@article{feng_cross-cultural_2025,
	title = {Cross-{Cultural} {Differences} on {Affective}, {Cognitive}, and {Psychiatric} {Measures}: {Evidence} {From} a {British}-{Chinese} {Comparison}},
	volume = {3},
	copyright = {© 2025 The Author(s). Mental Health Science published by Wiley Periodicals LLC.},
	issn = {2642-3588},
	shorttitle = {Cross-{Cultural} {Differences} on {Affective}, {Cognitive}, and {Psychiatric} {Measures}},
	url = {https://onlinelibrary.wiley.com/doi/abs/10.1002/mhs2.70020},
	doi = {10.1002/mhs2.70020},
	abstract = {Individuals worldwide share basic affective and cognitive abilities, and receive mental health diagnoses using similar scales. However, these measures have been predominantly developed and validated in Western contexts. Here, we compared British (N = 187; age 19–73 years) and Chinese participants (N = 194; age 19–60 years) on behavioral tasks of facial emotion recognition and sustained attention, evaluating affect and cognition, as well as mental health measures of anxiety, depression, obsessive-compulsive disorder, and impulsivity. Comparing British and Chinese populations is particularly important as they represent distinct cultural traditions in emotional expression, cognitive processing, and mental health conceptualization. We found that British participants were significantly better at recognizing emotions, especially negative ones; while Chinese participants showed higher obsessive-compulsive symptoms, driven primarily by the number-meaning item, the tendency to assign significance to numerical information. The groups showed negligible differences in sustained attention and other mental health measures. This study provides novel evidence that culture has a greater influence on affective abilities than cognitive ones, and highlights concerns about cultural biases in established mental health scales. However, these findings may not generalize beyond British and Chinese populations, which calls for broader cross-cultural research.},
	language = {en},
	number = {2},
	urldate = {2025-06-06},
	journal = {Mental Health Science},
	author = {Feng, Boyin and Sheehan, Rosanna and Utama, Priyanka and Wang, Yixuan and Bao, Jiamin and Robinson, Oliver J. and Zang, Yinyin and Carlisi, Christina O.},
	year = {2025},
	note = {\_eprint: https://onlinelibrary.wiley.com/doi/pdf/10.1002/mhs2.70020},
	keywords = {context effects, cultural differences, emotion recognition, mental health, psychopathology, sustained attention},
	pages = {e70020},
}

Individuals worldwide share basic affective and cognitive abilities, and receive mental health diagnoses using similar scales. However, these measures have been predominantly developed and validated in Western contexts. Here, we compared British (N = 187; age 19–73 years) and Chinese participants (N = 194; age 19–60 years) on behavioral tasks of facial emotion recognition and sustained attention, evaluating affect and cognition, as well as mental health measures of anxiety, depression, obsessive-compulsive disorder, and impulsivity. Comparing British and Chinese populations is particularly important as they represent distinct cultural traditions in emotional expression, cognitive processing, and mental health conceptualization. We found that British participants were significantly better at recognizing emotions, especially negative ones; while Chinese participants showed higher obsessive-compulsive symptoms, driven primarily by the number-meaning item, the tendency to assign significance to numerical information. The groups showed negligible differences in sustained attention and other mental health measures. This study provides novel evidence that culture has a greater influence on affective abilities than cognitive ones, and highlights concerns about cultural biases in established mental health scales. However, these findings may not generalize beyond British and Chinese populations, which calls for broader cross-cultural research.

