demonstrate clear avoidance biases in their decision making.  These findings suggest that this may be driven by a reduced propensity to take  risks rather than a stronger aversion to losses. This important clarification  suggests that psychological interventions for anxiety should focus on reducing  risk sensitivity rather than reducing sensitivity to negative outcomes per se.},\n\tlanguage = {eng},\n\tnumber = {12},\n\tjournal = {Biological psychiatry},\n\tauthor = {Charpentier, Caroline J. and Aylward, Jessica and Roiser, Jonathan P. and Robinson, Oliver J.},\n\tmonth = jun,\n\tyear = {2017},\n\tpmid = {28126210},\n\tpmcid = {PMC5466268},\n\tnote = {Place: United States},\n\tkeywords = {*Avoidance Learning, *Risk-Taking, Adult, Anxiety, Anxiety/*psychology, Case-Control Studies, Decision Making, Decision making, Emotion, Female, Gambling/psychology, Humans, Loss aversion, Male, Memory, Risk aversion, Young Adult},\n\tpages = {1014--1022},\n}\n\n
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\n BACKGROUND: Anxiety disorders are associated with disruptions in both emotional processing and decision making. As a result, anxious individuals often make decisions that favor harm avoidance. However, this bias could be driven by enhanced aversion to uncertainty about the decision outcome (e.g., risk) or aversion to negative outcomes (e.g., loss). Distinguishing between these possibilities may provide a better cognitive understanding of anxiety disorders and hence inform treatment strategies. METHODS: To address this question, unmedicated individuals with pathological anxiety (n = 25) and matched healthy control subjects (n = 23) completed a gambling task featuring a decision between a gamble and a safe (certain) option on every trial. Choices on one type of gamble-involving weighing a potential win against a potential loss (mixed)-could be driven by both loss and risk aversion, whereas choices on the other type-featuring only wins (gain only)-were exclusively driven by risk aversion. By fitting a computational prospect theory model to participants' choices, we were able to reliably estimate risk and loss aversion and their respective contribution to gambling decisions. RESULTS: Relative to healthy control subjects, pathologically anxious participants exhibited enhanced risk aversion but equivalent levels of loss aversion. CONCLUSIONS: Individuals with pathological anxiety demonstrate clear avoidance biases in their decision making. These findings suggest that this may be driven by a reduced propensity to take risks rather than a stronger aversion to losses. This important clarification suggests that psychological interventions for anxiety should focus on reducing risk sensitivity rather than reducing sensitivity to negative outcomes per se.\n
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\n \n\n \n \n \n \n \n The impact of threat of shock-induced anxiety on memory encoding and retrieval.\n \n \n \n\n\n \n Bolton, S.; and Robinson, O. J.\n\n\n \n\n\n\n Learning & memory (Cold Spring Harbor, N.Y.), 24(10): 532–542. October 2017.\n Place: United States\n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n  \n \n 1 download\n \n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n
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@article{bolton_impact_2017,\n\ttitle = {The impact of threat of shock-induced anxiety on memory encoding and retrieval.},\n\tvolume = {24},\n\tcopyright = {© 2017 Bolton and Robinson; Published by Cold Spring Harbor Laboratory Press.},\n\tissn = {1549-5485 1072-0502},\n\tdoi = {10.1101/lm.045187.117},\n\tabstract = {Anxiety disorders are the most common mental health disorders, and daily transient feelings of anxiety (or "stress") are ubiquitous. However, the precise  impact of both transient and pathological anxiety on higher-order cognitive  functions, including short- and long-term memory, is poorly understood. A clearer  understanding of the anxiety-memory relationship is important as one of the core  symptoms of anxiety, most prominently in post-traumatic stress disorder (PTSD),  is intrusive reexperiencing of traumatic events in the form of vivid memories.  This study therefore aimed to examine the impact of induced anxiety (threat of  shock) on memory encoding and retrieval. Eighty-six healthy participants  completed tasks assessing: visuospatial working memory, verbal recognition, face  recognition, and associative memory. Critically, anxiety was manipulated  within-subjects: information was both encoded and retrieved under threat of shock  and safe (no shock) conditions. Results revealed that visuospatial working memory  was enhanced when information was encoded and subsequently retrieved under  threat, and that threat impaired the encoding of faces regardless of the  condition in which it was retrieved. Episodic memory and verbal short-term  recognition were, however, unimpaired. These findings indicate that transient  anxiety in healthy individuals has domain-specific, rather than domain-general,  impacts on memory. Future studies would benefit from expanding these findings  into anxiety disorder patients to delineate the differences between adaptive and  maladaptive responding.},\n\tlanguage = {eng},\n\tnumber = {10},\n\tjournal = {Learning \\& memory (Cold Spring Harbor, N.Y.)},\n\tauthor = {Bolton, Sorcha and Robinson, Oliver J.},\n\tmonth = oct,\n\tyear = {2017},\n\tpmid = {28916628},\n\tpmcid = {PMC5602344},\n\tnote = {Place: United States},\n\tkeywords = {*Memory, Adolescent, Adult, Analysis of Variance, Anxiety/*psychology, Electroshock, Fear/*psychology, Female, Humans, Male, Middle Aged, Neuropsychological Tests, Wrist, Young Adult},\n\tpages = {532--542},\n}\n\n
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\n Anxiety disorders are the most common mental health disorders, and daily transient feelings of anxiety (or \"stress\") are ubiquitous. However, the precise impact of both transient and pathological anxiety on higher-order cognitive functions, including short- and long-term memory, is poorly understood. A clearer understanding of the anxiety-memory relationship is important as one of the core symptoms of anxiety, most prominently in post-traumatic stress disorder (PTSD), is intrusive reexperiencing of traumatic events in the form of vivid memories. This study therefore aimed to examine the impact of induced anxiety (threat of shock) on memory encoding and retrieval. Eighty-six healthy participants completed tasks assessing: visuospatial working memory, verbal recognition, face recognition, and associative memory. Critically, anxiety was manipulated within-subjects: information was both encoded and retrieved under threat of shock and safe (no shock) conditions. Results revealed that visuospatial working memory was enhanced when information was encoded and subsequently retrieved under threat, and that threat impaired the encoding of faces regardless of the condition in which it was retrieved. Episodic memory and verbal short-term recognition were, however, unimpaired. These findings indicate that transient anxiety in healthy individuals has domain-specific, rather than domain-general, impacts on memory. Future studies would benefit from expanding these findings into anxiety disorder patients to delineate the differences between adaptive and maladaptive responding.\n
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\n \n\n \n \n \n \n \n The impact of induced anxiety on affective response inhibition.\n \n \n \n\n\n \n Aylward, J.; Valton, V.; Goer, F.; Mkrtchian, A.; Lally, N.; Peters, S.; Limbachya, T.; and Robinson, O. J.\n\n\n \n\n\n\n Royal Society open science, 4(6): 170084. June 2017.\n Place: England\n\n\n\n
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@article{aylward_impact_2017,\n\ttitle = {The impact of induced anxiety on affective response inhibition.},\n\tvolume = {4},\n\tcopyright = {All rights reserved},\n\tissn = {2054-5703},\n\tdoi = {10.1098/rsos.170084},\n\tabstract = {Studying the effects of experimentally induced anxiety in healthy volunteers may increase our understanding of the mechanisms underpinning anxiety disorders.  Experimentally induced stress (via threat of unpredictable shock) improves  accuracy at withholding a response on the sustained attention to response task  (SART), and in separate studies improves accuracy to classify fearful faces,  creating an affective bias. Integrating these findings, participants at two  public science engagement events (n = 46, n = 55) were recruited to explore the  effects of experimentally induced stress on an affective version of the SART. We  hypothesized that we would see an improved accuracy at withholding a response to  affectively congruent stimuli (i.e. increased accuracy at withholding a response  to fearful 'no-go' distractors) under threat of shock. Induced anxiety slowed  reaction time, and at the second event quicker responses were made to fearful  stimuli. However, we did not observe improved inhibition overall during induced  anxiety, and there was no evidence to suggest an interaction between induced  anxiety and stimulus valence on response accuracy. Indeed Bayesian analysis  provided decisive evidence against this hypothesis. We suggest that the presence  of emotional stimuli might make the safe condition more anxiogenic, reducing the  differential between conditions and knocking out any threat-potentiated  improvement.},\n\tlanguage = {eng},\n\tnumber = {6},\n\tjournal = {Royal Society open science},\n\tauthor = {Aylward, Jessica and Valton, Vincent and Goer, Franziska and Mkrtchian, Anahit and Lally, Níall and Peters, Sarah and Limbachya, Tarun and Robinson, Oliver J.},\n\tmonth = jun,\n\tyear = {2017},\n\tpmid = {28680667},\n\tpmcid = {PMC5493909},\n\tnote = {Place: England},\n\tkeywords = {affective response inhibition, mood and anxiety disorders, stress, threat of shock},\n\tpages = {170084},\n}\n\n
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\n\n\n
\n Studying the effects of experimentally induced anxiety in healthy volunteers may increase our understanding of the mechanisms underpinning anxiety disorders. Experimentally induced stress (via threat of unpredictable shock) improves accuracy at withholding a response on the sustained attention to response task (SART), and in separate studies improves accuracy to classify fearful faces, creating an affective bias. Integrating these findings, participants at two public science engagement events (n = 46, n = 55) were recruited to explore the effects of experimentally induced stress on an affective version of the SART. We hypothesized that we would see an improved accuracy at withholding a response to affectively congruent stimuli (i.e. increased accuracy at withholding a response to fearful 'no-go' distractors) under threat of shock. Induced anxiety slowed reaction time, and at the second event quicker responses were made to fearful stimuli. However, we did not observe improved inhibition overall during induced anxiety, and there was no evidence to suggest an interaction between induced anxiety and stimulus valence on response accuracy. Indeed Bayesian analysis provided decisive evidence against this hypothesis. We suggest that the presence of emotional stimuli might make the safe condition more anxiogenic, reducing the differential between conditions and knocking out any threat-potentiated improvement.\n
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\n \n\n \n \n \n \n \n Towards an emotional 'stress test': a reliable, non-subjective cognitive measure of anxious responding.\n \n \n \n\n\n \n Aylward, J.; and Robinson, O. J.\n\n\n \n\n\n\n Scientific reports, 7: 40094. January 2017.\n Place: England\n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n  \n \n 1 download\n \n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n
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@article{aylward_towards_2017,\n\ttitle = {Towards an emotional 'stress test': a reliable, non-subjective cognitive measure of anxious responding.},\n\tvolume = {7},\n\tcopyright = {All rights reserved},\n\tissn = {2045-2322},\n\tdoi = {10.1038/srep40094},\n\tabstract = {Response to stress or external threats is a key factor in mood and anxiety disorder aetiology. Current measures of anxious responding to threats are limited  because they largely rely on retrospective self-report. Objectively quantifying  individual differences in threat response would be a valuable step towards  improving our understanding of anxiety disorder vulnerability. Our goal is to  therefore develop a reliable, objective, within-subject 'stress-test' of anxious  responding. To this end, we examined threat-potentiated performance on an  inhibitory control task from baseline to 2-4 weeks (n = 50) and again after 5-9  months (n = 22). We also describe single session data for a larger sample  (n = 157) to provide better population-level estimates of task performance  variance. Replicating previous findings, threat of shock improved distractor  accuracy and slowed target reaction time on our task. Critically, both  within-subject self-report measures of anxiety (ICC = 0.66) and  threat-potentiated task performance (ICC = 0.58) showed clinically useful  test-retest reliability. Threat-potentiated task performance may therefore hold  promise as a non-subjective measure of individual anxious responding.},\n\tlanguage = {eng},\n\tjournal = {Scientific reports},\n\tauthor = {Aylward, Jessica and Robinson, Oliver J.},\n\tmonth = jan,\n\tyear = {2017},\n\tpmid = {28071668},\n\tpmcid = {PMC5223119},\n\tnote = {Place: England},\n\tkeywords = {Adolescent, Adult, Anxiety/*diagnosis, Diagnostic Tests, Diagnostic Tests, Routine/*methods, Female, Healthy Volunteers, Humans, Male, Psychological/*diagnosis, Retrospective Studies, Routine/*methods, Stress, Stress, Psychological/*diagnosis, Young Adult},\n\tpages = {40094},\n}\n\n
