@article{pike_test-retest_2024,
	title = {Test-{Retest} {Reliability} of {Two} {Computationally}-{Characterised} {Affective} {Bias} {Tasks}},
	volume = {8},
	issn = {2379-6227},
	doi = {10.5334/cpsy.92},
	abstract = {Affective biases are commonly seen in disorders such as depression and anxiety, where individuals may show attention towards and preferential processing of negative or threatening stimuli. Affective biases have been shown to change with effective intervention: randomized controlled trials into these biases and the mechanisms that underpin them may allow greater understanding of how interventions can be improved and their success be maximized. For such trials to be informative, we must have reliable ways of measuring affective bias over time, so we can detect how and whether they are altered by interventions: the test-retest reliability of our measures puts an upper bound on our ability to detect any changes. In this online study we therefore examined the test-retest reliability of two behavioural affective bias tasks (an 'Ambiguous Midpoint' and a 'Go-Nogo' task). 58 individuals recruited from the general population completed the tasks twice, with at least 14 days in between sessions. We analysed the reliability of both summary statistics and parameters from computational models using Pearson's correlations and intra-class correlations. Standard summary statistic measures from these affective bias tasks had reliabilities ranging from 0.18 (poor) to 0.49 (moderate). Parameters from computational modelling of these tasks were in many cases less reliable than summary statistics. However, embedding the covariance between sessions within the generative modelling framework resulted in higher estimates of stability. We conclude that measures from these affective bias tasks are moderately reliable, but further work to improve the reliability of these tasks would improve still further our ability to draw inferences in randomized trials.},
	language = {eng},
	number = {1},
	journal = {Computational Psychiatry (Cambridge, Mass.)},
	author = {Pike, Alexandra C. and Tan, Katrina H. T. and Tromblee, Hoda and Wing, Michelle and Robinson, Oliver J.},
	year = {2024},
	pmid = {39713087},
	pmcid = {PMC11661199},
	keywords = {affective bias, anxiety, depression, measurement, psychometrics, test-retest reliability},
	pages = {217--232},
}

Affective biases are commonly seen in disorders such as depression and anxiety, where individuals may show attention towards and preferential processing of negative or threatening stimuli. Affective biases have been shown to change with effective intervention: randomized controlled trials into these biases and the mechanisms that underpin them may allow greater understanding of how interventions can be improved and their success be maximized. For such trials to be informative, we must have reliable ways of measuring affective bias over time, so we can detect how and whether they are altered by interventions: the test-retest reliability of our measures puts an upper bound on our ability to detect any changes. In this online study we therefore examined the test-retest reliability of two behavioural affective bias tasks (an 'Ambiguous Midpoint' and a 'Go-Nogo' task). 58 individuals recruited from the general population completed the tasks twice, with at least 14 days in between sessions. We analysed the reliability of both summary statistics and parameters from computational models using Pearson's correlations and intra-class correlations. Standard summary statistic measures from these affective bias tasks had reliabilities ranging from 0.18 (poor) to 0.49 (moderate). Parameters from computational modelling of these tasks were in many cases less reliable than summary statistics. However, embedding the covariance between sessions within the generative modelling framework resulted in higher estimates of stability. We conclude that measures from these affective bias tasks are moderately reliable, but further work to improve the reliability of these tasks would improve still further our ability to draw inferences in randomized trials.

@article{buehler_independent_2024,
	title = {Independent replications reveal anterior and posterior cingulate cortex activation underlying state anxiety-attenuated face encoding},
	volume = {2},
	issn = {2731-9121},
	doi = {10.1038/s44271-024-00128-y},
	abstract = {Anxiety involves the anticipation of aversive outcomes and can impair neurocognitive processes, such as the ability to recall faces encoded during the anxious state. It is important to precisely delineate and determine the replicability of these effects using causal state anxiety inductions in the general population. This study therefore aimed to replicate prior research on the distinct impacts of threat-of-shock-induced anxiety on the encoding and recognition stage of emotional face processing, in a large asymptomatic sample (n = 92). We successfully replicated previous results demonstrating impaired recognition of faces encoded under threat-of-shock. This was supported by a mega-analysis across three independent studies using the same paradigm (n = 211). Underlying this, a whole-brain fMRI analysis revealed enhanced activation in the posterior cingulate cortex (PCC), alongside previously seen activity in the anterior cingulate cortex (ACC) when combined in a mega-analysis with the fMRI findings we aimed to replicate. We further found replications of hippocampus activation when the retrieval and encoding states were congruent. Our results support the notion that state anxiety disrupts face recognition, potentially due to attentional demands of anxious arousal competing with affective stimuli processing during encoding and suggest that regions of the cingulate cortex play pivotal roles in this.},
	language = {eng},
	journal = {Communications Psychology},
	author = {Buehler, Sarah K. and Lowther, Millie and Lukow, Paulina B. and Kirk, Peter A. and Pike, Alexandra C. and Yamamori, Yumeya and Chavanne, Alice V. and Gormley, Siobhan and Goble, Talya and Tuominen, Ella W. and Aylward, Jessica and McCloud, Tayla and Rodriguez-Sanchez, Julia and Robinson, Oliver J.},
	year = {2024},
	pmid = {39184223},
	pmcid = {PMC11343718},
	keywords = {Cognitive control, Short-term memory},
	pages = {80},
}

Anxiety involves the anticipation of aversive outcomes and can impair neurocognitive processes, such as the ability to recall faces encoded during the anxious state. It is important to precisely delineate and determine the replicability of these effects using causal state anxiety inductions in the general population. This study therefore aimed to replicate prior research on the distinct impacts of threat-of-shock-induced anxiety on the encoding and recognition stage of emotional face processing, in a large asymptomatic sample (n = 92). We successfully replicated previous results demonstrating impaired recognition of faces encoded under threat-of-shock. This was supported by a mega-analysis across three independent studies using the same paradigm (n = 211). Underlying this, a whole-brain fMRI analysis revealed enhanced activation in the posterior cingulate cortex (PCC), alongside previously seen activity in the anterior cingulate cortex (ACC) when combined in a mega-analysis with the fMRI findings we aimed to replicate. We further found replications of hippocampus activation when the retrieval and encoding states were congruent. Our results support the notion that state anxiety disrupts face recognition, potentially due to attentional demands of anxious arousal competing with affective stimuli processing during encoding and suggest that regions of the cingulate cortex play pivotal roles in this.

@article{lukow_amygdala_2024,
	title = {Amygdala activity after subchronic escitalopram administration in healthy volunteers: {A} pharmaco-functional magnetic resonance imaging study},
	volume = {38},
	issn = {0269-8811, 1461-7285},
	shorttitle = {Amygdala activity after subchronic escitalopram administration in healthy volunteers},
	url = {https://journals.sagepub.com/doi/10.1177/02698811241286773},
	doi = {10.1177/02698811241286773},
	abstract = {Background:
              Selective serotonin reuptake inhibitors (SSRIs) are used for the treatment of several conditions including anxiety disorders, but the basic neurobiology of serotonin function remains unclear. The amygdala and prefrontal cortex are strongly innervated by serotonergic projections and have been suggested to play an important role in anxiety expression. However, serotonergic function in behaviour and SSRI-mediated neurobiological changes remain incompletely understood.
            
            
              Aims:
              To investigate the neural correlates of subchronic antidepressant administration.
            
            
              Methods:
              We investigated whether the 2- to 3-week administration of a highly selective SSRI (escitalopram) would alter brain activation on a task robustly shown to recruit the bilateral amygdala and frontal cortices in a large healthy volunteer sample. Participants performed the task during a functional magnetic resonance imaging acquisition before ( n = 96) and after subchronic escitalopram ( n = 46, days of administration mean (SD) = 15.7 (2.70)) or placebo ( n = 40 days of administration mean (SD) = 16.2 (2.90)) self-administration.
            
            
              Results:
              Compared to placebo, we found an elevation in right amygdala activation to the task after escitalopram administration without significant changes in mood. This effect was not seen in the left amygdala, the dorsomedial region of interest, the subgenual anterior cingulate cortex or the right fusiform area. There were no significant changes in connectivity between the dorsomedial cortex and amygdala or the subgenual anterior cingulate cortex after escitalopram administration.
            