@article{sporrer_induced_2024,
	title = {Induced worry increases risk aversion in patients with generalized anxiety},
	volume = {474},
	issn = {0166-4328},
	url = {https://www.sciencedirect.com/science/article/pii/S0166432824003486},
	doi = {10.1016/j.bbr.2024.115192},
	abstract = {Generalized anxiety disorder is characterized by disruptions in decision-making, including an enhanced aversion to uncertain outcomes (i.e., risk aversion), which is not specific to negative outcomes (i.e., no loss aversion). It is unknown if this uncertainty bias is a trait-like causal factor contributing to anxiety symptoms, or a state-like feature triggered by anxiety symptoms such as worry chains. Here, in-patients with Major Depression Disorder (MDD), with (N = 16) or without (N = 24) Generalized anxiety (GA) symptoms, and healthy controls (N = 23), completed an economic decision-making task before and after worry induction. They were asked to choose between a certain monetary payoff, and an uncertain gamble, allowing for estimation of risk and loss aversion through a computational prospect-theoretic model. There were no significant differences in risk and loss aversion between any of the three groups at baseline. After worry induction, patients with GA symptoms, compared to those without, showed increased risk aversion. This increase was modulated by the severity of anxiety symptoms. These findings suggest that decision-making disruptions in anxiety disorder may be driven by anxiety symptoms such as worry, rather than causing them. This could shape etiological models, motivate standardization of emotional state in research on decision-making in anxiety disorders, support treatment strategies primarily aimed at worry management, and could guide novel interventions focusing on uncertainty exposure across aversive and appetitive domains.},
	urldate = {2025-06-06},
	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},
	keywords = {Anxiety, Decision making, Depression, Loss aversion, Risk aversion, Worry},
	pages = {115192},
}

Generalized anxiety disorder is characterized by disruptions in decision-making, including an enhanced aversion to uncertain outcomes (i.e., risk aversion), which is not specific to negative outcomes (i.e., no loss aversion). It is unknown if this uncertainty bias is a trait-like causal factor contributing to anxiety symptoms, or a state-like feature triggered by anxiety symptoms such as worry chains. Here, in-patients with Major Depression Disorder (MDD), with (N = 16) or without (N = 24) Generalized anxiety (GA) symptoms, and healthy controls (N = 23), completed an economic decision-making task before and after worry induction. They were asked to choose between a certain monetary payoff, and an uncertain gamble, allowing for estimation of risk and loss aversion through a computational prospect-theoretic model. There were no significant differences in risk and loss aversion between any of the three groups at baseline. After worry induction, patients with GA symptoms, compared to those without, showed increased risk aversion. This increase was modulated by the severity of anxiety symptoms. These findings suggest that decision-making disruptions in anxiety disorder may be driven by anxiety symptoms such as worry, rather than causing them. This could shape etiological models, motivate standardization of emotional state in research on decision-making in anxiety disorders, support treatment strategies primarily aimed at worry management, and could guide novel interventions focusing on uncertainty exposure across aversive and appetitive domains.

@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{harada-laszlo_series_2023,
	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.},
	year = {2023},
	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.

@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{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{charpentier_how_2021,
	title = {How representative are neuroimaging samples? {Large}-scale evidence for trait anxiety differences between {fMRI} and behaviour-only research participants},
	volume = {16},
	issn = {1749-5024},
	shorttitle = {How representative are neuroimaging samples?},
	doi = {10.1093/scan/nsab057},
	abstract = {Over the past three decades, functional magnetic resonance imaging (fMRI) has become crucial to study how cognitive processes are implemented in the human brain. However, the question of whether participants recruited into fMRI studies differ from participants recruited into other study contexts has received little to no attention. This is particularly pertinent when effects fail to generalize across study contexts: for example, a behavioural effect discovered in a non-imaging context not replicating in a neuroimaging environment. Here, we tested the hypothesis, motivated by preliminary findings (N = 272), that fMRI participants differ from behaviour-only participants on one fundamental individual difference variable: trait anxiety. Analysing trait anxiety scores and possible confounding variables from healthy volunteers across multiple institutions (N = 3317), we found robust support for lower trait anxiety in fMRI study participants, consistent with a sampling or self-selection bias. The bias was larger in studies that relied on phone screening (compared with full in-person psychiatric screening), recruited at least partly from convenience samples (compared with community samples), and in pharmacology studies. Our findings highlight the need for surveying trait anxiety at recruitment and for appropriate screening procedures or sampling strategies to mitigate this bias.},
	language = {eng},
	number = {10},
	journal = {Social Cognitive and Affective Neuroscience},
	author = {Charpentier, Caroline J. and Faulkner, Paul and Pool, Eva R. and Ly, Verena and Tollenaar, Marieke S. and Kluen, Lisa M. and Fransen, Aniek and Yamamori, Yumeya and Lally, Níall and Mkrtchian, Anahit and Valton, Vincent and Huys, Quentin J. M. and Sarigiannidis, Ioannis and Morrow, Kelly A. and Krenz, Valentina and Kalbe, Felix and Cremer, Anna and Zerbes, Gundula and Kausche, Franziska M. and Wanke, Nadine and Giarrizzo, Alessio and Pulcu, Erdem and Murphy, Susannah and Kaltenboeck, Alexander and Browning, Michael and Paul, Lynn K. and Cools, Roshan and Roelofs, Karin and Pessoa, Luiz and Harmer, Catherine J. and Chase, Henry W. and Grillon, Christian and Schwabe, Lars and Roiser, Jonathan P. and Robinson, Oliver J. and O'Doherty, John P.},
	month = sep,
	year = {2021},
	pmid = {33950220},
	pmcid = {PMC8483285},
	keywords = {Anxiety, Anxiety Disorders, Attention, Humans, Magnetic Resonance Imaging, Neuroimaging, behaviour, neuroimaging, sampling bias, trait anxiety},
	pages = {1057--1070},
}