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\n Response to stress or external threats is a key factor in mood and anxiety disorder aetiology. Current measures of anxious responding to threats are limited because they largely rely on retrospective self-report. Objectively quantifying individual differences in threat response would be a valuable step towards improving our understanding of anxiety disorder vulnerability. Our goal is to therefore develop a reliable, objective, within-subject 'stress-test' of anxious responding. To this end, we examined threat-potentiated performance on an inhibitory control task from baseline to 2-4 weeks (n = 50) and again after 5-9 months (n = 22). We also describe single session data for a larger sample (n = 157) to provide better population-level estimates of task performance variance. Replicating previous findings, threat of shock improved distractor accuracy and slowed target reaction time on our task. Critically, both within-subject self-report measures of anxiety (ICC = 0.66) and threat-potentiated task performance (ICC = 0.58) showed clinically useful test-retest reliability. Threat-potentiated task performance may therefore hold promise as a non-subjective measure of individual anxious responding.\n
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\n  \n 2016\n \n \n (4)\n \n \n
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\n \n\n \n \n \n \n \n Anxiety-potentiated amygdala-medial frontal coupling and attentional control.\n \n \n \n\n\n \n Robinson, O. J.; Krimsky, M.; Lieberman, L.; Vytal, K.; Ernst, M.; and Grillon, C.\n\n\n \n\n\n\n Translational psychiatry, 6(6): e833. June 2016.\n Place: United States\n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n
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@article{robinson_anxiety-potentiated_2016,\n\ttitle = {Anxiety-potentiated amygdala-medial frontal coupling and attentional control.},\n\tvolume = {6},\n\tcopyright = {All rights reserved},\n\tissn = {2158-3188},\n\tdoi = {10.1038/tp.2016.105},\n\tabstract = {Anxiety disorders can be treated both pharmacologically and psychologically, but many individuals either fail to respond to treatment or relapse. Improving  outcomes is difficult, in part because we have incomplete understanding of the  neurobiological mechanisms underlying current treatments. In a sequence of  studies, we have identified 'affective bias-related' amygdala-medial cortical  coupling as a candidate substrate underlying adaptive anxiety (that is, anxiety  elicited by threat of shock in healthy individuals) and shown that it is also  chronically engaged in maladaptive anxiety disorders. We have provided evidence  that this circuit can be modulated pharmacologically, but whether this mechanism  can be shifted by simple psychological instruction is unknown. In this functional  magnetic resonance imaging study, we extend a previously used translational  anxiety induction (threat of shock) in healthy subjects (N=43) and cognitive task  to include an element of instructed attentional control. Replicating our previous  findings, we show that induced anxiety engages 'affective bias-related'  amygdala-dorsal medial frontal coupling during the processing of emotional faces.  By contrast, instructing subjects to attend to neutral shapes (and ignore faces)  disengages this circuitry and increases putative 'attentional control-related'  coupling between the amygdala and a more rostral prefrontal region. These neural  coupling changes are accompanied by corresponding modulation of behavioural  performance. Taken together, these findings serve to further highlight the  potential role of amygdala-medial frontal coupling in the pathogenesis of anxiety  and highlight a mechanism by which it can be modulated via psychological  instructions. This, in turn, generates hypotheses for future work exploring the  mechanisms underlying psychological therapeutic interventions for anxiety.},\n\tlanguage = {eng},\n\tnumber = {6},\n\tjournal = {Translational psychiatry},\n\tauthor = {Robinson, O. J. and Krimsky, M. and Lieberman, L. and Vytal, K. and Ernst, M. and Grillon, C.},\n\tmonth = jun,\n\tyear = {2016},\n\tpmid = {27271859},\n\tpmcid = {PMC4931603},\n\tnote = {Place: United States},\n\tkeywords = {*Magnetic Resonance Imaging, Adult, Amygdala/diagnostic imaging/*physiopathology, Anxiety Disorders/diagnostic imaging/*physiopathology, Arousal/physiology, Attention/*physiology, Electroshock, Facial Expression, Facial Recognition/physiology, Female, Frontal Lobe/diagnostic imaging/*physiopathology, Human behaviour, Humans, Male, Middle Aged, Nerve Net/diagnostic imaging/*physiopathology, Neuroscience, Pattern Recognition, Pattern Recognition, Visual/physiology, Reaction Time/physiology, Reference Values, Visual/physiology, Young Adult},\n\tpages = {e833},\n}\n\n
\n
\n\n\n
\n Anxiety disorders can be treated both pharmacologically and psychologically, but many individuals either fail to respond to treatment or relapse. Improving outcomes is difficult, in part because we have incomplete understanding of the neurobiological mechanisms underlying current treatments. In a sequence of studies, we have identified 'affective bias-related' amygdala-medial cortical coupling as a candidate substrate underlying adaptive anxiety (that is, anxiety elicited by threat of shock in healthy individuals) and shown that it is also chronically engaged in maladaptive anxiety disorders. We have provided evidence that this circuit can be modulated pharmacologically, but whether this mechanism can be shifted by simple psychological instruction is unknown. In this functional magnetic resonance imaging study, we extend a previously used translational anxiety induction (threat of shock) in healthy subjects (N=43) and cognitive task to include an element of instructed attentional control. Replicating our previous findings, we show that induced anxiety engages 'affective bias-related' amygdala-dorsal medial frontal coupling during the processing of emotional faces. By contrast, instructing subjects to attend to neutral shapes (and ignore faces) disengages this circuitry and increases putative 'attentional control-related' coupling between the amygdala and a more rostral prefrontal region. These neural coupling changes are accompanied by corresponding modulation of behavioural performance. Taken together, these findings serve to further highlight the potential role of amygdala-medial frontal coupling in the pathogenesis of anxiety and highlight a mechanism by which it can be modulated via psychological instructions. This, in turn, generates hypotheses for future work exploring the mechanisms underlying psychological therapeutic interventions for anxiety.\n
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\n \n\n \n \n \n \n \n The neural basis of improved cognitive performance by threat of shock.\n \n \n \n\n\n \n Torrisi, S.; Robinson, O.; O'Connell, K.; Davis, A.; Balderston, N.; Ernst, M.; and Grillon, C.\n\n\n \n\n\n\n Social cognitive and affective neuroscience, 11(11): 1677–1686. November 2016.\n Place: England\n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n
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@article{torrisi_neural_2016,\n\ttitle = {The neural basis of improved cognitive performance by threat of shock.},\n\tvolume = {11},\n\tcopyright = {Published by Oxford University Press 2016. This work is written by US Government employees and is in the public domain in the United States.},\n\tissn = {1749-5024 1749-5016},\n\tdoi = {10.1093/scan/nsw088},\n\tabstract = {Anxiety can have both detrimental and facilitatory cognitive effects. This study investigates the neural substrates of a replicated facilitatory effect of anxiety  on sustained attention and response inhibition. This effect consisted of improved  performance on the Sustained Attention to Response Task (a Go-NoGo task  consisting of 91\\% Go and 9\\% NoGo trials) in threat (unpredictable electrical  shock) vs safe (no shock) conditions. This study uses the same experimental  design with fMRI and relies on an event-related analysis of BOLD signal changes.  Findings reveal that threat-related cognitive facilitation (improved NoGo  accuracy) is associated with greater activation of a right-lateralized  frontoparietal group of regions previously implicated in sustained attention and  response inhibition. Moreover, these same regions show decreased activation in  the Go trials preceding NoGo errors. During NoGo trials, striatal activity is  also greater in the threat vs safe condition, consistent with the notion of  enhanced inhibitory processing under threat. These findings identify potential  mechanisms by which threat of unpredictable shock can facilitate distinct  cognitive functions. A greater understanding of the complex interaction of the  anxious state and cognitive processes may have critical clinical implications.},\n\tlanguage = {eng},\n\tnumber = {11},\n\tjournal = {Social cognitive and affective neuroscience},\n\tauthor = {Torrisi, Salvatore and Robinson, Oliver and O'Connell, Katherine and Davis, Andrew and Balderston, Nicholas and Ernst, Monique and Grillon, Christian},\n\tmonth = nov,\n\tyear = {2016},\n\tpmid = {27369069},\n\tpmcid = {PMC5091680},\n\tnote = {Place: England},\n\tkeywords = {*Electroshock, *Inhibition, *Inhibition, Psychological, *Magnetic Resonance Imaging, Adult, Anxiety/*physiopathology, Arousal/physiology, Attention/*physiology, Brain Mapping, Caudate Nucleus/*physiopathology, Cerebral Cortex/*physiopathology, Cerebral/physiology, Cognition/*physiology, Dominance, Dominance, Cerebral/physiology, Evoked Potentials/physiology, Female, Go/NoGo, Humans, Male, Oxygen/blood, Psychological, Reaction Time/physiology, Young Adult, fMRI, response inhibition, sustained attention, threat of shock},\n\tpages = {1677--1686},\n}\n\n
\n
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\n Anxiety can have both detrimental and facilitatory cognitive effects. This study investigates the neural substrates of a replicated facilitatory effect of anxiety on sustained attention and response inhibition. This effect consisted of improved performance on the Sustained Attention to Response Task (a Go-NoGo task consisting of 91% Go and 9% NoGo trials) in threat (unpredictable electrical shock) vs safe (no shock) conditions. This study uses the same experimental design with fMRI and relies on an event-related analysis of BOLD signal changes. Findings reveal that threat-related cognitive facilitation (improved NoGo accuracy) is associated with greater activation of a right-lateralized frontoparietal group of regions previously implicated in sustained attention and response inhibition. Moreover, these same regions show decreased activation in the Go trials preceding NoGo errors. During NoGo trials, striatal activity is also greater in the threat vs safe condition, consistent with the notion of enhanced inhibitory processing under threat. These findings identify potential mechanisms by which threat of unpredictable shock can facilitate distinct cognitive functions. A greater understanding of the complex interaction of the anxious state and cognitive processes may have critical clinical implications.\n
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\n \n\n \n \n \n \n \n Effect of attention control on sustained attention during induced anxiety.\n \n \n \n\n\n \n Grillon, C.; Robinson, O. J.; Mathur, A.; and Ernst, M.\n\n\n \n\n\n\n Cognition & emotion, 30(4): 700–712. 2016.\n Place: England\n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n
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@article{grillon_effect_2016,\n\ttitle = {Effect of attention control on sustained attention during induced anxiety.},\n\tvolume = {30},\n\tcopyright = {All rights reserved},\n\tissn = {1464-0600 0269-9931},\n\tdoi = {10.1080/02699931.2015.1024614},\n\tabstract = {Anxiety has wide-reaching and complex effects on cognitive performance. Although it can intrude on cognition and interfere with performance, it can also  facilitate information processing and behavioural responses. In a previous study,  we showed that anxiety induced by threat of shock facilitates performance on the  Sustained Attention to Response Task, a vigilance test, which probes response  inhibition to infrequent nogo stimuli. The present study sought to identify  factors that may have contributed to such improved performance, including on- and  off-task thinking (assessed with thought probes) and individual differences in  attention control, as measured with the Attention Control Scale. Replicating our  prior finding, we showed that shock threat significantly reduced errors of  commission on the nogo trials. However, we extended this finding in demonstrating  that this effect was driven by subjects with low attention control. We therefore  confirm that anxiety increases inhibitory control of prepotent responses--a  mechanism which is adaptive under threat--and show that this effect is greater in  those who rely more upon such prepotent responding, i.e., those with low  attentional control.},\n\tlanguage = {eng},\n\tnumber = {4},\n\tjournal = {Cognition \\& emotion},\n\tauthor = {Grillon, Christian and Robinson, Oliver J. and Mathur, Ambika and Ernst, Monique},\n\tyear = {2016},\n\tpmid = {25899613},\n\tpmcid = {PMC4618278},\n\tnote = {Place: England},\n\tkeywords = {*Attention, Anxiety, Anxiety/*psychology, Fear, Psychomotor Performance, Reflex, Reflex, Startle, SART, Startle, Stress, Threat of shock, Vigilance},\n\tpages = {700--712},\n}\n\n
\n
\n\n\n
\n Anxiety has wide-reaching and complex effects on cognitive performance. Although it can intrude on cognition and interfere with performance, it can also facilitate information processing and behavioural responses. In a previous study, we showed that anxiety induced by threat of shock facilitates performance on the Sustained Attention to Response Task, a vigilance test, which probes response inhibition to infrequent nogo stimuli. The present study sought to identify factors that may have contributed to such improved performance, including on- and off-task thinking (assessed with thought probes) and individual differences in attention control, as measured with the Attention Control Scale. Replicating our prior finding, we showed that shock threat significantly reduced errors of commission on the nogo trials. However, we extended this finding in demonstrating that this effect was driven by subjects with low attention control. We therefore confirm that anxiety increases inhibitory control of prepotent responses–a mechanism which is adaptive under threat–and show that this effect is greater in those who rely more upon such prepotent responding, i.e., those with low attentional control.\n