            
              Conclusions:
              To date, this most highly powered study of subchronic SSRI administration indicates that, contrary to effects often seen in patients with anxiety disorders, subchronic SSRI treatment may increase amygdala activation in healthy controls. This finding highlights important gaps in our understanding of the functional role of serotonin.},
	language = {en},
	number = {12},
	urldate = {2024-11-06},
	journal = {Journal of Psychopharmacology},
	author = {Lukow, Paulina B and Lowther, Millie and Pike, Alexandra C and Yamamori, Yumeya and Chavanne, Alice V and Gormley, Siobhan and Aylward, Jessica and McCloud, Tayla and Goble, Talya and Rodriguez-Sanchez, Julia and Tuominen, Ella W and Buehler, Sarah K and Kirk, Peter and Robinson, Oliver J},
	month = dec,
	year = {2024},
	pages = {1071--1082},
}

Background: Selective serotonin reuptake inhibitors (SSRIs) are used for the treatment of several conditions including anxiety disorders, but the basic neurobiology of serotonin function remains unclear. The amygdala and prefrontal cortex are strongly innervated by serotonergic projections and have been suggested to play an important role in anxiety expression. However, serotonergic function in behaviour and SSRI-mediated neurobiological changes remain incompletely understood. Aims: To investigate the neural correlates of subchronic antidepressant administration. Methods: We investigated whether the 2- to 3-week administration of a highly selective SSRI (escitalopram) would alter brain activation on a task robustly shown to recruit the bilateral amygdala and frontal cortices in a large healthy volunteer sample. Participants performed the task during a functional magnetic resonance imaging acquisition before ( n = 96) and after subchronic escitalopram ( n = 46, days of administration mean (SD) = 15.7 (2.70)) or placebo ( n = 40 days of administration mean (SD) = 16.2 (2.90)) self-administration. Results: Compared to placebo, we found an elevation in right amygdala activation to the task after escitalopram administration without significant changes in mood. This effect was not seen in the left amygdala, the dorsomedial region of interest, the subgenual anterior cingulate cortex or the right fusiform area. There were no significant changes in connectivity between the dorsomedial cortex and amygdala or the subgenual anterior cingulate cortex after escitalopram administration. Conclusions: To date, this most highly powered study of subchronic SSRI administration indicates that, contrary to effects often seen in patients with anxiety disorders, subchronic SSRI treatment may increase amygdala activation in healthy controls. This finding highlights important gaps in our understanding of the functional role of serotonin.

@article{lutkenherm_reward_2024,
	title = {Reward {Sensitivity} and {Noise} {Contribute} to {Negative} {Affective} {Bias}: {A} {Learning} {Signal} {Detection} {Theory} {Approach} in {Decision}-{Making}},
	volume = {8},
	issn = {2379-6227},
	shorttitle = {Reward {Sensitivity} and {Noise} {Contribute} to {Negative} {Affective} {Bias}},
	url = {https://account.cpsyjournal.org/index.php/up-j-cp/article/view/102},
	doi = {10.5334/cpsy.102},
	abstract = {In patients with mood disorders, negative affective biases – systematically prioritising and interpreting information negatively – are common. A translational cognitive task testing this bias has shown that depressed patients have a reduced preference for a high reward under ambiguous decision-making conditions. The precise mechanisms underscoring this bias are, however, not yet understood. We therefore developed a set of measures to probe the underlying source of the behavioural bias by testing its relationship to a participant’s reward sensitivity, value sensitivity and reward learning rate. One-hundred-forty-eight participants completed three online behavioural tasks: the original ambiguous-cue decision-making task probing negative affective bias, a probabilistic reward learning task probing reward sensitivity and reward learning rate, and a gambling task probing value sensitivity. We modelled the learning task through a dynamic signal detection theory model and the gambling task through an expectation-maximisation prospect theory model. Reward sensitivity from the probabilistic reward task (β = 0.131, p = 0.024) and setting noise from the probabilistic reward task (β = –0.187, p = 0.028) both predicted the affective bias score in a logistic regression. Increased negative affective bias, at least on this specific task, may therefore be driven in part by a combination of reduced sensitivity to rewards and more variable responses.},
	number = {1},
	urldate = {2024-11-06},
	journal = {Computational Psychiatry},
	author = {Lütkenherm, Isabel K. and Locke, Shannon M. and Robinson, Oliver J.},
	month = may,
	year = {2024},
}

In patients with mood disorders, negative affective biases – systematically prioritising and interpreting information negatively – are common. A translational cognitive task testing this bias has shown that depressed patients have a reduced preference for a high reward under ambiguous decision-making conditions. The precise mechanisms underscoring this bias are, however, not yet understood. We therefore developed a set of measures to probe the underlying source of the behavioural bias by testing its relationship to a participant’s reward sensitivity, value sensitivity and reward learning rate. One-hundred-forty-eight participants completed three online behavioural tasks: the original ambiguous-cue decision-making task probing negative affective bias, a probabilistic reward learning task probing reward sensitivity and reward learning rate, and a gambling task probing value sensitivity. We modelled the learning task through a dynamic signal detection theory model and the gambling task through an expectation-maximisation prospect theory model. Reward sensitivity from the probabilistic reward task (β = 0.131, p = 0.024) and setting noise from the probabilistic reward task (β = –0.187, p = 0.028) both predicted the affective bias score in a logistic regression. Increased negative affective bias, at least on this specific task, may therefore be driven in part by a combination of reduced sensitivity to rewards and more variable responses.

@article{yamamori_thinking_2024,
	title = {Thinking computationally in translational psychiatry. {A} commentary on {Neville} et al. (2024)},
	volume = {24},
	issn = {1530-7026, 1531-135X},
	url = {https://link.springer.com/10.3758/s13415-024-01172-1},
	doi = {10.3758/s13415-024-01172-1},
	abstract = {Abstract
            
              There is a growing focus on the computational aspects of psychiatric disorders in humans. This idea also is gaining traction in nonhuman animal studies. Commenting on a new comprehensive overview of the benefits of applying this approach in translational research by Neville et al. (
              Cognitive Affective \& Behavioral Neuroscience
              1–14, 2024), we discuss the implications for translational model validity within this framework. We argue that thinking computationally in translational psychiatry calls for a change in the way that we evaluate animal models of human psychiatric processes, with a shift in focus towards symptom-producing computations rather than the symptoms themselves. Further, in line with Neville et al.'s adoption of the reinforcement learning framework to model animal behaviour, we illustrate how this approach can be applied beyond simple decision-making paradigms to model more naturalistic behaviours.},
	language = {en},
	number = {2},
	urldate = {2024-11-06},
	journal = {Cognitive, Affective, \& Behavioral Neuroscience},
	author = {Yamamori, Yumeya and Robinson, Oliver J.},
	month = apr,
	year = {2024},
	pages = {384--387},
}

Abstract There is a growing focus on the computational aspects of psychiatric disorders in humans. This idea also is gaining traction in nonhuman animal studies. Commenting on a new comprehensive overview of the benefits of applying this approach in translational research by Neville et al. ( Cognitive Affective & Behavioral Neuroscience 1–14, 2024), we discuss the implications for translational model validity within this framework. We argue that thinking computationally in translational psychiatry calls for a change in the way that we evaluate animal models of human psychiatric processes, with a shift in focus towards symptom-producing computations rather than the symptoms themselves. Further, in line with Neville et al.'s adoption of the reinforcement learning framework to model animal behaviour, we illustrate how this approach can be applied beyond simple decision-making paradigms to model more naturalistic behaviours.

@article{kirk_preliminary_2024,
	title = {Preliminary evidence for altered brain-heart coherence during anxiogenic movies},
	volume = {2},
	issn = {2837-6056},
	url = {https://direct.mit.edu/imag/article/doi/10.1162/imag_a_00156/120593/Preliminary-evidence-for-altered-brain-heart},
	doi = {10.1162/imag_a_00156},
	abstract = {Abstract
            During states of anxiety, fundamental threat circuitry in the brain can increase heart rate via alterations in autonomic balance (increased sympathetic activity and parasympathetic withdrawal) and may serve to promote interoceptive integration and awareness of cardiac signals. Moreover, evidence indicates pathological anxiety could be associated with increased communication between the brain and the heart. Yet, this phenomenon remains not well understood. For instance, studies in this area have been conducted within the confines of tightly controlled experimental paradigms. Whether anxiety impacts brain-heart communication outside of such experimental settings, and in relatively more naturalistic contexts, is less clear. Here, we used a suspenseful movie fMRI paradigm to study induced anxiety (n = 29 healthy volunteers; Caltech Conte dataset; Kliemann et al., 2022). We predicted that brain responses across an anxiety-relevant “defensive response network” (amygdala, hypothalamus, periaqueductal gray, bed nucleus of the stria terminalis, dorsomedial prefrontal cortex, ventromedial prefrontal cortex, subgenual anterior cingulate, and anterior insula; Abend et al., 2022) would show increased coherence with heart rate as participants watched a suspenseful movie clip compared to a non-suspenseful movie clip. Counter to our predictions, we found decreased coherence between heart rate and brain responses during increased anxiety, namely in amygdala-prefrontal circuitry. We suggest these alterations may be underpinned by parasympathetic withdrawal and/or decreased interoceptive awareness during suspenseful movie-watching.},
	language = {en},
	urldate = {2024-11-06},
	journal = {Imaging Neuroscience},
	author = {Kirk, Peter A. and Robinson, Oliver J.},
	month = may,
	year = {2024},
	pages = {1--15},
}