Over the past three decades, functional magnetic resonance imaging (fMRI) has become crucial to study how cognitive processes are implemented in the human brain. However, the question of whether participants recruited into fMRI studies differ from participants recruited into other study contexts has received little to no attention. This is particularly pertinent when effects fail to generalize across study contexts: for example, a behavioural effect discovered in a non-imaging context not replicating in a neuroimaging environment. Here, we tested the hypothesis, motivated by preliminary findings (N = 272), that fMRI participants differ from behaviour-only participants on one fundamental individual difference variable: trait anxiety. Analysing trait anxiety scores and possible confounding variables from healthy volunteers across multiple institutions (N = 3317), we found robust support for lower trait anxiety in fMRI study participants, consistent with a sampling or self-selection bias. The bias was larger in studies that relied on phone screening (compared with full in-person psychiatric screening), recruited at least partly from convenience samples (compared with community samples), and in pharmacology studies. Our findings highlight the need for surveying trait anxiety at recruitment and for appropriate screening procedures or sampling strategies to mitigate this bias.

@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{aylward_translating_2020,
	title = {Translating a rodent measure of negative bias into humans: the impact of induced anxiety and unmedicated mood and anxiety disorders},
	volume = {50},
	issn = {1469-8978},
	shorttitle = {Translating a rodent measure of negative bias into humans},
	doi = {10.1017/S0033291718004117},
	abstract = {BACKGROUND: Mood and anxiety disorders are ubiquitous but current treatment options are ineffective for many sufferers. Moreover, a number of promising pre-clinical interventions have failed to translate into clinical efficacy in humans. Improved treatments are unlikely without better animal-human translational pipelines. Here, we translate a rodent measure of negative affective bias into humans, exploring its relationship with (1) pathological mood and anxiety symptoms and (2) transient induced anxiety.
METHODS: Adult participants (age = 29 ± 11) who met criteria for mood or anxiety disorder symptomatology according to a face-to-face neuropsychiatric interview were included in the symptomatic group. Study 1 included N = 77 (47 = asymptomatic [female = 21]; 30 = symptomatic [female = 25]), study 2 included N = 47 asymptomatic participants (25 = female). Outcome measures were choice ratios, reaction times and parameters recovered from a computational model of reaction time - the drift diffusion model (DDM) - from a two-alternative-forced-choice task in which ambiguous and unambiguous auditory stimuli were paired with high and low rewards.
RESULTS: Both groups showed over 93\% accuracy on unambiguous tones indicating intact discrimination, but symptomatic individuals demonstrated increased negative affective bias on ambiguous tones [proportion high reward = 0.42 (s.d. = 0.14)] relative to asymptomatic individuals [0.53 (s.d. = 0.17)] as well as a significantly reduced DDM drift rate. No significant effects were observed for the within-subjects anxiety-induction.
CONCLUSIONS: Humans with pathological anxiety symptoms directly mimic rodents undergoing anxiogenic manipulation. The lack of sensitivity to transient anxiety suggests the paradigm might be more sensitive to clinically relevant symptoms. Our results establish a direct translational pipeline (and candidate therapeutics screen) from negative affective bias in rodents to pathological mood and anxiety symptoms in humans.},
	language = {eng},
	number = {2},
	journal = {Psychological Medicine},
	author = {Aylward, Jessica and Hales, Claire and Robinson, Emma and Robinson, Oliver J.},
	month = jan,
	year = {2020},
	pmid = {30683161},
	pmcid = {PMC7083556},
	keywords = {Adolescent, Adult, Affect, Affective bias, Animals, Anxiety Disorders, Bias, Disease Models, Animal, Female, Humans, Male, Mood Disorders, Reaction Time, Reward, Rodentia, Translational Research, Biomedical, Young Adult, anxiety, back-translation, computational psychiatry, depression, drift diffusion model},
	pages = {237--246},
}