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\n \n\n \n \n \n \n \n Anxiety promotes memory for mood-congruent faces but does not alter loss aversion.\n \n \n \n\n\n \n Charpentier, C. J.; Hindocha, C.; Roiser, J. P.; and Robinson, O. J.\n\n\n \n\n\n\n Scientific reports, 6: 24746. April 2016.\n Place: England\n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n
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@article{charpentier_anxiety_2016,\n\ttitle = {Anxiety promotes memory for mood-congruent faces but does not alter loss aversion.},\n\tvolume = {6},\n\tcopyright = {All rights reserved},\n\tissn = {2045-2322},\n\tdoi = {10.1038/srep24746},\n\tabstract = {Pathological anxiety is associated with disrupted cognitive processing, including working memory and decision-making. In healthy individuals,  experimentally-induced state anxiety or high trait anxiety often results in the  deployment of adaptive harm-avoidant behaviours. However, how these processes  affect cognition is largely unknown. To investigate this question, we implemented  a translational within-subjects anxiety induction, threat of shock, in healthy  participants reporting a wide range of trait anxiety scores. Participants  completed a gambling task, embedded within an emotional working memory task, with  some blocks under unpredictable threat and others safe from shock. Relative to  the safe condition, threat of shock improved recall of threat-congruent (fearful)  face location, especially in highly trait anxious participants. This suggests  that threat boosts working memory for mood-congruent stimuli in vulnerable  individuals, mirroring memory biases in clinical anxiety. By contrast, Bayesian  analysis indicated that gambling decisions were better explained by models that  did not include threat or treat anxiety, suggesting that: (i) higher-level  executive functions are robust to these anxiety manipulations; and (ii) decreased  risk-taking may be specific to pathological anxiety. These findings provide  insight into the complex interactions between trait anxiety, acute state anxiety  and cognition, and may help understand the cognitive mechanisms underlying  adaptive anxiety.},\n\tlanguage = {eng},\n\tjournal = {Scientific reports},\n\tauthor = {Charpentier, Caroline J. and Hindocha, Chandni and Roiser, Jonathan P. and Robinson, Oliver J.},\n\tmonth = apr,\n\tyear = {2016},\n\tpmid = {27098489},\n\tpmcid = {PMC4838853},\n\tnote = {Place: England},\n\tkeywords = {*Affect, *Facial Expression, *Memory, Adult, Anxiety Disorders/*psychology, Anxiety/*psychology, Cognition, Decision Making, Emotions, Female, Gambling, Heritable, Humans, Male, Memory, Memory, Short-Term, Psychological, Quantitative Trait, Quantitative Trait, Heritable, Reaction Time, Short-Term, Stress, Stress, Psychological, Surveys and Questionnaires, Young Adult},\n\tpages = {24746},\n}\n\n
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\n Pathological anxiety is associated with disrupted cognitive processing, including working memory and decision-making. In healthy individuals, experimentally-induced state anxiety or high trait anxiety often results in the deployment of adaptive harm-avoidant behaviours. However, how these processes affect cognition is largely unknown. To investigate this question, we implemented a translational within-subjects anxiety induction, threat of shock, in healthy participants reporting a wide range of trait anxiety scores. Participants completed a gambling task, embedded within an emotional working memory task, with some blocks under unpredictable threat and others safe from shock. Relative to the safe condition, threat of shock improved recall of threat-congruent (fearful) face location, especially in highly trait anxious participants. This suggests that threat boosts working memory for mood-congruent stimuli in vulnerable individuals, mirroring memory biases in clinical anxiety. By contrast, Bayesian analysis indicated that gambling decisions were better explained by models that did not include threat or treat anxiety, suggesting that: (i) higher-level executive functions are robust to these anxiety manipulations; and (ii) decreased risk-taking may be specific to pathological anxiety. These findings provide insight into the complex interactions between trait anxiety, acute state anxiety and cognition, and may help understand the cognitive mechanisms underlying adaptive anxiety.\n
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\n  \n 2015\n \n \n (2)\n \n \n
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\n \n\n \n \n \n \n \n The impact of threat of shock on the framing effect and temporal discounting: executive functions unperturbed by acute stress?.\n \n \n \n\n\n \n Robinson, O. J.; Bond, R. L.; and Roiser, J. P.\n\n\n \n\n\n\n Frontiers in psychology, 6: 1315. 2015.\n Place: Switzerland\n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n
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@article{robinson_impact_2015,\n\ttitle = {The impact of threat of shock on the framing effect and temporal discounting: executive functions unperturbed by acute stress?},\n\tvolume = {6},\n\tcopyright = {All rights reserved},\n\tissn = {1664-1078},\n\tdoi = {10.3389/fpsyg.2015.01315},\n\tabstract = {Anxiety and stress-related disorders constitute a large global health burden, but are still poorly understood. Prior work has demonstrated clear impacts of stress  upon basic cognitive function: biasing attention toward unexpected and  potentially threatening information and instantiating a negative affective bias.  However, the impact that these changes have on higher-order, executive,  decision-making processes is unclear. In this study, we examined the impact of a  translational within-subjects stress induction (threat of unpredictable shock) on  two well-established executive decision-making biases: the framing effect (N =  83), and temporal discounting (N = 36). In both studies, we demonstrate (a) clear  subjective effects of stress, and (b) clear executive decision-making biases but  (c) no impact of stress on these decision-making biases. Indeed, Bayes factor  analyses confirmed substantial preference for decision-making models that did not  include stress. We posit that while stress may induce subjective mood change and  alter low-level perceptual and action processes (Robinson et al., 2013c), some  higher-level executive processes remain unperturbed by these impacts. As such,  although stress can induce a transient affective biases and altered mood, these  need not result in poor financial decision-making.},\n\tlanguage = {eng},\n\tjournal = {Frontiers in psychology},\n\tauthor = {Robinson, Oliver J. and Bond, Rebecca L. and Roiser, Jonathan P.},\n\tyear = {2015},\n\tpmid = {26441705},\n\tpmcid = {PMC4562307},\n\tnote = {Place: Switzerland},\n\tkeywords = {Bayesian models, anxiety, depression, executive function, framing effect, stress, temporal discounting, threat of shock},\n\tpages = {1315},\n}\n\n
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\n Anxiety and stress-related disorders constitute a large global health burden, but are still poorly understood. Prior work has demonstrated clear impacts of stress upon basic cognitive function: biasing attention toward unexpected and potentially threatening information and instantiating a negative affective bias. However, the impact that these changes have on higher-order, executive, decision-making processes is unclear. In this study, we examined the impact of a translational within-subjects stress induction (threat of unpredictable shock) on two well-established executive decision-making biases: the framing effect (N = 83), and temporal discounting (N = 36). In both studies, we demonstrate (a) clear subjective effects of stress, and (b) clear executive decision-making biases but (c) no impact of stress on these decision-making biases. Indeed, Bayes factor analyses confirmed substantial preference for decision-making models that did not include stress. We posit that while stress may induce subjective mood change and alter low-level perceptual and action processes (Robinson et al., 2013c), some higher-level executive processes remain unperturbed by these impacts. As such, although stress can induce a transient affective biases and altered mood, these need not result in poor financial decision-making.\n
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\n \n\n \n \n \n \n \n The impact of stress on financial decision-making varies as a function of depression and anxiety symptoms.\n \n \n \n\n\n \n Robinson, O. J.; Bond, R. L.; and Roiser, J. P.\n\n\n \n\n\n\n PeerJ, 3: e770. 2015.\n Place: United States\n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n
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@article{robinson_impact_2015-1,\n\ttitle = {The impact of stress on financial decision-making varies as a function of depression and anxiety symptoms.},\n\tvolume = {3},\n\tcopyright = {All rights reserved},\n\tissn = {2167-8359},\n\tdoi = {10.7717/peerj.770},\n\tabstract = {Stress can precipitate the onset of mood and anxiety disorders. This may occur, at least in part, via a modulatory effect of stress on decision-making. Some  individuals are, however, more resilient to the effects of stress than others.  The mechanisms underlying such vulnerability differences are nevertheless  unknown. In this study we attempted to begin quantifying individual differences  in vulnerability by exploring the effect of experimentally induced stress on  decision-making. The threat of unpredictable shock was used to induce stress in  healthy volunteers (N = 47) using a within-subjects, within-session design, and  its impact on a financial decision-making task (the Iowa Gambling Task) was  assessed alongside anxious and depressive symptomatology. As expected,  participants learned to select advantageous decks and avoid disadvantageous  decks. Importantly, we found that stress provoked a pattern of harm-avoidant  behaviour (decreased selection of disadvantageous decks) in individuals with low  levels of trait anxiety. By contrast, individuals with high trait anxiety  demonstrated the opposite pattern: stress-induced risk-seeking (increased  selection of disadvantageous decks). These contrasting influences of stress  depending on mood and anxiety symptoms might provide insight into vulnerability  to common mental illness. In particular, we speculate that those who adopt a more  harm-avoidant strategy may be better able to regulate their exposure to further  environmental stress, reducing their susceptibility to mood and anxiety  disorders.},\n\tlanguage = {eng},\n\tjournal = {PeerJ},\n\tauthor = {Robinson, Oliver J. and Bond, Rebecca L. and Roiser, Jonathan P.},\n\tyear = {2015},\n\tpmid = {25699215},\n\tpmcid = {PMC4330902},\n\tnote = {Place: United States},\n\tkeywords = {Anxiety, Depression, Harm-avoidance, Iowa Gambling Task, Resilience, Risk-seeking, Stress, Threat of shock, Vulnerablity},\n\tpages = {e770},\n}\n\n
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\n Stress can precipitate the onset of mood and anxiety disorders. This may occur, at least in part, via a modulatory effect of stress on decision-making. Some individuals are, however, more resilient to the effects of stress than others. The mechanisms underlying such vulnerability differences are nevertheless unknown. In this study we attempted to begin quantifying individual differences in vulnerability by exploring the effect of experimentally induced stress on decision-making. The threat of unpredictable shock was used to induce stress in healthy volunteers (N = 47) using a within-subjects, within-session design, and its impact on a financial decision-making task (the Iowa Gambling Task) was assessed alongside anxious and depressive symptomatology. As expected, participants learned to select advantageous decks and avoid disadvantageous decks. Importantly, we found that stress provoked a pattern of harm-avoidant behaviour (decreased selection of disadvantageous decks) in individuals with low levels of trait anxiety. By contrast, individuals with high trait anxiety demonstrated the opposite pattern: stress-induced risk-seeking (increased selection of disadvantageous decks). These contrasting influences of stress depending on mood and anxiety symptoms might provide insight into vulnerability to common mental illness. In particular, we speculate that those who adopt a more harm-avoidant strategy may be better able to regulate their exposure to further environmental stress, reducing their susceptibility to mood and anxiety disorders.\n
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\n  \n 2014\n \n \n (2)\n \n \n
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\n \n\n \n \n \n \n \n Sustained anxiety increases amygdala-dorsomedial prefrontal coupling: a mechanism for maintaining an anxious state in healthy adults.\n \n \n \n\n\n \n Vytal, K. E.; Overstreet, C.; Charney, D. R.; Robinson, O. J.; and Grillon, C.\n\n\n \n\n\n\n Journal of psychiatry & neuroscience : JPN, 39(5): 321–329. September 2014.\n Place: Canada\n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n