Abstract During states of anxiety, fundamental threat circuitry in the brain can increase heart rate via alterations in autonomic balance (increased sympathetic activity and parasympathetic withdrawal) and may serve to promote interoceptive integration and awareness of cardiac signals. Moreover, evidence indicates pathological anxiety could be associated with increased communication between the brain and the heart. Yet, this phenomenon remains not well understood. For instance, studies in this area have been conducted within the confines of tightly controlled experimental paradigms. Whether anxiety impacts brain-heart communication outside of such experimental settings, and in relatively more naturalistic contexts, is less clear. Here, we used a suspenseful movie fMRI paradigm to study induced anxiety (n = 29 healthy volunteers; Caltech Conte dataset; Kliemann et al., 2022). We predicted that brain responses across an anxiety-relevant “defensive response network” (amygdala, hypothalamus, periaqueductal gray, bed nucleus of the stria terminalis, dorsomedial prefrontal cortex, ventromedial prefrontal cortex, subgenual anterior cingulate, and anterior insula; Abend et al., 2022) would show increased coherence with heart rate as participants watched a suspenseful movie clip compared to a non-suspenseful movie clip. Counter to our predictions, we found decreased coherence between heart rate and brain responses during increased anxiety, namely in amygdala-prefrontal circuitry. We suggest these alterations may be underpinned by parasympathetic withdrawal and/or decreased interoceptive awareness during suspenseful movie-watching.

@article{kirk_neuroanatomical_2024,
	title = {Neuroanatomical {Subtyping} of {Phobias}: {Implications} for {Function} and {Development}},
	volume = {181},
	issn = {0002-953X, 1535-7228},
	shorttitle = {Neuroanatomical {Subtyping} of {Phobias}},
	url = {https://psychiatryonline.org/doi/10.1176/appi.ajp.20240502},
	doi = {10.1176/appi.ajp.20240502},
	language = {en},
	number = {8},
	urldate = {2024-11-06},
	journal = {American Journal of Psychiatry},
	author = {Kirk, Peter A. and Robinson, Oliver J.},
	month = aug,
	year = {2024},
	pages = {693--695},
}

@article{wang_similarities_2024,
	title = {Similarities and differences between post-traumatic stress disorder and major depressive disorder: {Evidence} from task-evoked functional magnetic resonance imaging meta-analysis},
	volume = {361},
	issn = {01650327},
	shorttitle = {Similarities and differences between post-traumatic stress disorder and major depressive disorder},
	url = {https://linkinghub.elsevier.com/retrieve/pii/S0165032724010280},
	doi = {10.1016/j.jad.2024.06.095},
	language = {en},
	urldate = {2024-11-06},
	journal = {Journal of Affective Disorders},
	author = {Wang, Zuxing and He, Danmei and Yang, Lin and Wang, Peijia and Xiao, Jun and Zou, Zhili and Min, Wenjiao and He, Ying and Yuan, Cui and Zhu, Hongru and Robinson, Oliver J.},
	month = sep,
	year = {2024},
	pages = {712--719},
}

@article{sporrer_induced_2024,
	title = {Induced worry increases risk aversion in patients with generalized anxiety},
	volume = {474},
	issn = {01664328},
	url = {https://linkinghub.elsevier.com/retrieve/pii/S0166432824003486},
	doi = {10.1016/j.bbr.2024.115192},
	language = {en},
	urldate = {2024-11-06},
	journal = {Behavioural Brain Research},
	author = {Sporrer, Juliana K. and Johann, Alexandra and Chumbley, Justin and Robinson, Oliver J. and Bach, Dominik R.},
	month = oct,
	year = {2024},
	pages = {115192},
}

@article{kirk_anxiety_2023,
	title = {Anxiety {Shapes} {Amygdala}-{Prefrontal} {Dynamics} {During} {Movie} {Watching}},
	volume = {3},
	issn = {26671743},
	url = {https://linkinghub.elsevier.com/retrieve/pii/S2667174322000489},
	doi = {10.1016/j.bpsgos.2022.03.009},
	language = {en},
	number = {3},
	urldate = {2024-11-06},
	journal = {Biological Psychiatry Global Open Science},
	author = {Kirk, Peter A. and Holmes, Avram J. and Robinson, Oliver J.},
	month = jul,
	year = {2023},
	pages = {409--417},
}

@article{slaninadavies_eating_2023,
	title = {Eating disorder symptoms and control‐seeking behavior},
	volume = {13},
	copyright = {All rights reserved},
	issn = {2162-3279, 2162-3279},
	url = {https://onlinelibrary.wiley.com/doi/10.1002/brb3.3105},
	doi = {10.1002/brb3.3105},
	abstract = {Abstract
            
              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 (
                r
                s
                 = .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.},
	language = {en},
	number = {8},
	urldate = {2024-11-06},
	journal = {Brain and Behavior},
	author = {Slanina‐Davies, Ashley and Robinson, Oliver J. and Pike, Alexandra C.},
	month = aug,
	year = {2023},
	pages = {e3105},
}

Abstract 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 ( r s  = .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.

@article{pitman_influence_2023,
	title = {The influence of peer non-suicidal self-harm on young adults’ urges to self-harm: experimental study},
	issn = {0924-2708, 1601-5215},
	shorttitle = {The influence of peer non-suicidal self-harm on young adults’ urges to self-harm},
	url = {https://www.cambridge.org/core/journals/acta-neuropsychiatrica/article/influence-of-peer-nonsuicidal-selfharm-on-young-adults-urges-to-selfharm-experimental-study/520B54D3ECB58C1725F87CCD3AFE9248},
	doi = {10.1017/neu.2023.51},
	abstract = {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.},
	language = {en},
	urldate = {2024-01-10},
	journal = {Acta Neuropsychiatrica},
	author = {Pitman, Alexandra and Lowther, Millie and Pike, Alexandra and Davies, Jessica and Cates, Angharad de and Buckman, Joshua E. J. and Robinson, Oliver},
	month = nov,
	year = {2023},
	note = {Publisher: Cambridge University Press},
	keywords = {Self-harm, adolescent, cognition, peer influence, self-injurious behaviour},
	pages = {1--13},
}

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.

@article{pike_catastrophizing_2023,
	title = {Catastrophizing and {Risk}-{Taking}},
	volume = {7},
	issn = {2379-6227},
	url = {https://cpsyjournal.org/article/10.5334/cpsy.91/},
	doi = {10.5334/cpsy.91},
	abstract = {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.},
	language = {en},
	number = {1},
	urldate = {2023-12-21},
	journal = {Computational Psychiatry},
	author = {Pike, Alexandra C. and Alves Anet, Ágatha and Peleg, Nina and Robinson, Oliver J.},
	month = jan,
	year = {2023},
	pages = {1},
}

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.

@article{suddell_emotional_2023,
	title = {Emotional bias training as a treatment for anxiety and depression: evidence from experimental medicine studies in healthy and medicated samples},
	volume = {53},
	issn = {0033-2917, 1469-8978},
	shorttitle = {Emotional bias training as a treatment for anxiety and depression},
	url = {https://www.cambridge.org/core/product/identifier/S0033291721002014/type/journal_article},
	doi = {10.1017/S0033291721002014},
	abstract = {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.},
	language = {en},
	number = {3},
	urldate = {2023-12-21},
	journal = {Psychological Medicine},
	author = {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.},
	month = feb,
	year = {2023},
	pages = {696--705},
}

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.

@article{yamamori_approach-avoidance_2023,
	title = {Approach-avoidance reinforcement learning as a translational and computational model of anxiety-related avoidance},
	volume = {12},
	issn = {2050-084X},
	url = {https://elifesciences.org/articles/87720},
	doi = {10.7554/eLife.87720},
	abstract = {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.},
	language = {en},
	urldate = {2023-12-21},
	journal = {eLife},
	author = {Yamamori, Yumeya and Robinson, Oliver J and Roiser, Jonathan P},
	month = nov,
	year = {2023},
	pages = {RP87720},
}

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.

@article{yamamori_computational_2023,
	title = {Computational perspectives on human fear and anxiety.},
	volume = {144},
	copyright = {Copyright © 2022 The Authors. Published by Elsevier Ltd.. All rights reserved.},
	issn = {1873-7528 0149-7634},
	doi = {10.1016/j.neubiorev.2022.104959},
	abstract = {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.},
	language = {eng},
	journal = {Neuroscience and biobehavioral reviews},
	author = {Yamamori, Yumeya and Robinson, Oliver J.},
	month = jan,
	year = {2023},
	pmid = {36375584},
	note = {Place: United States},
	keywords = {*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},
	pages = {104959},
}

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.