BACKGROUND: Mood and anxiety disorders are ubiquitous but current treatment options are ineffective for many sufferers. Moreover, a number of promising pre-clinical interventions have failed to translate into clinical efficacy in humans. Improved treatments are unlikely without better animal-human translational pipelines. Here, we translate a rodent measure of negative affective bias into humans, exploring its relationship with (1) pathological mood and anxiety symptoms and (2) transient induced anxiety. METHODS: Adult participants (age = 29 ± 11) who met criteria for mood or anxiety disorder symptomatology according to a face-to-face neuropsychiatric interview were included in the symptomatic group. Study 1 included N = 77 (47 = asymptomatic [female = 21]; 30 = symptomatic [female = 25]), study 2 included N = 47 asymptomatic participants (25 = female). Outcome measures were choice ratios, reaction times and parameters recovered from a computational model of reaction time - the drift diffusion model (DDM) - from a two-alternative-forced-choice task in which ambiguous and unambiguous auditory stimuli were paired with high and low rewards. RESULTS: Both groups showed over 93% accuracy on unambiguous tones indicating intact discrimination, but symptomatic individuals demonstrated increased negative affective bias on ambiguous tones [proportion high reward = 0.42 (s.d. = 0.14)] relative to asymptomatic individuals [0.53 (s.d. = 0.17)] as well as a significantly reduced DDM drift rate. No significant effects were observed for the within-subjects anxiety-induction. CONCLUSIONS: Humans with pathological anxiety symptoms directly mimic rodents undergoing anxiogenic manipulation. The lack of sensitivity to transient anxiety suggests the paradigm might be more sensitive to clinically relevant symptoms. Our results establish a direct translational pipeline (and candidate therapeutics screen) from negative affective bias in rodents to pathological mood and anxiety symptoms in humans.

@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{aylward_altered_2019,
	title = {Altered learning under uncertainty in unmedicated mood and anxiety disorders},
	volume = {3},
	issn = {2397-3374},
	doi = {10.1038/s41562-019-0628-0},
	abstract = {Anxiety is characterized by altered responses under uncertain conditions, but the precise mechanism by which uncertainty changes the behaviour of anxious individuals is unclear. Here we probe the computational basis of learning under uncertainty in healthy individuals and individuals suffering from a mix of mood and anxiety disorders. Participants were asked to choose between four competing slot machines with fluctuating reward and punishment outcomes during safety and stress. We predicted that anxious individuals under stress would learn faster about punishments and exhibit choices that were more affected by those punishments, thus formalizing our predictions as parameters in reinforcement learning accounts of behaviour. Overall, the data suggest that anxious individuals are quicker to update their behaviour in response to negative outcomes (increased punishment learning rates). When treating anxiety, it may therefore be more fruitful to encourage anxious individuals to integrate information over longer horizons when bad things happen, rather than try to blunt their responses to negative outcomes.},
	language = {eng},
	number = {10},
	journal = {Nature Human Behaviour},
	author = {Aylward, Jessica and Valton, Vincent and Ahn, Woo-Young and Bond, Rebecca L. and Dayan, Peter and Roiser, Jonathan P. and Robinson, Oliver J.},
	month = oct,
	year = {2019},
	pmid = {31209369},
	pmcid = {PMC6790140},
	keywords = {Adolescent, Adult, Anxiety Disorders, Case-Control Studies, Depressive Disorder, Major, Female, Humans, Learning, Male, Mood Disorders, Panic Disorder, Punishment, Reward, Stress, Psychological, Uncertainty, Young Adult},
	pages = {1116--1123},
}