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@article{vytal_sustained_2014,\n\ttitle = {Sustained anxiety increases amygdala-dorsomedial prefrontal coupling: a mechanism for maintaining an anxious state in healthy adults.},\n\tvolume = {39},\n\tcopyright = {All rights reserved},\n\tissn = {1488-2434 1180-4882},\n\tdoi = {10.1503/jpn.130145},\n\tabstract = {BACKGROUND: Neuroimaging research has traditionally explored fear and anxiety in response to discrete threat cues (e.g., during fear conditioning). However,  anxiety is a sustained aversive state that can persist in the absence of discrete  threats. Little is known about mechanisms that maintain anxiety states over a  prolonged period. Here, we used a robust translational paradigm (threat of shock)  to induce sustained anxiety. Recent translational work has implicated an  amygdala-prefrontal cortex (PFC) circuit in the maintenance of anxiety in  rodents. To explore the functional homologues of this circuitry in humans, we  used a novel paradigm to examine the impact of sustained anticipatory anxiety on  amygdala-PFC intrinsic connectivity. METHODS: Task-independent fMRI data were  collected in healthy participants during long-duration periods of shock  anticipation and safety. We examined intrinsic functional connectivity. RESULTS:  Our study involved 20 healthy participants. During sustained anxiety, amygdala  activity was positively coupled with dorsomedial PFC (DMPFC) activity. High trait  anxiety was associated with increased amygdala-DMPFC coupling. In addition,  induced anxiety was associated with positive coupling between regions involved in  defensive responding, and decreased coupling between regions involved in  emotional control and the default mode network. LIMITATIONS: Inferences regarding  anxious pathology should be made with caution because this study was conducted in  healthy participants. CONCLUSION: Findings suggest that anticipatory anxiety  increases intrinsic amygdala-DMPFC coupling and that the DMPFC may serve as a  functional homologue for the rodent prefrontal regions by sustaining anxiety.  Future research may use this defensive neural context to identify biomarkers of  risk for anxious pathology and target these circuits for therapeutic  intervention.},\n\tlanguage = {eng},\n\tnumber = {5},\n\tjournal = {Journal of psychiatry \\& neuroscience : JPN},\n\tauthor = {Vytal, Katherine E. and Overstreet, Cassie and Charney, Danielle R. and Robinson, Oliver J. and Grillon, Christian},\n\tmonth = sep,\n\tyear = {2014},\n\tpmid = {24886788},\n\tpmcid = {PMC4160361},\n\tnote = {Place: Canada},\n\tkeywords = {Adult, Amygdala/*physiopathology, Anticipation, Anticipation, Psychological/physiology, Anxiety/*physiopathology, Brain Mapping, Electroshock, Fear/physiology, Female, Humans, Magnetic Resonance Imaging, Male, Neural Pathways/physiopathology, Neuropsychological Tests, Personality, Prefrontal Cortex/*physiopathology, Psychological/physiology, Psychophysics, Young Adult},\n\tpages = {321--329},\n}\n\n
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\n\n\n
\n BACKGROUND: Neuroimaging research has traditionally explored fear and anxiety in response to discrete threat cues (e.g., during fear conditioning). However, anxiety is a sustained aversive state that can persist in the absence of discrete threats. Little is known about mechanisms that maintain anxiety states over a prolonged period. Here, we used a robust translational paradigm (threat of shock) to induce sustained anxiety. Recent translational work has implicated an amygdala-prefrontal cortex (PFC) circuit in the maintenance of anxiety in rodents. To explore the functional homologues of this circuitry in humans, we used a novel paradigm to examine the impact of sustained anticipatory anxiety on amygdala-PFC intrinsic connectivity. METHODS: Task-independent fMRI data were collected in healthy participants during long-duration periods of shock anticipation and safety. We examined intrinsic functional connectivity. RESULTS: Our study involved 20 healthy participants. During sustained anxiety, amygdala activity was positively coupled with dorsomedial PFC (DMPFC) activity. High trait anxiety was associated with increased amygdala-DMPFC coupling. In addition, induced anxiety was associated with positive coupling between regions involved in defensive responding, and decreased coupling between regions involved in emotional control and the default mode network. LIMITATIONS: Inferences regarding anxious pathology should be made with caution because this study was conducted in healthy participants. CONCLUSION: Findings suggest that anticipatory anxiety increases intrinsic amygdala-DMPFC coupling and that the DMPFC may serve as a functional homologue for the rodent prefrontal regions by sustaining anxiety. Future research may use this defensive neural context to identify biomarkers of risk for anxious pathology and target these circuits for therapeutic intervention.\n
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\n \n\n \n \n \n \n \n \n Towards a mechanistic understanding of pathological anxiety: the dorsal medial prefrontal-amygdala ‘aversive amplification’ circuit in unmedicated generalized and social anxiety disorders.\n \n \n \n \n\n\n \n Robinson, O. J; Krimsky, M.; Lieberman, L.; Allen, P.; Vytal, K.; and Grillon, C.\n\n\n \n\n\n\n The Lancet. Psychiatry, 1(4): 294–302. September 2014.\n \n\n\n\n
\n\n\n\n \n \n \"TowardsPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n
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@article{robinson_towards_2014,\n\ttitle = {Towards a mechanistic understanding of pathological anxiety: the dorsal medial prefrontal-amygdala ‘aversive amplification’ circuit in unmedicated generalized and social anxiety disorders},\n\tvolume = {1},\n\tcopyright = {All rights reserved},\n\tissn = {2215-0366},\n\tshorttitle = {Towards a mechanistic understanding of pathological anxiety},\n\turl = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4337019/},\n\tdoi = {10.1016/S2215-0366(14)70305-0},\n\tabstract = {Background\nWe have delineated, across four prior studies, the role of positive dorsal medial prefrontal/anterior cingulate cortex (dmPFC/ACC)-amygdala circuit coupling during aversive processing in healthy individuals under stress. This translational circuit, termed the ‘aversive amplification circuit’, is thought to drive adaptive, harm-avoidant behavior in threatening environments. Here, in a natural progression of this prior work, we confirm that this circuit also plays a role in the pathological manifestation of anxiety disorders.\n\nMethods\nForty-five unmedicated participants (N=22 generalized and social anxiety disorder/N=23 controls) recruited from Washington DC metropolitan area completed a simple emotion identification task during functional magnetic resonance imaging at the National Institutes of Health, Bethesda, MD, USA.\n\nFindings\nAs predicted, a diagnosis by valence interaction was seen in whole-brain amygdala connectivity within the dmPFC/ACC clusters identified in our prior study; driven by significantly greater circuit coupling during fearful versus happy face processing in anxious, but not healthy, participants. Critically, and in accordance with contemporary theoretical approaches to psychiatry, circuit coupling correlated positively with self-reported anxious symptoms, providing evidence of a continuous circuit-subjective symptomatology relationship.\n\nInterpretation\nWe track the functional role of a single neural circuit from its involvement in adaptive threat-biases under stress, to its chronic engagement in anxiety disorders in the absence of experimentally induced stress. Thus, we uniquely map a mood and anxiety related circuit across its adaptive and maladaptive stages. Clinically, this may provide a step towards a more mechanistic spectrum-based approach to anxiety disorder diagnosis and may ultimately lead to more targeted treatments.},\n\tnumber = {4},\n\turldate = {2022-08-22},\n\tjournal = {The Lancet. Psychiatry},\n\tauthor = {Robinson, Oliver J and Krimsky, Marissa and Lieberman, Lynne and Allen, Phillip and Vytal, Katherine and Grillon, Christian},\n\tmonth = sep,\n\tyear = {2014},\n\tpmid = {25722962},\n\tpmcid = {PMC4337019},\n\tkeywords = {Anxiety, Aversive amplification, amygdala, connectivity, dmPFC/DACC},\n\tpages = {294--302},\n}\n\n
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\n Background We have delineated, across four prior studies, the role of positive dorsal medial prefrontal/anterior cingulate cortex (dmPFC/ACC)-amygdala circuit coupling during aversive processing in healthy individuals under stress. This translational circuit, termed the ‘aversive amplification circuit’, is thought to drive adaptive, harm-avoidant behavior in threatening environments. Here, in a natural progression of this prior work, we confirm that this circuit also plays a role in the pathological manifestation of anxiety disorders. Methods Forty-five unmedicated participants (N=22 generalized and social anxiety disorder/N=23 controls) recruited from Washington DC metropolitan area completed a simple emotion identification task during functional magnetic resonance imaging at the National Institutes of Health, Bethesda, MD, USA. Findings As predicted, a diagnosis by valence interaction was seen in whole-brain amygdala connectivity within the dmPFC/ACC clusters identified in our prior study; driven by significantly greater circuit coupling during fearful versus happy face processing in anxious, but not healthy, participants. Critically, and in accordance with contemporary theoretical approaches to psychiatry, circuit coupling correlated positively with self-reported anxious symptoms, providing evidence of a continuous circuit-subjective symptomatology relationship. Interpretation We track the functional role of a single neural circuit from its involvement in adaptive threat-biases under stress, to its chronic engagement in anxiety disorders in the absence of experimentally induced stress. Thus, we uniquely map a mood and anxiety related circuit across its adaptive and maladaptive stages. Clinically, this may provide a step towards a more mechanistic spectrum-based approach to anxiety disorder diagnosis and may ultimately lead to more targeted treatments.\n
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\n  \n 2013\n \n \n (4)\n \n \n
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\n \n\n \n \n \n \n \n \n The Impact of Anxiety Upon Cognition: Perspectives from Human Threat of Shock Studies.\n \n \n \n \n\n\n \n Robinson, O. J.; Vytal, K.; Cornwell, B. R; and Grillon, C.\n\n\n \n\n\n\n Frontiers in Human Neuroscience, 7. May 2013.\n \n\n\n\n
\n\n\n\n \n \n \"ThePaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n
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@article{robinson_impact_2013,\n\ttitle = {The {Impact} of {Anxiety} {Upon} {Cognition}: {Perspectives} from {Human} {Threat} of {Shock} {Studies}},\n\tvolume = {7},\n\tcopyright = {All rights reserved},\n\tissn = {1662-5161},\n\tshorttitle = {The impact of anxiety on cognition},\n\turl = {http://www.frontiersin.org/Journal/Abstract.aspx?s=537&name=human_neuroscience&ART_DOI=10.3389/fnhum.2013.00203},\n\tdoi = {10.3389/fnhum.2013.00203},\n\tabstract = {Anxiety disorders constitute a sizeable worldwide health burden with profound social and economic consequences. The symptoms are wide-ranging; from hyperarousal to difficulties with concentrating. This latter effect falls under the broad category of altered cognitive performance; in this review we examine studies quantifying such impacts of anxiety on cognition. Specifically, we focus on the translational threat of unpredictable shock paradigm, a method previously used to characterize emotional responses and defensive mechanisms that is now emerging as valuable tool for examining the interaction between anxiety and cognition. In particular, we compare the impact of threat of shock on cognition in humans to that of pathological anxiety disorders. We highlight that both threat of shock and anxiety disorders promote mechanisms associated with harm avoidance across multiple levels of cognition (from perception to attention to learning and executive function) – a ‘hot’ cognitive function which can be both adaptive and maladaptive depending upon the circumstances. This mechanism comes at a cost to other functions such as working memory, but leaves some functions, such as planning, unperturbed. We also highlight a number of cognitive effects that differ across anxiety disorders and threat of shock. These discrepant effects are largely seen in ‘cold’ cognitive functions involving control mechanisms and may reveal boundaries between adaptive (e.g. response to threat) and maladaptive (e.g. pathological) anxiety. We conclude by raising a number of unresolved questions regarding the role of anxiety in cognition that may provide fruitful avenues for future research.},\n\tlanguage = {English},\n\tjournal = {Frontiers in Human Neuroscience},\n\tauthor = {Robinson, Oliver Joe and Vytal, Katherine and Cornwell, Brian R and Grillon, Christian},\n\tmonth = may,\n\tyear = {2013},\n\tkeywords = {Anxiety Disorders, Attention, Cognition, Perception, Threat of shock, anxiety, anxiety disorders, attention, cognition, executive function, learning and memory, perception, threat of shock},\n}\n\n
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\n Anxiety disorders constitute a sizeable worldwide health burden with profound social and economic consequences. The symptoms are wide-ranging; from hyperarousal to difficulties with concentrating. This latter effect falls under the broad category of altered cognitive performance; in this review we examine studies quantifying such impacts of anxiety on cognition. Specifically, we focus on the translational threat of unpredictable shock paradigm, a method previously used to characterize emotional responses and defensive mechanisms that is now emerging as valuable tool for examining the interaction between anxiety and cognition. In particular, we compare the impact of threat of shock on cognition in humans to that of pathological anxiety disorders. We highlight that both threat of shock and anxiety disorders promote mechanisms associated with harm avoidance across multiple levels of cognition (from perception to attention to learning and executive function) – a ‘hot’ cognitive function which can be both adaptive and maladaptive depending upon the circumstances. This mechanism comes at a cost to other functions such as working memory, but leaves some functions, such as planning, unperturbed. We also highlight a number of cognitive effects that differ across anxiety disorders and threat of shock. These discrepant effects are largely seen in ‘cold’ cognitive functions involving control mechanisms and may reveal boundaries between adaptive (e.g. response to threat) and maladaptive (e.g. pathological) anxiety. We conclude by raising a number of unresolved questions regarding the role of anxiety in cognition that may provide fruitful avenues for future research.\n
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\n \n\n \n \n \n \n \n \n Stress increases aversive prediction error signal in the ventral striatum.\n \n \n \n \n\n\n \n Robinson, O. J.; Overstreet, C.; Charney, D. R.; Vytal, K.; and Grillon, C.\n\n\n \n\n\n\n Proceedings of the National Academy of Sciences, 110(10): 4129–4133. March 2013.\n \n\n\n\n