@article{fleming_measuring_2023,
	title = {Measuring cognitive effort without difficulty.},
	copyright = {© 2023. The Author(s).},
	issn = {1531-135X 1530-7026},
	doi = {10.3758/s13415-023-01065-9},
	abstract = {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.},
	language = {eng},
	journal = {Cognitive, affective \& behavioral neuroscience},
	author = {Fleming, Hugo and Robinson, Oliver J. and Roiser, Jonathan P.},
	month = feb,
	year = {2023},
	pmid = {36750498},
	note = {Place: United States},
	keywords = {Anhedonia, Cognitive effort, Computational psychiatry, Depression, Individual differences, New measures},
}

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.

@article{chelliah_efficacy_2022,
	title = {Efficacy of attention bias modification via smartphones in a large population sample},
	volume = {9},
	issn = {2054-5703},
	url = {https://royalsocietypublishing.org/doi/10.1098/rsos.211629},
	doi = {10.1098/rsos.211629},
	abstract = {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.},
	language = {en},
	number = {8},
	urldate = {2023-12-21},
	journal = {Royal Society Open Science},
	author = {Chelliah, Alysha and Robinson, Oliver},
	month = aug,
	year = {2022},
	pages = {211629},
}

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.

@article{wise_identifying_2022,
	title = {Identifying {Transdiagnostic} {Mechanisms} in {Mental} {Health} {Using} {Computational} {Factor} {Modeling}.},
	copyright = {Copyright © 2022 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved.},
	issn = {1873-2402 0006-3223},
	doi = {10.1016/j.biopsych.2022.09.034},
	abstract = {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.},
	language = {eng},
	journal = {Biological psychiatry},
	author = {Wise, Toby and Robinson, Oliver J. and Gillan, Claire M.},
	month = oct,
	year = {2022},
	pmid = {36725393},
	note = {Place: United States},
	keywords = {Cognition, Computational factor modeling, Computational modeling, Factor analysis, RDoC, Transdiagnostic},
	pages = {S0006--3223(22)01661--4},
}

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.

@article{schmidt_ejn_2022,
	title = {{EJN} stress, brain and behaviour special issue.},
	volume = {55},
	copyright = {All rights reserved},
	issn = {1460-9568 0953-816X},
	doi = {10.1111/ejn.15718},
	language = {eng},
	number = {9-10},
	journal = {The European journal of neuroscience},
	author = {Schmidt, Mathias V. and Robinson, Oliver J. and Sandi, Carmen},
	month = may,
	year = {2022},
	pmid = {35569819},
	note = {Place: France},
	keywords = {*Brain, *Head},
	pages = {2053--2057},
}

@article{pike_reinforcement_2022,
	title = {Reinforcement {Learning} in {Patients} {With} {Mood} and {Anxiety} {Disorders} vs {Control} {Individuals}: {A} {Systematic} {Review} and {Meta}-analysis},
	volume = {79},
	copyright = {All rights reserved},
	issn = {2168-622X},
	shorttitle = {Reinforcement {Learning} in {Patients} {With} {Mood} and {Anxiety} {Disorders} vs {Control} {Individuals}},
	url = {https://doi.org/10.1001/jamapsychiatry.2022.0051},
	doi = {10.1001/jamapsychiatry.2022.0051},
	abstract = {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.},
	number = {4},
	urldate = {2022-08-02},
	journal = {JAMA Psychiatry},
	author = {Pike, Alexandra C. and Robinson, Oliver J.},
	month = apr,
	year = {2022},
	keywords = {*Anxiety Disorders/diagnosis/therapy, *Anxiety/therapy, Affect, Bayes Theorem, Humans, Reward},
	pages = {313--322},
}

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.

@article{kirk_anxiety_2022,
	title = {Anxiety and amygdala connectivity during movie-watching},
	volume = {169},
	copyright = {All rights reserved},
	issn = {1873-3514},
	doi = {10.1016/j.neuropsychologia.2022.108194},
	abstract = {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.},
	language = {eng},
	journal = {Neuropsychologia},
	author = {Kirk, Peter A. and Robinson, Oliver J. and Skipper, Jeremy I.},
	month = may,
	year = {2022},
	pmid = {35245529},
	pmcid = {PMC8987737},
	keywords = {*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},
	pages = {108194},
}

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.

@article{kirk_threat_2022,
	title = {Threat vigilance and intrinsic amygdala connectivity},
	volume = {43},
	copyright = {All rights reserved},
	issn = {1097-0193},
	doi = {10.1002/hbm.25851},
	abstract = {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.},
	language = {eng},
	number = {10},
	journal = {Human Brain Mapping},
	author = {Kirk, Peter A. and Holmes, Avram J. and Robinson, Oliver J.},
	month = jul,
	year = {2022},
	pmid = {35362645},
	pmcid = {PMC9188965},
	keywords = {*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},
	pages = {3283--3292},
}

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.

@article{kirk_rapidhrv_2022,
	title = {{RapidHRV}: an open-source toolbox for extracting heart rate and heart rate variability.},
	volume = {10},
	copyright = {© 2022 Kirk et al.},
	issn = {2167-8359},
	doi = {10.7717/peerj.13147},
	abstract = {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.},
	language = {eng},
	journal = {PeerJ},
	author = {Kirk, Peter A. and Davidson Bryan, Alexander and Garfinkel, Sarah N. and Robinson, Oliver J.},
	year = {2022},
	pmid = {35345583},
	pmcid = {PMC8957280},
	note = {Place: United States},
	keywords = {*Algorithms, *Electrocardiography, Heart Rate/physiology, Heart rate variability, Photoplethysmography, Python, Remote sensing, Toolbox, Wrist},
	pages = {e13147},
}

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.

@article{daniel-watanabe_association_2022,
	title = {Association {Between} a {Directly} {Translated} {Cognitive} {Measure} of {Negative} {Bias} and {Self}-reported {Psychiatric} {Symptoms}},
	volume = {7},
	copyright = {All rights reserved},
	issn = {2451-9022},
	url = {https://www.sciencedirect.com/science/article/pii/S2451902220300537},
	doi = {10.1016/j.bpsc.2020.02.010},
	abstract = {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.},
	language = {en},
	number = {2},
	urldate = {2022-09-01},
	journal = {Biological Psychiatry: Cognitive Neuroscience and Neuroimaging},
	author = {Daniel-Watanabe, Lucie and McLaughlin, Martha and Gormley, Siobhan and Robinson, Oliver J.},
	month = feb,
	year = {2022},
	keywords = {*Affect, *Anxiety Disorders, Animals, Anxiety, Bias, Cognition, Computational psychiatry, Depression, Humans, Individual differences, Negative affective bias, Online testing, Self Report, Structural equation modeling},
	pages = {201--209},
}

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.

@article{suddell_emotional_2021,
	title = {Emotional bias training as a treatment for anxiety and depression: evidence from experimental medicine studies in healthy and medicated samples.},
	copyright = {All rights reserved},
	issn = {1469-8978 0033-2917},
	doi = {10.1017/S0033291721002014},
	abstract = {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.},
	language = {eng},
	journal = {Psychological medicine},
	author = {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.},
	month = may,
	year = {2021},
	pmid = {34057058},
	note = {Place: England},
	keywords = {Anxiety, cognitive training, depression, digital intervention, emotional processing},
	pages = {1--10},
}

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.

@article{pike_development_2021,
	title = {The development and psychometric properties of a self-report {Catastrophizing} {Questionnaire}.},
	volume = {8},
	copyright = {© 2021 The Authors.},
	issn = {2054-5703},
	doi = {10.1098/rsos.201362},
	abstract = {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.},
	language = {eng},
	number = {1},
	journal = {Royal Society open science},
	author = {Pike, Alexandra C. and Serfaty, Jade R. and Robinson, Oliver J.},
	month = jan,
	year = {2021},
	pmid = {33614077},
	pmcid = {PMC7890513},
	note = {Place: England},
	keywords = {anxiety disorders, catastrophizing, cognitive distortions, mood disorders, psychiatry, self-report questionnaire},
	pages = {201362},
}

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.

@article{pike_importance_2021,
	title = {The {Importance} of {Common} {Currency} {Tasks} in {Translational} {Psychiatry}},
	volume = {8},
	copyright = {All rights reserved},
	issn = {2196-2979},
	url = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7904709/},
	doi = {10.1007/s40473-021-00225-w},
	abstract = {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.},
	number = {1},
	urldate = {2022-08-22},
	journal = {Current Behavioral Neuroscience Reports},
	author = {Pike, Alexandra C. and Lowther, Millie and Robinson, Oliver J.},
	year = {2021},
	pmid = {33708469},
	pmcid = {PMC7904709},
	keywords = {Animal models, Behavioural assay, Common currency tasks, Translational psychiatry, Translational tasks, Validity},
	pages = {1--10},
}

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.

@article{packer_assessing_2021,
	title = {Assessing the {Effectiveness} of {Front} of {Pack} {Labels}: {Findings} from an {Online} {Randomised}-{Controlled} {Experiment} in a {Representative} {British} {Sample}.},
	volume = {13},
	copyright = {All rights reserved},
	issn = {2072-6643},
	doi = {10.3390/nu13030900},
	abstract = {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.},
	language = {eng},
	number = {3},
	journal = {Nutrients},
	author = {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},
	month = mar,
	year = {2021},
	pmid = {33802115},
	pmcid = {PMC7999818},
	note = {Place: Switzerland},
	keywords = {*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},
}

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.