Anxiety is characterized by altered responses under uncertain conditions, but the precise mechanism by which uncertainty changes the behaviour of anxious individuals is unclear. Here we probe the computational basis of learning under uncertainty in healthy individuals and individuals suffering from a mix of mood and anxiety disorders. Participants were asked to choose between four competing slot machines with fluctuating reward and punishment outcomes during safety and stress. We predicted that anxious individuals under stress would learn faster about punishments and exhibit choices that were more affected by those punishments, thus formalizing our predictions as parameters in reinforcement learning accounts of behaviour. Overall, the data suggest that anxious individuals are quicker to update their behaviour in response to negative outcomes (increased punishment learning rates). When treating anxiety, it may therefore be more fruitful to encourage anxious individuals to integrate information over longer horizons when bad things happen, rather than try to blunt their responses to negative outcomes.

@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{charpentier_enhanced_2017,
	title = {Enhanced {Risk} {Aversion}, {But} {Not} {Loss} {Aversion}, in {Unmedicated} {Pathological} {Anxiety}},
	volume = {81},
	issn = {1873-2402},
	doi = {10.1016/j.biopsych.2016.12.010},
	abstract = {BACKGROUND: Anxiety disorders are associated with disruptions in both emotional processing and decision making. As a result, anxious individuals often make decisions that favor harm avoidance. However, this bias could be driven by enhanced aversion to uncertainty about the decision outcome (e.g., risk) or aversion to negative outcomes (e.g., loss). Distinguishing between these possibilities may provide a better cognitive understanding of anxiety disorders and hence inform treatment strategies.
METHODS: To address this question, unmedicated individuals with pathological anxiety (n = 25) and matched healthy control subjects (n = 23) completed a gambling task featuring a decision between a gamble and a safe (certain) option on every trial. Choices on one type of gamble-involving weighing a potential win against a potential loss (mixed)-could be driven by both loss and risk aversion, whereas choices on the other type-featuring only wins (gain only)-were exclusively driven by risk aversion. By fitting a computational prospect theory model to participants' choices, we were able to reliably estimate risk and loss aversion and their respective contribution to gambling decisions.
RESULTS: Relative to healthy control subjects, pathologically anxious participants exhibited enhanced risk aversion but equivalent levels of loss aversion.
CONCLUSIONS: Individuals with pathological anxiety demonstrate clear avoidance biases in their decision making. These findings suggest that this may be driven by a reduced propensity to take risks rather than a stronger aversion to losses. This important clarification suggests that psychological interventions for anxiety should focus on reducing risk sensitivity rather than reducing sensitivity to negative outcomes per se.},
	language = {eng},
	number = {12},
	journal = {Biological Psychiatry},
	author = {Charpentier, Caroline J. and Aylward, Jessica and Roiser, Jonathan P. and Robinson, Oliver J.},
	month = jun,
	year = {2017},
	pmid = {28126210},
	pmcid = {PMC5466268},
	keywords = {Adult, Anxiety, Avoidance Learning, Case-Control Studies, Decision Making, Decision making, Emotion, Female, Gambling, Humans, Loss aversion, Male, Memory, Risk aversion, Risk-Taking, Young Adult},
	pages = {1014--1022},
}

BACKGROUND: Anxiety disorders are associated with disruptions in both emotional processing and decision making. As a result, anxious individuals often make decisions that favor harm avoidance. However, this bias could be driven by enhanced aversion to uncertainty about the decision outcome (e.g., risk) or aversion to negative outcomes (e.g., loss). Distinguishing between these possibilities may provide a better cognitive understanding of anxiety disorders and hence inform treatment strategies. METHODS: To address this question, unmedicated individuals with pathological anxiety (n = 25) and matched healthy control subjects (n = 23) completed a gambling task featuring a decision between a gamble and a safe (certain) option on every trial. Choices on one type of gamble-involving weighing a potential win against a potential loss (mixed)-could be driven by both loss and risk aversion, whereas choices on the other type-featuring only wins (gain only)-were exclusively driven by risk aversion. By fitting a computational prospect theory model to participants' choices, we were able to reliably estimate risk and loss aversion and their respective contribution to gambling decisions. RESULTS: Relative to healthy control subjects, pathologically anxious participants exhibited enhanced risk aversion but equivalent levels of loss aversion. CONCLUSIONS: Individuals with pathological anxiety demonstrate clear avoidance biases in their decision making. These findings suggest that this may be driven by a reduced propensity to take risks rather than a stronger aversion to losses. This important clarification suggests that psychological interventions for anxiety should focus on reducing risk sensitivity rather than reducing sensitivity to negative outcomes per se.