\n\n\n\n \n \n \"StressPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n  \n \n 1 download\n \n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{robinson_stress_2013,\n\ttitle = {Stress increases aversive prediction error signal in the ventral striatum},\n\tvolume = {110},\n\tcopyright = {All rights reserved},\n\tissn = {0027-8424, 1091-6490},\n\turl = {https://pnas.org/doi/full/10.1073/pnas.1213923110},\n\tdoi = {10.1073/pnas.1213923110},\n\tabstract = {From job interviews to the heat of battle, it is evident that people think and learn differently when stressed. In fact, learning under stress may have long-term consequences; stress facilitates aversive conditioning and associations learned during extreme stress may result in debilitating emotional responses in posttraumatic stress disorder. The mechanisms underpinning such stress-related associations, however, are unknown. Computational neuroscience has successfully characterized several mechanisms critical for associative learning under normative conditions. One such mechanism, the detection of a mismatch between expected and observed outcomes within the ventral striatum (i.e., “prediction errors”), is thought to be a critical precursor to the formation of new stimulus–outcome associations. An untested possibility, therefore, is that stress may affect learning via modulation of this mechanism. Here we combine a translational model of stress with a cognitive neuroimaging paradigm to demonstrate that stress significantly increases ventral striatum aversive (but not appetitive) prediction error signal. This provides a unique account of the propensity to form threat-related associations under stress with direct implications for our understanding of both normal stress and stress-related disorders.},\n\tlanguage = {en},\n\tnumber = {10},\n\turldate = {2023-04-06},\n\tjournal = {Proceedings of the National Academy of Sciences},\n\tauthor = {Robinson, Oliver J. and Overstreet, Cassie and Charney, Danielle R. and Vytal, Katherine and Grillon, Christian},\n\tmonth = mar,\n\tyear = {2013},\n\tpages = {4129--4133},\n}\n\n
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\n From job interviews to the heat of battle, it is evident that people think and learn differently when stressed. In fact, learning under stress may have long-term consequences; stress facilitates aversive conditioning and associations learned during extreme stress may result in debilitating emotional responses in posttraumatic stress disorder. The mechanisms underpinning such stress-related associations, however, are unknown. Computational neuroscience has successfully characterized several mechanisms critical for associative learning under normative conditions. One such mechanism, the detection of a mismatch between expected and observed outcomes within the ventral striatum (i.e., “prediction errors”), is thought to be a critical precursor to the formation of new stimulus–outcome associations. An untested possibility, therefore, is that stress may affect learning via modulation of this mechanism. Here we combine a translational model of stress with a cognitive neuroimaging paradigm to demonstrate that stress significantly increases ventral striatum aversive (but not appetitive) prediction error signal. This provides a unique account of the propensity to form threat-related associations under stress with direct implications for our understanding of both normal stress and stress-related disorders.\n
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\n \n\n \n \n \n \n \n \n The role of serotonin in the neurocircuitry of negative affective bias: Serotonergic modulation of the dorsal medial prefrontal-amygdala ‘aversive amplification’ circuit.\n \n \n \n \n\n\n \n Robinson, O. J.; Overstreet, C.; Allen, P. S.; Letkiewicz, A.; Vytal, K.; Pine, D. S.; and Grillon, C.\n\n\n \n\n\n\n Neuroimage, 78: 217–223. 2013.\n 0\n\n\n\n
\n\n\n\n \n \n \"ThePaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n
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@article{robinson_role_2013,\n\ttitle = {The role of serotonin in the neurocircuitry of negative affective bias: {Serotonergic} modulation of the dorsal medial prefrontal-amygdala ‘aversive amplification’ circuit},\n\tvolume = {78},\n\tcopyright = {All rights reserved},\n\tissn = {1053-8119},\n\tshorttitle = {The role of serotonin in the neurocircuitry of negative affective bias: {Serotonergic} modulation of the dorsal medial prefrontal-amygdala ‘aversive amplification’ circuit},\n\turl = {http://www.sciencedirect.com/science/article/pii/S1053811913003303},\n\tdoi = {10.1016/j.neuroimage.2013.03.075},\n\tjournal = {Neuroimage},\n\tauthor = {Robinson, Oliver J. and Overstreet, Cassie and Allen, Philip S. and Letkiewicz, Alison and Vytal, Katherine and Pine, Daniel S. and Grillon, Christian},\n\tyear = {2013},\n\tnote = {0},\n\tkeywords = {ATD, Adult, Affect/drug effects/physiology, Affective Symptoms, Amygdala, Amygdala/*metabolism/physiopathology, Anxiety/metabolism/physiopathology, Aversive amplification, Bias, Computer-Assisted, Cross-Over Studies, DMPFC, Depression/metabolism/physiopathology, Double-Blind Method, Emotions/drug effects/physiology, Female, Humans, Image Interpretation, Image Interpretation, Computer-Assisted, Magnetic Resonance Imaging, Male, Negative bias, Neural Pathways/*metabolism/physiopathology, Prefrontal Cortex/*metabolism/physiopathology, Serotonin Receptor Agonists/pharmacology, Serotonin/*metabolism, Tryptophan/pharmacology, serotonin},\n\tpages = {217--223},\n}\n\n
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\n \n\n \n \n \n \n \n The impact of induced anxiety on response inhibition.\n \n \n \n\n\n \n Robinson, O. J.; Krimsky, M.; and Grillon, C.\n\n\n \n\n\n\n Frontiers in human neuroscience, 7: 69. 2013.\n Place: Switzerland\n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n
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@article{robinson_impact_2013-1,\n\ttitle = {The impact of induced anxiety on response inhibition.},\n\tvolume = {7},\n\tcopyright = {All rights reserved},\n\tissn = {1662-5161},\n\tdoi = {10.3389/fnhum.2013.00069},\n\tabstract = {Anxiety has wide reaching effects on cognition; evidenced most prominently by the "difficulties concentrating" seen in anxiety disorders, and by adaptive  harm-avoidant behaviors adopted under threatening circumstances. Despite having  critical implications for daily-living, the precise impact of anxiety on  cognition is as yet poorly quantified. Here we attempt to clarify the impact of  anxiety on sustained attention and response inhibition via a translational  anxiety induction in healthy individuals (N = 22). Specifically, in a  within-subjects design, participants completed the Sustained Attention to  Response Task (SART) in which subjects withhold responses to infrequent no-go  stimuli under threat of unpredictable electrical shock (anxious) and safe  (non-anxious) conditions. Different studies have argued that this task measures  either (1) attention lapses due to off-task thinking or (2) response inhibition;  two cognitive functions which are likely impacted by anxiety. We show that threat  of shock significantly reduces errors of commission on the no-go trials relative  to the safe condition whilst having no effect on go trials or overall reaction  time (RT). We suggest that this is because threat of shock during SART promotes  response inhibition. In particular we argue that, by virtue of frequency,  subjects acquire a habitual bias toward a go response which impairs no-go  performance and that threat of shock improves the ability to withhold these  prepotent responses. This improved response inhibition likely falls within the  range of adaptive cognitive functions which promote cautious harm avoidance under  threatening conditions, although a range of alternative explanations for this  effect is discussed.},\n\tlanguage = {eng},\n\tjournal = {Frontiers in human neuroscience},\n\tauthor = {Robinson, Oliver J. and Krimsky, Marissa and Grillon, Christian},\n\tyear = {2013},\n\tpmid = {23471118},\n\tpmcid = {PMC3590569},\n\tnote = {Place: Switzerland},\n\tkeywords = {anxiety, mind-wandering, response inhibition, threat, threat of shock},\n\tpages = {69},\n}\n\n
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\n Anxiety has wide reaching effects on cognition; evidenced most prominently by the \"difficulties concentrating\" seen in anxiety disorders, and by adaptive harm-avoidant behaviors adopted under threatening circumstances. Despite having critical implications for daily-living, the precise impact of anxiety on cognition is as yet poorly quantified. Here we attempt to clarify the impact of anxiety on sustained attention and response inhibition via a translational anxiety induction in healthy individuals (N = 22). Specifically, in a within-subjects design, participants completed the Sustained Attention to Response Task (SART) in which subjects withhold responses to infrequent no-go stimuli under threat of unpredictable electrical shock (anxious) and safe (non-anxious) conditions. Different studies have argued that this task measures either (1) attention lapses due to off-task thinking or (2) response inhibition; two cognitive functions which are likely impacted by anxiety. We show that threat of shock significantly reduces errors of commission on the no-go trials relative to the safe condition whilst having no effect on go trials or overall reaction time (RT). We suggest that this is because threat of shock during SART promotes response inhibition. In particular we argue that, by virtue of frequency, subjects acquire a habitual bias toward a go response which impairs no-go performance and that threat of shock improves the ability to withhold these prepotent responses. This improved response inhibition likely falls within the range of adaptive cognitive functions which promote cautious harm avoidance under threatening conditions, although a range of alternative explanations for this effect is discussed.\n
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\n  \n 2012\n \n \n (6)\n \n \n
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\n \n\n \n \n \n \n \n \n Ventral Striatum Response During Reward and Punishment Reversal Learning in Unmedicated Major Depressive Disorder.\n \n \n \n \n\n\n \n Robinson, O. J.; Cools, R.; Carlisi, C. O.; Sahakian, B. J.; and Drevets, W. C.\n\n\n \n\n\n\n American Journal of Psychiatry, 169(2): 152–159. February 2012.\n Publisher: American Psychiatric Publishing\n\n\n\n
\n\n\n\n \n \n \"VentralPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{robinson_ventral_2012,\n\ttitle = {Ventral {Striatum} {Response} {During} {Reward} and {Punishment} {Reversal} {Learning} in {Unmedicated} {Major} {Depressive} {Disorder}},\n\tvolume = {169},\n\tcopyright = {All rights reserved},\n\tissn = {0002-953X},\n\turl = {https://ajp.psychiatryonline.org/doi/full/10.1176/appi.ajp.2011.11010137},\n\tdoi = {10.1176/appi.ajp.2011.11010137},\n\tabstract = {Objective:\n\nAffective biases may underlie many of the key symptoms of major depressive disorder, from anhedonia to altered cognitive performance. Understanding the cause of these biases is therefore critical in the quest for improved treatments. Depression is associated, for example, with a negative affective bias in reversal learning. However, despite the fact that reversal learning is associated with striatal response in healthy individuals and depressed individuals exhibit attenuated striatal function on multiple tasks, studies to date have not demonstrated striatal involvement in the negative bias in reversal learning in depression. In this study, the authors sought to determine whether this may be because reversal learning tasks conventionally used to study behavior examine reversals only on the basis of unexpected punishment and therefore do not adequately separate reward- and punishment-based behavior.\n\nMethod:\n\nThe authors used functional MRI to compare the hemodynamic response to a reversal learning task with mixed reward- and punishment-based reversal stages between individuals with unmedicated major depressive disorder (N=13) and healthy comparison subjects (N=14).\n\nResults:\n\nImpaired reward (but not punishment) reversal accuracy was found alongside attenuated anteroventral striatal response to unexpected reward in depression.\n\nConclusions:\n\nAttenuated neurophysiological response of the anteroventral striatum may reflect dysfunction in circuits involving afferent projections from the orbitofrontal, limbic, and/or mesostriatal dopaminergic pathways, which conceivably may, together with the ventral striatum, underlie anhedonia in depression. Learning to appreciate and enjoy positive life experiences is critical for recovery from depression. This study pinpoints a neural target for such recovery.},\n\tnumber = {2},\n\turldate = {2023-04-14},\n\tjournal = {American Journal of Psychiatry},\n\tauthor = {Robinson, Oliver J. and Cools, Roshan and Carlisi, Christina O. and Sahakian, Barbara J. and Drevets, Wayne C.},\n\tmonth = feb,\n\tyear = {2012},\n\tnote = {Publisher: American Psychiatric Publishing},\n\tpages = {152--159},\n}\n\n
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\n Objective: Affective biases may underlie many of the key symptoms of major depressive disorder, from anhedonia to altered cognitive performance. Understanding the cause of these biases is therefore critical in the quest for improved treatments. Depression is associated, for example, with a negative affective bias in reversal learning. However, despite the fact that reversal learning is associated with striatal response in healthy individuals and depressed individuals exhibit attenuated striatal function on multiple tasks, studies to date have not demonstrated striatal involvement in the negative bias in reversal learning in depression. In this study, the authors sought to determine whether this may be because reversal learning tasks conventionally used to study behavior examine reversals only on the basis of unexpected punishment and therefore do not adequately separate reward- and punishment-based behavior. Method: The authors used functional MRI to compare the hemodynamic response to a reversal learning task with mixed reward- and punishment-based reversal stages between individuals with unmedicated major depressive disorder (N=13) and healthy comparison subjects (N=14). Results: Impaired reward (but not punishment) reversal accuracy was found alongside attenuated anteroventral striatal response to unexpected reward in depression. Conclusions: Attenuated neurophysiological response of the anteroventral striatum may reflect dysfunction in circuits involving afferent projections from the orbitofrontal, limbic, and/or mesostriatal dopaminergic pathways, which conceivably may, together with the ventral striatum, underlie anhedonia in depression. Learning to appreciate and enjoy positive life experiences is critical for recovery from depression. This study pinpoints a neural target for such recovery.\n