@article{locke_affective_2021,
	title = {Affective {Bias} {Through} the {Lens} of {Signal} {Detection} {Theory}.},
	volume = {5},
	copyright = {All rights reserved},
	issn = {2379-6227},
	doi = {10.5334/cpsy.58},
	abstract = {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.},
	language = {eng},
	number = {1},
	journal = {Computational psychiatry (Cambridge, Mass.)},
	author = {Locke, Shannon M. and Robinson, Oliver J.},
	year = {2021},
	pmid = {34268450},
	pmcid = {PMC7611246},
	note = {Place: England},
	keywords = {affective bias, anxiety disorders, decision-making, mood disorders, signal detection theory},
	pages = {4--20},
}

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.

@article{kirk_trait_2021,
	title = {Trait anxiety does not correlate with metacognitive confidence or reminder usage in a delayed intentions task.},
	volume = {74},
	copyright = {All rights reserved},
	issn = {1747-0226 1747-0218},
	doi = {10.1177/1747021820970156},
	abstract = {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.},
	language = {eng},
	number = {4},
	journal = {Quarterly journal of experimental psychology (2006)},
	author = {Kirk, Peter A. and Robinson, Oliver J. and Gilbert, Sam J.},
	month = apr,
	year = {2021},
	pmid = {33084484},
	pmcid = {PMC8044609},
	note = {Place: England},
	keywords = {*Memory, *Memory, Episodic, *Metacognition, Anxiety, Bayes Theorem, Episodic, Humans, Intention, Memory, Prospective Studies, anxiety, metacognition},
	pages = {634--644},
}

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.

@article{sarigiannidis_does_2020,
	title = {Does overloading cognitive resources mimic the impact of anxiety on temporal cognition?},
	volume = {46},
	copyright = {All rights reserved},
	issn = {1939-1285 0278-7393},
	doi = {10.1037/xlm0000845},
	abstract = {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).},
	language = {eng},
	number = {10},
	journal = {Journal of experimental psychology. Learning, memory, and cognition},
	author = {Sarigiannidis, Ioannis and Kirk, Peter A. and Roiser, Jonathan P. and Robinson, Oliver J.},
	month = oct,
	year = {2020},
	pmid = {32378938},
	pmcid = {PMC7872305},
	note = {Place: United States},
	keywords = {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},
	pages = {1828--1835},
}

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).

@article{sarigiannidis_anxiety_2020,
	title = {Anxiety makes time pass quicker while fear has no effect.},
	volume = {197},
	copyright = {Copyright © 2020 The Authors. Published by Elsevier B.V. All rights reserved.},
	issn = {1873-7838 0010-0277},
	doi = {10.1016/j.cognition.2019.104116},
	abstract = {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).},
	language = {eng},
	journal = {Cognition},
	author = {Sarigiannidis, Ioannis and Grillon, Christian and Ernst, Monique and Roiser, Jonathan P. and Robinson, Oliver J.},
	month = apr,
	year = {2020},
	pmid = {31883966},
	pmcid = {PMC7033556},
	note = {Place: Netherlands},
	keywords = {*Fear, *Time Perception, Anxiety, Anxiety Disorders, Cognition, Emotion, Fear, Humans, Threat-of-shock, Time perception},
	pages = {104116},
}

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).

@article{love_bigger_2020,
	title = {"{Bigger}" or "better": the roles of magnitude and valence in "affective bias".},
	volume = {34},
	copyright = {All rights reserved},
	issn = {1464-0600 0269-9931},
	doi = {10.1080/02699931.2019.1662373},
	abstract = {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.},
	language = {eng},
	number = {4},
	journal = {Cognition \& emotion},
	author = {Love, Jack and Robinson, Oliver J.},
	month = jun,
	year = {2020},
	pmid = {31496360},
	pmcid = {PMC7446041},
	note = {Place: England},
	keywords = {*Affect, *Punishment/psychology, *Reward, Affective bias, Anxiety/*psychology, Bias, Healthy Volunteers/*psychology, Humans, Role, anxiety, magnitude, two-alternative forced choice, valence},
	pages = {633--642},
}

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.

@article{robinson_translational_2019,
	title = {The translational neural circuitry of anxiety},
	volume = {90},
	copyright = {All rights reserved},
	issn = {1468-330X},
	doi = {10.1136/jnnp-2019-321400},
	abstract = {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.},
	language = {eng},
	number = {12},
	journal = {Journal of Neurology, Neurosurgery, and Psychiatry},
	author = {Robinson, Oliver J. and Pike, Alexandra C. and Cornwell, Brian and Grillon, Christian},
	month = dec,
	year = {2019},
	pmid = {31256001},
	keywords = {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},
	pages = {1353--1360},
}

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.

@article{nord_reliability_2019,
	title = {Reliability of {Fronto}-{Amygdala} {Coupling} during {Emotional} {Face} {Processing}.},
	volume = {9},
	copyright = {All rights reserved},
	issn = {2076-3425},
	doi = {10.3390/brainsci9040089},
	abstract = {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.},
	language = {eng},
	number = {4},
	journal = {Brain sciences},
	author = {Nord, Camilla L. and Gray, Alan and Robinson, Oliver J. and Roiser, Jonathan P.},
	month = apr,
	year = {2019},
	pmid = {31010224},
	pmcid = {PMC6523743},
	note = {Place: Switzerland},
	keywords = {amygdala, connectivity, emotion processing, functional magnetic resonance imaging (fMRI), prefrontal cortex, reliability},
}

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.

@article{grillon_modeling_2019,
	title = {Modeling anxiety in healthy humans: a key intermediate bridge between basic and clinical sciences.},
	volume = {44},
	copyright = {All rights reserved},
	issn = {1740-634X 0893-133X},
	doi = {10.1038/s41386-019-0445-1},
	abstract = {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.},
	language = {eng},
	number = {12},
	journal = {Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology},
	author = {Grillon, Christian and Robinson, Oliver J. and Cornwell, Brian and Ernst, Monique},
	month = nov,
	year = {2019},
	pmid = {31226707},
	pmcid = {PMC6897969},
	note = {Place: England},
	keywords = {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},
	pages = {1999--2010},
}

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.

@article{garibbo_impact_2019,
	title = {The impact of threat of shock-induced anxiety on the neural substrates of memory encoding and retrieval.},
	volume = {14},
	copyright = {© The Author(s) 2019. Published by Oxford University Press.},
	issn = {1749-5024 1749-5016},
	doi = {10.1093/scan/nsz080},
	abstract = {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.},
	language = {eng},
	number = {10},
	journal = {Social cognitive and affective neuroscience},
	author = {Garibbo, Michele and Aylward, Jessica and Robinson, Oliver J.},
	month = oct,
	year = {2019},
	pmid = {31680142},
	pmcid = {PMC6970151},
	note = {Place: England},
	keywords = {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},
	pages = {1087--1096},
}

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.

@article{robinson_learning_2017,
	title = {Learning and {Choice} in {Mood} {Disorders}: {Searching} for the {Computational} {Parameters} of {Anhedonia}.},
	volume = {1},
	copyright = {All rights reserved},
	issn = {2379-6227},
	doi = {10.1162/CPSY_a_00009},
	abstract = {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.},
	language = {eng},
	number = {1},
	journal = {Computational psychiatry (Cambridge, Mass.)},
	author = {Robinson, Oliver J. and Chase, Henry W.},
	year = {2017},
	pmid = {29400358},
	pmcid = {PMC5796642},
	note = {Place: England},
	keywords = {anxiety, computational psychiatry, decision making, mood disorders, reinforcement learning},
	pages = {208--233},
}

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.

@article{peters_cognitive_2017,
	title = {Cognitive bias modification for facial interpretation: a randomized controlled trial of transfer to self-report and cognitive measures in a healthy sample.},
	volume = {4},
	copyright = {All rights reserved},
	issn = {2054-5703},
	doi = {10.1098/rsos.170681},
	abstract = {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.},
	language = {eng},
	number = {12},
	journal = {Royal Society open science},
	author = {Peters, S. E. and Lumsden, J. and Peh, O. H. and Penton-Voak, I. S. and Munafò, M. R. and Robinson, O. J.},
	month = dec,
	year = {2017},
	pmid = {29308221},
	pmcid = {PMC5749989},
	note = {Place: England},
	keywords = {cognitive bias modification, facial interpretation, randomized controlled trial, translational research},
	pages = {170681},
}

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.