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\n \n\n \n \n \n \n \n \n Acute Tryptophan Depletion Increases Translational Indices of Anxiety but not Fear: Serotonergic Modulation of the Bed Nucleus of the Stria Terminalis?.\n \n \n \n \n\n\n \n Robinson, O. J.; Overstreet, C.; Allen, P. S.; Pine, D. S.; and Grillon, C.\n\n\n \n\n\n\n Neuropsychopharmacology. 2012.\n \n\n\n\n
\n\n\n\n \n \n \"AcutePaper\n  \n \n\n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n  \n \n 1 download\n \n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n
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@article{robinson_acute_2012,\n\ttitle = {Acute {Tryptophan} {Depletion} {Increases} {Translational} {Indices} of {Anxiety} but not {Fear}: {Serotonergic} {Modulation} of the {Bed} {Nucleus} of the {Stria} {Terminalis}?},\n\tcopyright = {All rights reserved},\n\tissn = {1740-634X},\n\tshorttitle = {Acute {Tryptophan} {Depletion} {Increases} {Translational} {Indices} of {Anxiety} but not {Fear}: {Serotonergic} {Modulation} of the {Bed} {Nucleus} of the {Stria} {Terminalis}?},\n\turl = {http://dx.doi.org/10.1038/npp.2012.43},\n\tjournal = {Neuropsychopharmacology},\n\tauthor = {Robinson, Oliver J. and Overstreet, Cassie and Allen, Phillip S. and Pine, Daniel S. and Grillon, Christian},\n\tyear = {2012},\n\tkeywords = {*Anxiety/blood/physiopathology, Adult, Double-Blind Method, Fear/*physiology, Female, Humans, Male, Reflex, Reflex, Startle/physiology, Septal Nuclei/metabolism/*physiology, Serotonin/metabolism/*physiology, Startle/physiology, Tryptophan/blood/*deficiency},\n}\n\n
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\n \n\n \n \n \n \n \n \n Depressed mood enhances anxiety to unpredictable threat.\n \n \n \n \n\n\n \n Robinson, O. J.; Overstreet, C.; Letkiewicz, A.; and Grillon, C.\n\n\n \n\n\n\n Psychol Med, 42: 1397–407. July 2012.\n 7\n\n\n\n
\n\n\n\n \n \n \"DepressedPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n
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@article{robinson_depressed_2012,\n\ttitle = {Depressed mood enhances anxiety to unpredictable threat},\n\tvolume = {42},\n\tcopyright = {All rights reserved},\n\tissn = {1469-8978 (Electronic) 0033-2917 (Linking)},\n\tshorttitle = {Depressed mood enhances anxiety to unpredictable threat},\n\turl = {http://www.ncbi.nlm.nih.gov/pubmed/22088577},\n\tdoi = {10.1017/S0033291711002583},\n\tlanguage = {eng},\n\turldate = {2011-01-01},\n\tjournal = {Psychol Med},\n\tauthor = {Robinson, O. J. and Overstreet, C. and Letkiewicz, A. and Grillon, C.},\n\tmonth = jul,\n\tyear = {2012},\n\tnote = {7},\n\tkeywords = {Amygdala/physiopathology, Analysis of Variance, Anticipation, Anticipation, Psychological, Anxiety Disorders/*complications/epidemiology, Anxiety/*complications/physiopathology, Arousal/physiology, Biological, Comorbidity, Cues, Depression/*complications/physiopathology, Depressive Disorder/*complications/epidemiology, Electric Stimulation, Fear/physiology, Female, Humans, Male, Models, Models, Biological, Psychological, Reflex, Reflex, Startle/*physiology, Self Report, Startle Reaction/*physiology, Startle/*physiology, Young Adult},\n\tpages = {1397--407},\n}\n\n
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\n \n\n \n \n \n \n \n \n Tryptophan depletion disinhibits punishment but not reward prediction: implications for resilience.\n \n \n \n \n\n\n \n Robinson, O. J.; Cools, R.; and Sahakian, B. J.\n\n\n \n\n\n\n Psychopharmacology (Berl), 219: 599–605. January 2012.\n 2\n\n\n\n
\n\n\n\n \n \n \"TryptophanPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n
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@article{robinson_tryptophan_2012,\n\ttitle = {Tryptophan depletion disinhibits punishment but not reward prediction: implications for resilience},\n\tvolume = {219},\n\tcopyright = {All rights reserved},\n\tissn = {1432-2072 (Electronic) 0033-3158 (Linking)},\n\tshorttitle = {Tryptophan depletion disinhibits punishment but not reward prediction: implications for resilience},\n\turl = {http://www.ncbi.nlm.nih.gov/pubmed/21769566},\n\tdoi = {10.1007/s00213-011-2410-5},\n\tlanguage = {eng},\n\tjournal = {Psychopharmacology (Berl)},\n\tauthor = {Robinson, O. J. and Cools, R. and Sahakian, B. J.},\n\tmonth = jan,\n\tyear = {2012},\n\tnote = {2},\n\tkeywords = {*Inhibition, *Inhibition (Psychology), *Inhibition, Psychological, *Reward, Adult, Affect/drug effects/physiology, Amino Acids/blood/pharmacology, Female, Humans, Neuropsychological Tests/statistics \\& numerical data, Psychological, Psychological/*drug effects, Punishment/*psychology, Resilience, Resilience, Psychological/*drug effects, Reversal Learning/drug effects/physiology, Tryptophan/blood/*deficiency/*physiology},\n\tpages = {599--605},\n}\n\n
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\n \n\n \n \n \n \n \n \n The adaptive threat bias in anxiety: Amygdala–dorsomedial prefrontal cortex coupling and aversive amplification.\n \n \n \n \n\n\n \n Robinson, O. J.; Charney, D. R.; Overstreet, C.; Vytal, K.; and Grillon, C.\n\n\n \n\n\n\n Neuroimage, 60: 523–529. 2012.\n 1\n\n\n\n
\n\n\n\n \n \n \"ThePaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n
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@article{robinson_adaptive_2012,\n\ttitle = {The adaptive threat bias in anxiety: {Amygdala}–dorsomedial prefrontal cortex coupling and aversive amplification},\n\tvolume = {60},\n\tcopyright = {All rights reserved},\n\tissn = {1053-8119},\n\tshorttitle = {The adaptive threat bias in anxiety: {Amygdala}–dorsomedial prefrontal cortex coupling and aversive amplification},\n\turl = {http://www.sciencedirect.com/science/article/pii/S1053811911014017},\n\tdoi = {10.1016/j.neuroimage.2011.11.096},\n\tjournal = {Neuroimage},\n\tauthor = {Robinson, Oliver J. and Charney, Danielle R. and Overstreet, Cassie and Vytal, Katherine and Grillon, Christian},\n\tyear = {2012},\n\tnote = {1},\n\tkeywords = {Adaptation, Adaptation, Psychological/*physiology, Adolescent, Adult, Amygdala, Amygdala/*physiopathology, Anxiety/*physiopathology, DMPFC, Female, Functional connectivity, Humans, Magnetic Resonance Imaging, Male, Middle Aged, Prefrontal Cortex/*physiopathology, Prelimbic, Psychological/*physiology, Threat bias, Young Adult, anxiety},\n\tpages = {523--529},\n}\n\n
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\n \n\n \n \n \n \n \n Reliance on habits at the expense of goal-directed control following dopamine precursor depletion.\n \n \n \n\n\n \n de Wit, S.; Standing, H. R.; Devito, E. E.; Robinson, O. J.; Ridderinkhof, K. R.; Robbins, T. W.; and Sahakian, B. J.\n\n\n \n\n\n\n Psychopharmacology, 219(2): 621–631. January 2012.\n Place: Germany\n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n
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@article{de_wit_reliance_2012,\n\ttitle = {Reliance on habits at the expense of goal-directed control following dopamine precursor depletion.},\n\tvolume = {219},\n\tcopyright = {All rights reserved},\n\tissn = {1432-2072 0033-3158},\n\tdoi = {10.1007/s00213-011-2563-2},\n\tabstract = {RATIONALE: Dopamine is well known to play an important role in learning and motivation. Recent animal studies have implicated dopamine in the reinforcement  of stimulus-response habits, as well as in flexible, goal-directed action.  However, the role of dopamine in human action control is still not well  understood. OBJECTIVES: We present the first investigation of the effect of  reducing dopamine function in healthy volunteers on the balance between habitual  and goal-directed action control. METHODS: The dietary intervention of acute  dietary phenylalanine and tyrosine depletion (APTD) was adopted to study the  effects of reduced global dopamine function on action control. Participants were  randomly assigned to either the APTD or placebo group (ns = 14) to allow for a  between-subjects comparison of performance on a novel three-stage experimental  paradigm. In the initial learning phase, participants learned to respond to  different stimuli in order to gain rewarding outcomes. Subsequently, an  outcome-devaluation test and a slips-of-action test were conducted to assess  whether participants were able to flexibly adjust their behaviour to changes in  the desirability of the outcomes. RESULTS: APTD did not prevent stimulus-response  learning, nor did we find evidence for impaired response-outcome learning in the  subsequent outcome-devaluation test. However, when goal-directed and habitual  systems competed for control in the slips-of-action test, APTD tipped the balance  towards habitual control. These findings were restricted to female volunteers.  CONCLUSIONS: We provide direct evidence that the balance between goal-directed  and habitual control in humans is dopamine dependent. The results are discussed  in light of gender differences in dopamine function and psychopathologies.},\n\tlanguage = {eng},\n\tnumber = {2},\n\tjournal = {Psychopharmacology},\n\tauthor = {de Wit, Sanne and Standing, Holly R. and Devito, Elise E. and Robinson, Oliver J. and Ridderinkhof, K. Richard and Robbins, Trevor W. and Sahakian, Barbara J.},\n\tmonth = jan,\n\tyear = {2012},\n\tpmid = {22134475},\n\tpmcid = {PMC3249188},\n\tnote = {Place: Germany},\n\tkeywords = {*Habits, Adaptation, Adaptation, Psychological/drug effects/*physiology, Adult, Amino Acids/blood/pharmacology, Conditioning, Conditioning, Operant/drug effects/*physiology, Dopamine/deficiency/*physiology, Female, Humans, Male, Middle Aged, Operant/drug effects/*physiology, Phenylalanine/blood/*deficiency, Psychological/drug effects/*physiology, Tyrosine/blood/*deficiency},\n\tpages = {621--631},\n}\n\n
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\n RATIONALE: Dopamine is well known to play an important role in learning and motivation. Recent animal studies have implicated dopamine in the reinforcement of stimulus-response habits, as well as in flexible, goal-directed action. However, the role of dopamine in human action control is still not well understood. OBJECTIVES: We present the first investigation of the effect of reducing dopamine function in healthy volunteers on the balance between habitual and goal-directed action control. METHODS: The dietary intervention of acute dietary phenylalanine and tyrosine depletion (APTD) was adopted to study the effects of reduced global dopamine function on action control. Participants were randomly assigned to either the APTD or placebo group (ns = 14) to allow for a between-subjects comparison of performance on a novel three-stage experimental paradigm. In the initial learning phase, participants learned to respond to different stimuli in order to gain rewarding outcomes. Subsequently, an outcome-devaluation test and a slips-of-action test were conducted to assess whether participants were able to flexibly adjust their behaviour to changes in the desirability of the outcomes. RESULTS: APTD did not prevent stimulus-response learning, nor did we find evidence for impaired response-outcome learning in the subsequent outcome-devaluation test. However, when goal-directed and habitual systems competed for control in the slips-of-action test, APTD tipped the balance towards habitual control. These findings were restricted to female volunteers. CONCLUSIONS: We provide direct evidence that the balance between goal-directed and habitual control in humans is dopamine dependent. The results are discussed in light of gender differences in dopamine function and psychopathologies.\n
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\n  \n 2011\n \n \n (3)\n \n \n
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\n \n\n \n \n \n \n \n \n The effect of induced anxiety on cognition: threat of shock enhances aversive processing in healthy individuals.\n \n \n \n \n\n\n \n Robinson, O.; Letkiewicz, A.; Overstreet, C.; Ernst, M.; and Grillon, C.\n\n\n \n\n\n\n Cognitive, Affective, & Behavioral Neuroscience, 11: 217–27. 2011.\n 2\n\n\n\n
\n\n\n\n \n \n \"ThePaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n
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@article{robinson_effect_2011,\n\ttitle = {The effect of induced anxiety on cognition: threat of shock enhances aversive processing in healthy individuals},\n\tvolume = {11},\n\tcopyright = {All rights reserved},\n\tissn = {1530-7026},\n\tshorttitle = {The effect of induced anxiety on cognition: threat of shock enhances aversive processing in healthy individuals},\n\turl = {http://dx.doi.org/10.3758/s13415-011-0030-5},\n\tdoi = {10.3758/s13415-011-0030-5},\n\tjournal = {Cognitive, Affective, \\& Behavioral Neuroscience},\n\tauthor = {Robinson, Oliver and Letkiewicz, Allison and Overstreet, Cassie and Ernst, Monique and Grillon, Christian},\n\tyear = {2011},\n\tnote = {2},\n\tkeywords = {*Adaptation, *Adaptation, Psychological, *Cognition, *Conflict, *Conflict, Psychological, Adult, Anxiety/*psychology, Electroshock/*psychology, Facial Expression, Female, Humans, Individuality, Male, Psychological, Psychology, Psychomotor Performance, Reaction Time, Stroop Test},\n\tpages = {217--27},\n}\n\n
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\n \n\n \n \n \n \n \n \n Brain burdens: Boost resilience to tackle mental illness.\n \n \n \n \n\n\n \n Robinson, O. J.\n\n\n \n\n\n\n Nature, 478: 459–459. 2011.\n 7370\n\n\n\n
\n\n\n\n \n \n \"BrainPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n