@article{nord_unreliability_2017,
	title = {Unreliability of putative {fMRI} biomarkers during emotional face processing.},
	volume = {156},
	copyright = {Copyright © 2017 The Authors. Published by Elsevier Inc. All rights reserved.},
	issn = {1095-9572 1053-8119},
	doi = {10.1016/j.neuroimage.2017.05.024},
	abstract = {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.},
	language = {eng},
	journal = {NeuroImage},
	author = {Nord, C. L. and Gray, A. and Charpentier, C. J. and Robinson, O. J. and Roiser, J. P.},
	month = aug,
	year = {2017},
	pmid = {28506872},
	pmcid = {PMC5553850},
	note = {Place: United States},
	keywords = {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},
	pages = {119--127},
}

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.

@article{mkrtchian_threat_2017,
	title = {Threat of shock and aversive inhibition: {Induced} anxiety modulates {Pavlovian}-instrumental interactions.},
	volume = {146},
	copyright = {(c) 2017 APA, all rights reserved).},
	issn = {1939-2222 0096-3445 0022-1015},
	doi = {10.1037/xge0000363},
	abstract = {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},
	language = {eng},
	number = {12},
	journal = {Journal of experimental psychology. General},
	author = {Mkrtchian, Anahit and Roiser, Jonathan P. and Robinson, Oliver J.},
	month = dec,
	year = {2017},
	pmid = {28910125},
	pmcid = {PMC5733814},
	note = {Place: United States},
	keywords = {*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},
	pages = {1694--1704},
}

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

@article{mkrtchian_modeling_2017,
	series = {Stress: {Mechanisms} in {Gut} and {Brain}},
	title = {Modeling {Avoidance} in {Mood} and {Anxiety} {Disorders} {Using} {Reinforcement} {Learning}},
	volume = {82},
	copyright = {All rights reserved},
	issn = {0006-3223},
	url = {https://www.sciencedirect.com/science/article/pii/S0006322317300914},
	doi = {10.1016/j.biopsych.2017.01.017},
	abstract = {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.},
	language = {en},
	number = {7},
	urldate = {2022-08-22},
	journal = {Biological Psychiatry},
	author = {Mkrtchian, Anahit and Aylward, Jessica and Dayan, Peter and Roiser, Jonathan P. and Robinson, Oliver J.},
	month = oct,
	year = {2017},
	keywords = {*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},
	pages = {532--539},
}

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.

@article{grillon_anxiety-mediated_2017,
	title = {Anxiety-mediated facilitation of behavioral inhibition: {Threat} processing and defensive reactivity during a go/no-go task.},
	volume = {17},
	copyright = {(c) 2017 APA, all rights reserved).},
	issn = {1931-1516 1528-3542},
	doi = {10.1037/emo0000214},
	abstract = {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},
	language = {eng},
	number = {2},
	journal = {Emotion (Washington, D.C.)},
	author = {Grillon, Christian and Robinson, Oliver J. and Krimsky, Marissa and O'Connell, Katherine and Alvarez, Gabriella and Ernst, Monique},
	month = mar,
	year = {2017},
	pmid = {27642657},
	pmcid = {PMC5328922},
	note = {Place: United States},
	keywords = {*Inhibition, *Inhibition, Psychological, Adult, Anxiety/*psychology, Fear/*psychology, Female, Humans, Male, Neuropsychological Tests, Psychological, Reflex, Reflex, Startle/*physiology, Startle/*physiology, Young Adult},
	pages = {259--266},
}

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

@article{grillon_clinical_2017,
	title = {Clinical anxiety promotes excessive response inhibition.},
	volume = {47},
	copyright = {All rights reserved},
	issn = {1469-8978 0033-2917},
	doi = {10.1017/S0033291716002555},
	abstract = {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.},
	language = {eng},
	number = {3},
	journal = {Psychological medicine},
	author = {Grillon, C. and Robinson, O. J. and O'Connell, K. and Davis, A. and Alvarez, G. and Pine, D. S. and Ernst, M.},
	month = feb,
	year = {2017},
	pmid = {27776562},
	pmcid = {PMC6100803},
	note = {Place: England},
	keywords = {*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},
	pages = {484--494},
}

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.

@article{robinson_anxiety-potentiated_2016,
	title = {Anxiety-potentiated amygdala-medial frontal coupling and attentional control.},
	volume = {6},
	copyright = {All rights reserved},
	issn = {2158-3188},
	doi = {10.1038/tp.2016.105},
	abstract = {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.},
	language = {eng},
	number = {6},
	journal = {Translational psychiatry},
	author = {Robinson, O. J. and Krimsky, M. and Lieberman, L. and Vytal, K. and Ernst, M. and Grillon, C.},
	month = jun,
	year = {2016},
	pmid = {27271859},
	pmcid = {PMC4931603},
	note = {Place: United States},
	keywords = {*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},
	pages = {e833},
}

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.

@article{torrisi_neural_2016,
	title = {The neural basis of improved cognitive performance by threat of shock.},
	volume = {11},
	copyright = {Published by Oxford University Press 2016. This work is written by US Government employees and is in the public domain in the United States.},
	issn = {1749-5024 1749-5016},
	doi = {10.1093/scan/nsw088},
	abstract = {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.},
	language = {eng},
	number = {11},
	journal = {Social cognitive and affective neuroscience},
	author = {Torrisi, Salvatore and Robinson, Oliver and O'Connell, Katherine and Davis, Andrew and Balderston, Nicholas and Ernst, Monique and Grillon, Christian},
	month = nov,
	year = {2016},
	pmid = {27369069},
	pmcid = {PMC5091680},
	note = {Place: England},
	keywords = {*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},
	pages = {1677--1686},
}

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.

@article{grillon_effect_2016,
	title = {Effect of attention control on sustained attention during induced anxiety.},
	volume = {30},
	copyright = {All rights reserved},
	issn = {1464-0600 0269-9931},
	doi = {10.1080/02699931.2015.1024614},
	abstract = {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.},
	language = {eng},
	number = {4},
	journal = {Cognition \& emotion},
	author = {Grillon, Christian and Robinson, Oliver J. and Mathur, Ambika and Ernst, Monique},
	year = {2016},
	pmid = {25899613},
	pmcid = {PMC4618278},
	note = {Place: England},
	keywords = {*Attention, Anxiety, Anxiety/*psychology, Fear, Psychomotor Performance, Reflex, Reflex, Startle, SART, Startle, Stress, Threat of shock, Vigilance},
	pages = {700--712},
}

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.

@article{robinson_impact_2015,
	title = {The impact of threat of shock on the framing effect and temporal discounting: executive functions unperturbed by acute stress?},
	volume = {6},
	copyright = {All rights reserved},
	issn = {1664-1078},
	doi = {10.3389/fpsyg.2015.01315},
	abstract = {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.},
	language = {eng},
	journal = {Frontiers in psychology},
	author = {Robinson, Oliver J. and Bond, Rebecca L. and Roiser, Jonathan P.},
	year = {2015},
	pmid = {26441705},
	pmcid = {PMC4562307},
	note = {Place: Switzerland},
	keywords = {Bayesian models, anxiety, depression, executive function, framing effect, stress, temporal discounting, threat of shock},
	pages = {1315},
}

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.

@article{robinson_impact_2015-1,
	title = {The impact of stress on financial decision-making varies as a function of depression and anxiety symptoms.},
	volume = {3},
	copyright = {All rights reserved},
	issn = {2167-8359},
	doi = {10.7717/peerj.770},
	abstract = {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.},
	language = {eng},
	journal = {PeerJ},
	author = {Robinson, Oliver J. and Bond, Rebecca L. and Roiser, Jonathan P.},
	year = {2015},
	pmid = {25699215},
	pmcid = {PMC4330902},
	note = {Place: United States},
	keywords = {Anxiety, Depression, Harm-avoidance, Iowa Gambling Task, Resilience, Risk-seeking, Stress, Threat of shock, Vulnerablity},
	pages = {e770},
}

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.

@article{vytal_sustained_2014,
	title = {Sustained anxiety increases amygdala-dorsomedial prefrontal coupling: a mechanism for maintaining an anxious state in healthy adults.},
	volume = {39},
	copyright = {All rights reserved},
	issn = {1488-2434 1180-4882},
	doi = {10.1503/jpn.130145},
	abstract = {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.},
	language = {eng},
	number = {5},
	journal = {Journal of psychiatry \& neuroscience : JPN},
	author = {Vytal, Katherine E. and Overstreet, Cassie and Charney, Danielle R. and Robinson, Oliver J. and Grillon, Christian},
	month = sep,
	year = {2014},
	pmid = {24886788},
	pmcid = {PMC4160361},
	note = {Place: Canada},
	keywords = {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},
	pages = {321--329},
}

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.

@article{robinson_towards_2014,
	title = {Towards a mechanistic understanding of pathological anxiety: the dorsal medial prefrontal-amygdala ‘aversive amplification’ circuit in unmedicated generalized and social anxiety disorders},
	volume = {1},
	copyright = {All rights reserved},
	issn = {2215-0366},
	shorttitle = {Towards a mechanistic understanding of pathological anxiety},
	url = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4337019/},
	doi = {10.1016/S2215-0366(14)70305-0},
	abstract = {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.},
	number = {4},
	urldate = {2022-08-22},
	journal = {The Lancet. Psychiatry},
	author = {Robinson, Oliver J and Krimsky, Marissa and Lieberman, Lynne and Allen, Phillip and Vytal, Katherine and Grillon, Christian},
	month = sep,
	year = {2014},
	pmid = {25722962},
	pmcid = {PMC4337019},
	keywords = {Anxiety, Aversive amplification, amygdala, connectivity, dmPFC/DACC},
	pages = {294--302},
}

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.

@article{robinson_impact_2013,
	title = {The {Impact} of {Anxiety} {Upon} {Cognition}: {Perspectives} from {Human} {Threat} of {Shock} {Studies}},
	volume = {7},
	copyright = {All rights reserved},
	issn = {1662-5161},
	shorttitle = {The impact of anxiety on cognition},
	url = {http://www.frontiersin.org/Journal/Abstract.aspx?s=537&name=human_neuroscience&ART_DOI=10.3389/fnhum.2013.00203},
	doi = {10.3389/fnhum.2013.00203},
	abstract = {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.},
	language = {English},
	journal = {Frontiers in Human Neuroscience},
	author = {Robinson, Oliver Joe and Vytal, Katherine and Cornwell, Brian R and Grillon, Christian},
	month = may,
	year = {2013},
	keywords = {Anxiety Disorders, Attention, Cognition, Perception, Threat of shock, anxiety, anxiety disorders, attention, cognition, executive function, learning and memory, perception, threat of shock},
}

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.

@article{robinson_stress_2013,
	title = {Stress increases aversive prediction error signal in the ventral striatum},
	volume = {110},
	copyright = {All rights reserved},
	issn = {0027-8424, 1091-6490},
	url = {https://pnas.org/doi/full/10.1073/pnas.1213923110},
	doi = {10.1073/pnas.1213923110},
	abstract = {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.},
	language = {en},
	number = {10},
	urldate = {2023-04-06},
	journal = {Proceedings of the National Academy of Sciences},
	author = {Robinson, Oliver J. and Overstreet, Cassie and Charney, Danielle R. and Vytal, Katherine and Grillon, Christian},
	month = mar,
	year = {2013},
	pages = {4129--4133},
}

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.

@article{robinson_role_2013,
	title = {The role of serotonin in the neurocircuitry of negative affective bias: {Serotonergic} modulation of the dorsal medial prefrontal-amygdala ‘aversive amplification’ circuit},
	volume = {78},
	copyright = {All rights reserved},
	issn = {1053-8119},
	shorttitle = {The role of serotonin in the neurocircuitry of negative affective bias: {Serotonergic} modulation of the dorsal medial prefrontal-amygdala ‘aversive amplification’ circuit},
	url = {http://www.sciencedirect.com/science/article/pii/S1053811913003303},
	doi = {10.1016/j.neuroimage.2013.03.075},
	journal = {Neuroimage},
	author = {Robinson, Oliver J. and Overstreet, Cassie and Allen, Philip S. and Letkiewicz, Alison and Vytal, Katherine and Pine, Daniel S. and Grillon, Christian},
	year = {2013},
	note = {0},
	keywords = {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},
	pages = {217--223},
}

@article{robinson_impact_2013-1,
	title = {The impact of induced anxiety on response inhibition.},
	volume = {7},
	copyright = {All rights reserved},
	issn = {1662-5161},
	doi = {10.3389/fnhum.2013.00069},
	abstract = {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.},
	language = {eng},
	journal = {Frontiers in human neuroscience},
	author = {Robinson, Oliver J. and Krimsky, Marissa and Grillon, Christian},
	year = {2013},
	pmid = {23471118},
	pmcid = {PMC3590569},
	note = {Place: Switzerland},
	keywords = {anxiety, mind-wandering, response inhibition, threat, threat of shock},
	pages = {69},
}

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.

@article{robinson_ventral_2012,
	title = {Ventral {Striatum} {Response} {During} {Reward} and {Punishment} {Reversal} {Learning} in {Unmedicated} {Major} {Depressive} {Disorder}},
	volume = {169},
	copyright = {All rights reserved},
	issn = {0002-953X},
	url = {https://ajp.psychiatryonline.org/doi/full/10.1176/appi.ajp.2011.11010137},
	doi = {10.1176/appi.ajp.2011.11010137},
	abstract = {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.},
	number = {2},
	urldate = {2023-04-14},
	journal = {American Journal of Psychiatry},
	author = {Robinson, Oliver J. and Cools, Roshan and Carlisi, Christina O. and Sahakian, Barbara J. and Drevets, Wayne C.},
	month = feb,
	year = {2012},
	note = {Publisher: American Psychiatric Publishing},
	pages = {152--159},
}

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.

@article{robinson_acute_2012,
	title = {Acute {Tryptophan} {Depletion} {Increases} {Translational} {Indices} of {Anxiety} but not {Fear}: {Serotonergic} {Modulation} of the {Bed} {Nucleus} of the {Stria} {Terminalis}?},
	copyright = {All rights reserved},
	issn = {1740-634X},
	shorttitle = {Acute {Tryptophan} {Depletion} {Increases} {Translational} {Indices} of {Anxiety} but not {Fear}: {Serotonergic} {Modulation} of the {Bed} {Nucleus} of the {Stria} {Terminalis}?},
	url = {http://dx.doi.org/10.1038/npp.2012.43},
	journal = {Neuropsychopharmacology},
	author = {Robinson, Oliver J. and Overstreet, Cassie and Allen, Phillip S. and Pine, Daniel S. and Grillon, Christian},
	year = {2012},
	keywords = {*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},
}

@article{robinson_depressed_2012,
	title = {Depressed mood enhances anxiety to unpredictable threat},
	volume = {42},
	copyright = {All rights reserved},
	issn = {1469-8978 (Electronic) 0033-2917 (Linking)},
	shorttitle = {Depressed mood enhances anxiety to unpredictable threat},
	url = {http://www.ncbi.nlm.nih.gov/pubmed/22088577},
	doi = {10.1017/S0033291711002583},
	language = {eng},
	urldate = {2011-01-01},
	journal = {Psychol Med},
	author = {Robinson, O. J. and Overstreet, C. and Letkiewicz, A. and Grillon, C.},
	month = jul,
	year = {2012},
	note = {7},
	keywords = {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},
	pages = {1397--407},
}

@article{robinson_tryptophan_2012,
	title = {Tryptophan depletion disinhibits punishment but not reward prediction: implications for resilience},
	volume = {219},
	copyright = {All rights reserved},
	issn = {1432-2072 (Electronic) 0033-3158 (Linking)},
	shorttitle = {Tryptophan depletion disinhibits punishment but not reward prediction: implications for resilience},
	url = {http://www.ncbi.nlm.nih.gov/pubmed/21769566},
	doi = {10.1007/s00213-011-2410-5},
	language = {eng},
	journal = {Psychopharmacology (Berl)},
	author = {Robinson, O. J. and Cools, R. and Sahakian, B. J.},
	month = jan,
	year = {2012},
	note = {2},
	keywords = {*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},
	pages = {599--605},
}

@article{robinson_adaptive_2012,
	title = {The adaptive threat bias in anxiety: {Amygdala}–dorsomedial prefrontal cortex coupling and aversive amplification},
	volume = {60},
	copyright = {All rights reserved},
	issn = {1053-8119},
	shorttitle = {The adaptive threat bias in anxiety: {Amygdala}–dorsomedial prefrontal cortex coupling and aversive amplification},
	url = {http://www.sciencedirect.com/science/article/pii/S1053811911014017},
	doi = {10.1016/j.neuroimage.2011.11.096},
	journal = {Neuroimage},
	author = {Robinson, Oliver J. and Charney, Danielle R. and Overstreet, Cassie and Vytal, Katherine and Grillon, Christian},
	year = {2012},
	note = {1},
	keywords = {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},
	pages = {523--529},
}

@article{de_wit_reliance_2012,
	title = {Reliance on habits at the expense of goal-directed control following dopamine precursor depletion.},
	volume = {219},
	copyright = {All rights reserved},
	issn = {1432-2072 0033-3158},
	doi = {10.1007/s00213-011-2563-2},
	abstract = {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.},
	language = {eng},
	number = {2},
	journal = {Psychopharmacology},
	author = {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.},
	month = jan,
	year = {2012},
	pmid = {22134475},
	pmcid = {PMC3249188},
	note = {Place: Germany},
	keywords = {*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},
	pages = {621--631},
}

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.