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@article{robinson_brain_2011,\n\ttitle = {Brain burdens: {Boost} resilience to tackle mental illness},\n\tvolume = {478},\n\tcopyright = {All rights reserved},\n\tissn = {0028-0836},\n\tshorttitle = {Brain burdens: {Boost} resilience to tackle mental illness},\n\turl = {http://dx.doi.org/10.1038/478459b},\n\tdoi = {10.1038/478459b},\n\tjournal = {Nature},\n\tauthor = {Robinson, Oliver J.},\n\tyear = {2011},\n\tnote = {7370},\n\tkeywords = {Female, Humans, Male, Mental Disorders/*economics/*epidemiology, Mental Health/*statistics \\& numerical data, Research Support as Topic/*economics},\n\tpages = {459--459},\n}\n\n
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\n \n\n \n \n \n \n \n \n Converging evidence for central 5-HT effects in acute tryptophan depletion.\n \n \n \n \n\n\n \n Crockett, M. J.; Clark, L.; Roiser, J. P.; Robinson, O. J.; Cools, R.; Chase, H. W.; den Ouden, H.; Apergis-Schoute, A.; Campbell-Meikeljohn, D.; Seymour, B.; Sahakian, B. J.; Rogers, R. D.; and Robbins, T. W.\n\n\n \n\n\n\n Mol Psychiatry. 2011.\n \n\n\n\n
\n\n\n\n \n \n \"ConvergingPaper\n  \n \n\n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n \n \n \n \n\n\n\n
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@article{crockett_converging_2011,\n\ttitle = {Converging evidence for central 5-{HT} effects in acute tryptophan depletion},\n\tcopyright = {All rights reserved},\n\tissn = {1476-5578},\n\tshorttitle = {Converging evidence for central 5-{HT} effects in acute tryptophan depletion},\n\turl = {http://dx.doi.org/10.1038/mp.2011.106},\n\tjournal = {Mol Psychiatry},\n\tauthor = {Crockett, M. J. and Clark, L. and Roiser, J. P. and Robinson, O. J. and Cools, R. and Chase, H. W. and den Ouden, H. and Apergis-Schoute, A. and Campbell-Meikeljohn, D. and Seymour, B. and Sahakian, B. J. and Rogers, R. D. and Robbins, T. W.},\n\tyear = {2011},\n\tkeywords = {Animals, Humans, Serotonin/*metabolism, Tryptophan/*deficiency},\n}\n\n
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\n  \n 2010\n \n \n (3)\n \n \n
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\n \n\n \n \n \n \n \n \n Dopamine precursor depletion improves punishment prediction during reversal learning in healthy females but not males.\n \n \n \n \n\n\n \n Robinson, O. J.; Standing, H.; DeVito, E.; Cools, R.; and Sahakian, B.\n\n\n \n\n\n\n Psychopharmacology, 211: 187–195. 2010.\n 2\n\n\n\n
\n\n\n\n \n \n \"DopaminePaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n
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@article{robinson_dopamine_2010,\n\ttitle = {Dopamine precursor depletion improves punishment prediction during reversal learning in healthy females but not males},\n\tvolume = {211},\n\tcopyright = {All rights reserved},\n\tissn = {0033-3158},\n\tshorttitle = {Dopamine precursor depletion improves punishment prediction during reversal learning in healthy females but not males},\n\turl = {http://dx.doi.org/10.1007/s00213-010-1880-1},\n\tdoi = {10.1007/s00213-010-1880-1},\n\tjournal = {Psychopharmacology},\n\tauthor = {Robinson, Oliver J. and Standing, Holly and DeVito, Elise and Cools, Roshan and Sahakian, Barbara},\n\tyear = {2010},\n\tnote = {2},\n\tkeywords = {*Punishment, *Reversal Learning, *Reward, Adult, Biomedical and Life Sciences, Cross-Over Studies, Dopamine/biosynthesis/*metabolism, Double-Blind Method, Female, Humans, Male, Middle Aged, Phenylalanine/deficiency, Sex Factors, Tyrosine/deficiency, Young Adult},\n\tpages = {187--195},\n}\n\n
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\n \n\n \n \n \n \n \n \n Dissociable responses to punishment in distinct striatal regions during reversal learning.\n \n \n \n \n\n\n \n Robinson, O. J.; Frank, M. J.; Sahakian, B. J.; and Cools, R.\n\n\n \n\n\n\n Neuroimage, 51: 1459–1467. 2010.\n 4\n\n\n\n
\n\n\n\n \n \n \"DissociablePaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n  \n \n 1 download\n \n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n
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@article{robinson_dissociable_2010,\n\ttitle = {Dissociable responses to punishment in distinct striatal regions during reversal learning},\n\tvolume = {51},\n\tcopyright = {All rights reserved},\n\tissn = {1053-8119},\n\tshorttitle = {Dissociable responses to punishment in distinct striatal regions during reversal learning},\n\turl = {http://www.sciencedirect.com/science/article/pii/S105381191000323X},\n\tdoi = {10.1016/j.neuroimage.2010.03.036},\n\tjournal = {Neuroimage},\n\tauthor = {Robinson, Oliver J. and Frank, Michael J. and Sahakian, Barbara J. and Cools, Roshan},\n\tyear = {2010},\n\tnote = {4},\n\tkeywords = {Adult, Computer-Assisted, Electrophysiology, Female, Humans, Image Processing, Image Processing, Computer-Assisted, Linear Models, Magnetic Resonance Imaging, Male, Neostriatum/*physiology, Oxygen/blood, Photic Stimulation, Psychomotor Performance/physiology, Punishment/*psychology, Reaction Time/physiology, Reversal Learning/*physiology, Reward, Young Adult},\n\tpages = {1459--1467},\n}\n\n
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\n \n\n \n \n \n \n \n \n Mood state moderates the role of serotonin in cognitive biases.\n \n \n \n \n\n\n \n Robinson, O.; Cools, R.; Crockett, M.; and Sahakian, B.\n\n\n \n\n\n\n Journal of Psychopharmacology, 24: 573–583. April 2010.\n 4\n\n\n\n
\n\n\n\n \n \n \"MoodPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n
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@article{robinson_mood_2010,\n\ttitle = {Mood state moderates the role of serotonin in cognitive biases},\n\tvolume = {24},\n\tcopyright = {All rights reserved},\n\tshorttitle = {Mood state moderates the role of serotonin in cognitive biases},\n\turl = {http://jop.sagepub.com/content/24/4/573.abstract},\n\tdoi = {10.1177/0269881108100257},\n\tabstract = {Reduction of the monoamine serotonin (5-HT) via the dietary manipulation of tryptophan (acute tryptophan depletion; ATD) has been shown to induce negative cognitive biases similar to those found in depression in healthy individuals. However, evidence also indicates that there can be positive effects of ATD on both mood and reinforcement processing. Here, we present two separate studies, with remarkably similar findings, which may help explain these discrepancies. In both experiments, we assessed cognitive biases following experimentally induced mood states under both a balanced amino acid drink (BAL) and ATD. A significant interaction between treatment, mood state and cognitive bias was observed in both experiments. In the first experiment, subjects undergoing positive mood induction demonstrated a positive cognitive bias on BAL, which was abolished by ATD. The same effect was observed in subjects undergoing neutral mood induction in the second experiment. These effects replicate findings in healthy individuals undergoing ATD. Subjects undergoing negative mood induction, by contrast, demonstrated the opposite pattern of results; in both experiments, they showed no bias under BAL but induction of a positive cognitive bias by ATD. These results mimic previous findings in currently depressed patients undergoing ATD. We therefore suggest that mood state moderates the effect of ATD on cognitive biases. This, in turn, has important implications for the understanding of the role of 5-HT in psychiatric disorders.},\n\tjournal = {Journal of Psychopharmacology},\n\tauthor = {Robinson, OJ and Cools, R. and Crockett, MJ and Sahakian, BJ},\n\tmonth = apr,\n\tyear = {2010},\n\tnote = {4},\n\tkeywords = {*Affect/drug effects, *Cognition/drug effects, Administration, Administration, Oral, Adult, Beverages, Brain/drug effects/*metabolism, Cross-Over Studies, Cues, Double-Blind Method, Female, Humans, Male, Mental Recall, Oral, Psychological, Reaction Time, Reward, Serotonin/*metabolism, Signal Detection, Signal Detection, Psychological, Tryptophan/administration \\& dosage/deficiency, Young Adult},\n\tpages = {573--583},\n}\n\n
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\n Reduction of the monoamine serotonin (5-HT) via the dietary manipulation of tryptophan (acute tryptophan depletion; ATD) has been shown to induce negative cognitive biases similar to those found in depression in healthy individuals. However, evidence also indicates that there can be positive effects of ATD on both mood and reinforcement processing. Here, we present two separate studies, with remarkably similar findings, which may help explain these discrepancies. In both experiments, we assessed cognitive biases following experimentally induced mood states under both a balanced amino acid drink (BAL) and ATD. A significant interaction between treatment, mood state and cognitive bias was observed in both experiments. In the first experiment, subjects undergoing positive mood induction demonstrated a positive cognitive bias on BAL, which was abolished by ATD. The same effect was observed in subjects undergoing neutral mood induction in the second experiment. These effects replicate findings in healthy individuals undergoing ATD. Subjects undergoing negative mood induction, by contrast, demonstrated the opposite pattern of results; in both experiments, they showed no bias under BAL but induction of a positive cognitive bias by ATD. These results mimic previous findings in currently depressed patients undergoing ATD. We therefore suggest that mood state moderates the effect of ATD on cognitive biases. This, in turn, has important implications for the understanding of the role of 5-HT in psychiatric disorders.\n
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\n  \n 2009\n \n \n (2)\n \n \n
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\n \n\n \n \n \n \n \n \n A Double Dissociation in the Roles of Serotonin and Mood in Healthy Subjects.\n \n \n \n \n\n\n \n Robinson, O. J.; and Sahakian, B. J.\n\n\n \n\n\n\n Biological Psychiatry, 65: 89–92. 2009.\n 1\n\n\n\n
\n\n\n\n \n \n \"APaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n  \n \n 1 download\n \n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n
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@article{robinson_double_2009,\n\ttitle = {A {Double} {Dissociation} in the {Roles} of {Serotonin} and {Mood} in {Healthy} {Subjects}},\n\tvolume = {65},\n\tcopyright = {All rights reserved},\n\tissn = {0006-3223},\n\tshorttitle = {A {Double} {Dissociation} in the {Roles} of {Serotonin} and {Mood} in {Healthy} {Subjects}},\n\turl = {http://www.sciencedirect.com/science/article/pii/S0006322308011980},\n\tdoi = {10.1016/j.biopsych.2008.10.001},\n\tjournal = {Biological Psychiatry},\n\tauthor = {Robinson, Oliver J. and Sahakian, Barbara J.},\n\tyear = {2009},\n\tnote = {1},\n\tkeywords = {Adult, Affect, Affect/*physiology, Cognition, Cognition/*physiology, Cross-Over Studies, Depression, Double-Blind Method, Female, Humans, Male, Mood, Mood Disorders/etiology, Placebos, Psychomotor Performance, Serotonin/*metabolism/physiology, Tryptophan/blood, mania, serotonin},\n\tpages = {89--92},\n}\n\n
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\n \n\n \n \n \n \n \n Acute tryptophan depletion evokes negative mood in healthy females who have previously experienced concurrent negative mood and tryptophan depletion.\n \n \n \n\n\n \n Robinson, O. J.; and Sahakian, B. J.\n\n\n \n\n\n\n Psychopharmacology, 205(2): 227–235. August 2009.\n Place: Germany\n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n  \n \n 1 download\n \n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n
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@article{robinson_acute_2009,\n\ttitle = {Acute tryptophan depletion evokes negative mood in healthy females who have previously experienced concurrent negative mood and tryptophan depletion.},\n\tvolume = {205},\n\tcopyright = {All rights reserved},\n\tissn = {1432-2072 0033-3158},\n\tdoi = {10.1007/s00213-009-1533-4},\n\tabstract = {INTRODUCTION: The majority of individuals who suffer an episode of depression go on to experience recurrences. We have proposed, based upon the observation that  reducing serotonin via acute tryptophan depletion (ATD) is more likely to induce  negative mood in recovered depressed individuals than never depressed  individuals, that this may be because associations form between negative mood and  reduced serotonin during an episode of depression (Robinson and Sahakian, Psychol  Med 38:315-318, 2008b). Such associations would mean that subsequent reductions  in serotonin are more likely to provoke depressed mood and hence trigger an  episode of depression. METHODS: In this study, we tested this hypothesis by  manipulating the mood state of healthy females undergoing ATD (or balanced  placebo) on two separate testing sessions. On the first session, subjects  received either negative or neutral mood induction, while on the second session  all subjects received neutral mood induction. RESULTS: Our findings demonstrate  significant ATD-induced negative mood exclusively on the second visit of subjects  who received both ATD and negative mood induction procedure on their first visit.  DISCUSSION: These findings may be explained by the formation of an association  between the negative mood and reduced serotonin states during the first visit. As  such, these findings provide preliminary support for the associative hypothesis  of recurrence in depression. CONCLUSION: Such associations might therefore  explain the discrepancy between the effects of ATD in recovered- and  never-depressed individuals and may, in turn, explain why an episode of  depression increases the risk of subsequent episodes.},\n\tlanguage = {eng},\n\tnumber = {2},\n\tjournal = {Psychopharmacology},\n\tauthor = {Robinson, Oliver J. and Sahakian, Barbara J.},\n\tmonth = aug,\n\tyear = {2009},\n\tpmid = {19370340},\n\tpmcid = {PMC2705725},\n\tnote = {Place: Germany},\n\tkeywords = {Affect/*physiology, Analysis of Variance, Association Learning/*physiology, Beverages, Depression/blood/*psychology, Female, Humans, Pain Measurement, Psychiatric Status Rating Scales, Time Factors, Tryptophan/blood/*deficiency},\n\tpages = {227--235},\n}\n\n