@article{robinson_effect_2011,
	title = {The effect of induced anxiety on cognition: threat of shock enhances aversive processing in healthy individuals},
	volume = {11},
	copyright = {All rights reserved},
	issn = {1530-7026},
	shorttitle = {The effect of induced anxiety on cognition: threat of shock enhances aversive processing in healthy individuals},
	url = {http://dx.doi.org/10.3758/s13415-011-0030-5},
	doi = {10.3758/s13415-011-0030-5},
	journal = {Cognitive, Affective, \& Behavioral Neuroscience},
	author = {Robinson, Oliver and Letkiewicz, Allison and Overstreet, Cassie and Ernst, Monique and Grillon, Christian},
	year = {2011},
	note = {2},
	keywords = {*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},
	pages = {217--27},
}

@article{robinson_brain_2011,
	title = {Brain burdens: {Boost} resilience to tackle mental illness},
	volume = {478},
	copyright = {All rights reserved},
	issn = {0028-0836},
	shorttitle = {Brain burdens: {Boost} resilience to tackle mental illness},
	url = {http://dx.doi.org/10.1038/478459b},
	doi = {10.1038/478459b},
	journal = {Nature},
	author = {Robinson, Oliver J.},
	year = {2011},
	note = {7370},
	keywords = {Female, Humans, Male, Mental Disorders/*economics/*epidemiology, Mental Health/*statistics \& numerical data, Research Support as Topic/*economics},
	pages = {459--459},
}

@article{crockett_converging_2011,
	title = {Converging evidence for central 5-{HT} effects in acute tryptophan depletion},
	copyright = {All rights reserved},
	issn = {1476-5578},
	shorttitle = {Converging evidence for central 5-{HT} effects in acute tryptophan depletion},
	url = {http://dx.doi.org/10.1038/mp.2011.106},
	journal = {Mol Psychiatry},
	author = {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.},
	year = {2011},
	keywords = {Animals, Humans, Serotonin/*metabolism, Tryptophan/*deficiency},
}

@article{robinson_dopamine_2010,
	title = {Dopamine precursor depletion improves punishment prediction during reversal learning in healthy females but not males},
	volume = {211},
	copyright = {All rights reserved},
	issn = {0033-3158},
	shorttitle = {Dopamine precursor depletion improves punishment prediction during reversal learning in healthy females but not males},
	url = {http://dx.doi.org/10.1007/s00213-010-1880-1},
	doi = {10.1007/s00213-010-1880-1},
	journal = {Psychopharmacology},
	author = {Robinson, Oliver J. and Standing, Holly and DeVito, Elise and Cools, Roshan and Sahakian, Barbara},
	year = {2010},
	note = {2},
	keywords = {*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},
	pages = {187--195},
}

@article{robinson_dissociable_2010,
	title = {Dissociable responses to punishment in distinct striatal regions during reversal learning},
	volume = {51},
	copyright = {All rights reserved},
	issn = {1053-8119},
	shorttitle = {Dissociable responses to punishment in distinct striatal regions during reversal learning},
	url = {http://www.sciencedirect.com/science/article/pii/S105381191000323X},
	doi = {10.1016/j.neuroimage.2010.03.036},
	journal = {Neuroimage},
	author = {Robinson, Oliver J. and Frank, Michael J. and Sahakian, Barbara J. and Cools, Roshan},
	year = {2010},
	note = {4},
	keywords = {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},
	pages = {1459--1467},
}

@article{robinson_mood_2010,
	title = {Mood state moderates the role of serotonin in cognitive biases},
	volume = {24},
	copyright = {All rights reserved},
	shorttitle = {Mood state moderates the role of serotonin in cognitive biases},
	url = {http://jop.sagepub.com/content/24/4/573.abstract},
	doi = {10.1177/0269881108100257},
	abstract = {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.},
	journal = {Journal of Psychopharmacology},
	author = {Robinson, OJ and Cools, R. and Crockett, MJ and Sahakian, BJ},
	month = apr,
	year = {2010},
	note = {4},
	keywords = {*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},
	pages = {573--583},
}

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.

@article{robinson_double_2009,
	title = {A {Double} {Dissociation} in the {Roles} of {Serotonin} and {Mood} in {Healthy} {Subjects}},
	volume = {65},
	copyright = {All rights reserved},
	issn = {0006-3223},
	shorttitle = {A {Double} {Dissociation} in the {Roles} of {Serotonin} and {Mood} in {Healthy} {Subjects}},
	url = {http://www.sciencedirect.com/science/article/pii/S0006322308011980},
	doi = {10.1016/j.biopsych.2008.10.001},
	journal = {Biological Psychiatry},
	author = {Robinson, Oliver J. and Sahakian, Barbara J.},
	year = {2009},
	note = {1},
	keywords = {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},
	pages = {89--92},
}

@article{robinson_acute_2009,
	title = {Acute tryptophan depletion evokes negative mood in healthy females who have previously experienced concurrent negative mood and tryptophan depletion.},
	volume = {205},
	copyright = {All rights reserved},
	issn = {1432-2072 0033-3158},
	doi = {10.1007/s00213-009-1533-4},
	abstract = {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.},
	language = {eng},
	number = {2},
	journal = {Psychopharmacology},
	author = {Robinson, Oliver J. and Sahakian, Barbara J.},
	month = aug,
	year = {2009},
	pmid = {19370340},
	pmcid = {PMC2705725},
	note = {Place: Germany},
	keywords = {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},
	pages = {227--235},
}

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.

@article{robinson_recurrence_2008,
	title = {Recurrence in major depressive disorder: a neurocognitive perspective},
	volume = {38},
	copyright = {All rights reserved},
	issn = {1469-8978, 0033-2917},
	shorttitle = {Recurrence in major depressive disorder},
	url = {https://www.cambridge.org/core/journals/psychological-medicine/article/recurrence-in-major-depressive-disorder-a-neurocognitive-perspective/CAA5ACDE5498E1E998227D4EF428CF26},
	doi = {10.1017/S0033291707001249},
	abstract = {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.},
	language = {en},
	number = {3},
	urldate = {2023-04-14},
	journal = {Psychological Medicine},
	author = {Robinson, O. J. and Sahakian, B. J.},
	month = mar,
	year = {2008},
	note = {Publisher: Cambridge University Press},
	pages = {315--318},
}

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.

@article{cools_acute_2007,
	title = {Acute {Tryptophan} {Depletion} in {Healthy} {Volunteers} {Enhances} {Punishment} {Prediction} but {Does} not {Affect} {Reward} {Prediction}},
	volume = {33},
	copyright = {All rights reserved},
	issn = {0893-133X},
	shorttitle = {Acute {Tryptophan} {Depletion} in {Healthy} {Volunteers} {Enhances} {Punishment} {Prediction} but {Does} not {Affect} {Reward} {Prediction}},
	url = {http://dx.doi.org/10.1038/sj.npp.1301598},
	journal = {Neuropsychopharmacology},
	author = {Cools, Roshan and Robinson, Oliver J. and Sahakian, Barbara},
	year = {2007},
	note = {9},
	keywords = {*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},
	pages = {2291--2299},
}

@article{reader_inter-order_2005,
	title = {Inter-{Order} {Interactions} {Between} {Flower}-{Visiting} {Insects}:{Foraging} {Bees} {Avoid} {Flowers} {Previously} {Visited} by {Hoverflies}},
	volume = {18},
	copyright = {All rights reserved},
	issn = {1572-8889},
	shorttitle = {Inter-{Order} {Interactions} {Between} {Flower}-{Visiting} {Insects}},
	url = {https://doi.org/10.1007/s10905-005-9346-8},
	doi = {10.1007/s10905-005-9346-8},
	language = {en},
	number = {1},
	urldate = {2023-04-14},
	journal = {Journal of Insect Behavior},
	author = {Reader, Tom and MacLeod, Ian and Elliott, Philip T. and Robinson, Oliver J. and Manica, Andrea},
	month = jan,
	year = {2005},
	keywords = {Bumble bees, competition, foraging, honey bees, hoverflies, inter-order interactions},
	pages = {51--57},
}

@article{harada-laszlo_series_nodate,
	title = {A series of unfortunate events: {Do} those who catastrophize learn more after negative outcomes?},
	volume = {n/a},
	copyright = {© 2023 The Authors. Mental Health Science published by Wiley Periodicals LLC.},
	issn = {2642-3588},
	shorttitle = {A series of unfortunate events},
	url = {https://onlinelibrary.wiley.com/doi/abs/10.1002/mhs2.49},
	doi = {10.1002/mhs2.49},
	abstract = {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.},
	language = {en},
	number = {n/a},
	urldate = {2024-01-10},
	journal = {Mental Health Science},
	author = {Harada-Laszlo, Mia and Talwar, Anahita and Robinson, Oliver J. and Pike, Alexandra C.},
	note = {\_eprint: https://onlinelibrary.wiley.com/doi/pdf/10.1002/mhs2.49},
	keywords = {catastrophizing, computational modeling, computational psychiatry, online, reinforcement learning, transdiagnostic},
	pages = {e49},
}

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.