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\n INTRODUCTION: The majority of individuals who suffer an episode of depression go on to experience recurrences. We have proposed, based upon the observation that reducing serotonin via acute tryptophan depletion (ATD) is more likely to induce negative mood in recovered depressed individuals than never depressed individuals, that this may be because associations form between negative mood and reduced serotonin during an episode of depression (Robinson and Sahakian, Psychol Med 38:315-318, 2008b). Such associations would mean that subsequent reductions in serotonin are more likely to provoke depressed mood and hence trigger an episode of depression. METHODS: In this study, we tested this hypothesis by manipulating the mood state of healthy females undergoing ATD (or balanced placebo) on two separate testing sessions. On the first session, subjects received either negative or neutral mood induction, while on the second session all subjects received neutral mood induction. RESULTS: Our findings demonstrate significant ATD-induced negative mood exclusively on the second visit of subjects who received both ATD and negative mood induction procedure on their first visit. DISCUSSION: These findings may be explained by the formation of an association between the negative mood and reduced serotonin states during the first visit. As such, these findings provide preliminary support for the associative hypothesis of recurrence in depression. CONCLUSION: Such associations might therefore explain the discrepancy between the effects of ATD in recovered- and never-depressed individuals and may, in turn, explain why an episode of depression increases the risk of subsequent episodes.\n
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\n  \n 2008\n \n \n (1)\n \n \n
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\n \n\n \n \n \n \n \n \n Recurrence in major depressive disorder: a neurocognitive perspective.\n \n \n \n \n\n\n \n Robinson, O. J.; and Sahakian, B. J.\n\n\n \n\n\n\n Psychological Medicine, 38(3): 315–318. March 2008.\n Publisher: Cambridge University Press\n\n\n\n
\n\n\n\n \n \n \"RecurrencePaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{robinson_recurrence_2008,\n\ttitle = {Recurrence in major depressive disorder: a neurocognitive perspective},\n\tvolume = {38},\n\tcopyright = {All rights reserved},\n\tissn = {1469-8978, 0033-2917},\n\tshorttitle = {Recurrence in major depressive disorder},\n\turl = {https://www.cambridge.org/core/journals/psychological-medicine/article/recurrence-in-major-depressive-disorder-a-neurocognitive-perspective/CAA5ACDE5498E1E998227D4EF428CF26},\n\tdoi = {10.1017/S0033291707001249},\n\tabstract = {Depressive disorders are amongst the leading causes of disability and mortality worldwide and, as such, it is predicted that by 2010 only cardio-ischaemic disorders will provide a greater burden. In addition to the sizable emotional, individual and social burden, depressive disorders cost an estimated US\\$83·1 billion per year in the United States alone. In spite of effective treatments, a large proportion of sufferers go on to experience recurrences. With successive recurrences, the likelihood of subsequent episodes increases. Despite this, research to date has tended to focus on first episodes or else has not distinguished between episodes. This editorial review highlights a number of differences between first and recurrent episodes which, in turn, recommend more longitudinal, recurrence-oriented, treatments. We also examine the findings from acute tryptophan depletion studies which, it is speculated, help to understand the differences between successive episodes. The overall aim, however, is to highlight the importance of recurrence in depression and to stimulate debate.},\n\tlanguage = {en},\n\tnumber = {3},\n\turldate = {2023-04-14},\n\tjournal = {Psychological Medicine},\n\tauthor = {Robinson, O. J. and Sahakian, B. J.},\n\tmonth = mar,\n\tyear = {2008},\n\tnote = {Publisher: Cambridge University Press},\n\tpages = {315--318},\n}\n\n
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\n Depressive disorders are amongst the leading causes of disability and mortality worldwide and, as such, it is predicted that by 2010 only cardio-ischaemic disorders will provide a greater burden. In addition to the sizable emotional, individual and social burden, depressive disorders cost an estimated US$83·1 billion per year in the United States alone. In spite of effective treatments, a large proportion of sufferers go on to experience recurrences. With successive recurrences, the likelihood of subsequent episodes increases. Despite this, research to date has tended to focus on first episodes or else has not distinguished between episodes. This editorial review highlights a number of differences between first and recurrent episodes which, in turn, recommend more longitudinal, recurrence-oriented, treatments. We also examine the findings from acute tryptophan depletion studies which, it is speculated, help to understand the differences between successive episodes. The overall aim, however, is to highlight the importance of recurrence in depression and to stimulate debate.\n
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\n  \n 2007\n \n \n (1)\n \n \n
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\n \n\n \n \n \n \n \n \n Acute Tryptophan Depletion in Healthy Volunteers Enhances Punishment Prediction but Does not Affect Reward Prediction.\n \n \n \n \n\n\n \n Cools, R.; Robinson, O. J.; and Sahakian, B.\n\n\n \n\n\n\n Neuropsychopharmacology, 33: 2291–2299. 2007.\n 9\n\n\n\n
\n\n\n\n \n \n \"AcutePaper\n  \n \n\n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n
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@article{cools_acute_2007,\n\ttitle = {Acute {Tryptophan} {Depletion} in {Healthy} {Volunteers} {Enhances} {Punishment} {Prediction} but {Does} not {Affect} {Reward} {Prediction}},\n\tvolume = {33},\n\tcopyright = {All rights reserved},\n\tissn = {0893-133X},\n\tshorttitle = {Acute {Tryptophan} {Depletion} in {Healthy} {Volunteers} {Enhances} {Punishment} {Prediction} but {Does} not {Affect} {Reward} {Prediction}},\n\turl = {http://dx.doi.org/10.1038/sj.npp.1301598},\n\tjournal = {Neuropsychopharmacology},\n\tauthor = {Cools, Roshan and Robinson, Oliver J. and Sahakian, Barbara},\n\tyear = {2007},\n\tnote = {9},\n\tkeywords = {*Punishment, Adolescent, Adult, Affect, Analysis of Variance, Conditioning, Conditioning, Operant, Discrimination Learning, Double-Blind Method, Female, Food, Food, Formulated, Formulated, Humans, Male, Neuropsychological Tests, Operant, Reaction Time, Reproducibility of Results, Reversal Learning/*physiology, Self Concept, Task Performance and Analysis, Tryptophan/*deficiency},\n\tpages = {2291--2299},\n}\n\n
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\n  \n 2005\n \n \n (1)\n \n \n
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\n \n\n \n \n \n \n \n \n Inter-Order Interactions Between Flower-Visiting Insects:Foraging Bees Avoid Flowers Previously Visited by Hoverflies.\n \n \n \n \n\n\n \n Reader, T.; MacLeod, I.; Elliott, P. T.; Robinson, O. J.; and Manica, A.\n\n\n \n\n\n\n Journal of Insect Behavior, 18(1): 51–57. January 2005.\n \n\n\n\n
\n\n\n\n \n \n \"Inter-OrderPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n
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@article{reader_inter-order_2005,\n\ttitle = {Inter-{Order} {Interactions} {Between} {Flower}-{Visiting} {Insects}:{Foraging} {Bees} {Avoid} {Flowers} {Previously} {Visited} by {Hoverflies}},\n\tvolume = {18},\n\tcopyright = {All rights reserved},\n\tissn = {1572-8889},\n\tshorttitle = {Inter-{Order} {Interactions} {Between} {Flower}-{Visiting} {Insects}},\n\turl = {https://doi.org/10.1007/s10905-005-9346-8},\n\tdoi = {10.1007/s10905-005-9346-8},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2023-04-14},\n\tjournal = {Journal of Insect Behavior},\n\tauthor = {Reader, Tom and MacLeod, Ian and Elliott, Philip T. and Robinson, Oliver J. and Manica, Andrea},\n\tmonth = jan,\n\tyear = {2005},\n\tkeywords = {Bumble bees, competition, foraging, honey bees, hoverflies, inter-order interactions},\n\tpages = {51--57},\n}\n\n
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\n \n\n \n \n \n \n \n \n A series of unfortunate events: Do those who catastrophize learn more after negative outcomes?.\n \n \n \n \n\n\n \n Harada-Laszlo, M.; Talwar, A.; Robinson, O. J.; and Pike, A. C.\n\n\n \n\n\n\n Mental Health Science, n/a(n/a): e49. .\n _eprint: https://onlinelibrary.wiley.com/doi/pdf/10.1002/mhs2.49\n\n\n\n
\n\n\n\n \n \n \"APaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n
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@article{harada-laszlo_series_nodate,\n\ttitle = {A series of unfortunate events: {Do} those who catastrophize learn more after negative outcomes?},\n\tvolume = {n/a},\n\tcopyright = {© 2023 The Authors. Mental Health Science published by Wiley Periodicals LLC.},\n\tissn = {2642-3588},\n\tshorttitle = {A series of unfortunate events},\n\turl = {https://onlinelibrary.wiley.com/doi/abs/10.1002/mhs2.49},\n\tdoi = {10.1002/mhs2.49},\n\tabstract = {Catastrophizing is a transdiagnostic construct that has been suggested to precipitate and maintain a multiplicity of psychiatric disorders, including anxiety, depression, post-traumatic stress disorder, and obsessive-compulsive disorder. However, the underlying cognitive mechanisms that result in catastrophizing are unknown. Relating reinforcement learning model parameters to catastrophizing may allow us to further understand the process of catastrophizing. Using a modified four-armed bandit task, we aimed to investigate the relationship between reinforcement learning parameters and self-report catastrophizing questionnaire scores to gain a mechanistic understanding of how catastrophizing may alter learning. We recruited 211 participants to complete a computerized four-armed bandit task and tested the fit of six reinforcement learning models on our data, including two novel models which both incorporated a scaling factor related to a history of negative outcomes variable. We investigated the relationship between self-report catastrophizing scores and free parameters from the overall best-fitting model, along with the best-fitting model to include history, using Pearson's correlations. Subsequently, we reassessed these relationships using multiple regression analyses to evaluate whether any observed relationships were altered when relevant IQ and mental health covariates were applied. Model-agnostic analyses indicated there were effects of outcome history on reaction time and accuracy, and that the effects on accuracy related to catastrophizing. The overall model of best fit was the Standard Rescorla–Wagner Model and the best-fitting model to include history was a model in which learning rate was scaled by history of negative outcome. We found no effect of catastrophizing on the scaling by history of negative outcome parameter (r = 0.003, p = 0.679), the learning rate parameter (r = 0.026, p = 0.703), or the inverse temperature parameter (r = 0.086, p = 0.220). We were unable to relate catastrophizing to any of the reinforcement learning parameters we investigated. This implies that catastrophizing is not straightforwardly linked to any changes to learning after a series of negative outcomes are received. Future research could incorporate further exploration of the space of models which include a history parameter.},\n\tlanguage = {en},\n\tnumber = {n/a},\n\turldate = {2024-01-10},\n\tjournal = {Mental Health Science},\n\tauthor = {Harada-Laszlo, Mia and Talwar, Anahita and Robinson, Oliver J. and Pike, Alexandra C.},\n\tnote = {\\_eprint: https://onlinelibrary.wiley.com/doi/pdf/10.1002/mhs2.49},\n\tkeywords = {catastrophizing, computational modeling, computational psychiatry, online, reinforcement learning, transdiagnostic},\n\tpages = {e49},\n}\n\n
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\n Catastrophizing is a transdiagnostic construct that has been suggested to precipitate and maintain a multiplicity of psychiatric disorders, including anxiety, depression, post-traumatic stress disorder, and obsessive-compulsive disorder. However, the underlying cognitive mechanisms that result in catastrophizing are unknown. Relating reinforcement learning model parameters to catastrophizing may allow us to further understand the process of catastrophizing. Using a modified four-armed bandit task, we aimed to investigate the relationship between reinforcement learning parameters and self-report catastrophizing questionnaire scores to gain a mechanistic understanding of how catastrophizing may alter learning. We recruited 211 participants to complete a computerized four-armed bandit task and tested the fit of six reinforcement learning models on our data, including two novel models which both incorporated a scaling factor related to a history of negative outcomes variable. We investigated the relationship between self-report catastrophizing scores and free parameters from the overall best-fitting model, along with the best-fitting model to include history, using Pearson's correlations. Subsequently, we reassessed these relationships using multiple regression analyses to evaluate whether any observed relationships were altered when relevant IQ and mental health covariates were applied. Model-agnostic analyses indicated there were effects of outcome history on reaction time and accuracy, and that the effects on accuracy related to catastrophizing. The overall model of best fit was the Standard Rescorla–Wagner Model and the best-fitting model to include history was a model in which learning rate was scaled by history of negative outcome. We found no effect of catastrophizing on the scaling by history of negative outcome parameter (r = 0.003, p = 0.679), the learning rate parameter (r = 0.026, p = 0.703), or the inverse temperature parameter (r = 0.086, p = 0.220). We were unable to relate catastrophizing to any of the reinforcement learning parameters we investigated. This implies that catastrophizing is not straightforwardly linked to any changes to learning after a series of negative outcomes are received. Future research could incorporate further exploration of the space of models which include a history parameter.\n
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