@article{aylward_impact_2017,
	title = {The impact of induced anxiety on affective response inhibition},
	volume = {4},
	issn = {2054-5703},
	doi = {10.1098/rsos.170084},
	abstract = {Studying the effects of experimentally induced anxiety in healthy volunteers may increase our understanding of the mechanisms underpinning anxiety disorders. Experimentally induced stress (via threat of unpredictable shock) improves accuracy at withholding a response on the sustained attention to response task (SART), and in separate studies improves accuracy to classify fearful faces, creating an affective bias. Integrating these findings, participants at two public science engagement events (n = 46, n = 55) were recruited to explore the effects of experimentally induced stress on an affective version of the SART. We hypothesized that we would see an improved accuracy at withholding a response to affectively congruent stimuli (i.e. increased accuracy at withholding a response to fearful 'no-go' distractors) under threat of shock. Induced anxiety slowed reaction time, and at the second event quicker responses were made to fearful stimuli. However, we did not observe improved inhibition overall during induced anxiety, and there was no evidence to suggest an interaction between induced anxiety and stimulus valence on response accuracy. Indeed Bayesian analysis provided decisive evidence against this hypothesis. We suggest that the presence of emotional stimuli might make the safe condition more anxiogenic, reducing the differential between conditions and knocking out any threat-potentiated improvement.},
	language = {eng},
	number = {6},
	journal = {Royal Society Open Science},
	author = {Aylward, Jessica and Valton, Vincent and Goer, Franziska and Mkrtchian, Anahit and Lally, Níall and Peters, Sarah and Limbachya, Tarun and Robinson, Oliver J.},
	month = jun,
	year = {2017},
	pmid = {28680667},
	pmcid = {PMC5493909},
	keywords = {affective response inhibition, mood and anxiety disorders, stress, threat of shock},
	pages = {170084},
}

Studying the effects of experimentally induced anxiety in healthy volunteers may increase our understanding of the mechanisms underpinning anxiety disorders. Experimentally induced stress (via threat of unpredictable shock) improves accuracy at withholding a response on the sustained attention to response task (SART), and in separate studies improves accuracy to classify fearful faces, creating an affective bias. Integrating these findings, participants at two public science engagement events (n = 46, n = 55) were recruited to explore the effects of experimentally induced stress on an affective version of the SART. We hypothesized that we would see an improved accuracy at withholding a response to affectively congruent stimuli (i.e. increased accuracy at withholding a response to fearful 'no-go' distractors) under threat of shock. Induced anxiety slowed reaction time, and at the second event quicker responses were made to fearful stimuli. However, we did not observe improved inhibition overall during induced anxiety, and there was no evidence to suggest an interaction between induced anxiety and stimulus valence on response accuracy. Indeed Bayesian analysis provided decisive evidence against this hypothesis. We suggest that the presence of emotional stimuli might make the safe condition more anxiogenic, reducing the differential between conditions and knocking out any threat-potentiated improvement.

@article{aylward_towards_2017,
	title = {Towards an emotional 'stress test': a reliable, non-subjective cognitive measure of anxious responding},
	volume = {7},
	issn = {2045-2322},
	shorttitle = {Towards an emotional 'stress test'},
	doi = {10.1038/srep40094},
	abstract = {Response to stress or external threats is a key factor in mood and anxiety disorder aetiology. Current measures of anxious responding to threats are limited because they largely rely on retrospective self-report. Objectively quantifying individual differences in threat response would be a valuable step towards improving our understanding of anxiety disorder vulnerability. Our goal is to therefore develop a reliable, objective, within-subject 'stress-test' of anxious responding. To this end, we examined threat-potentiated performance on an inhibitory control task from baseline to 2-4 weeks (n = 50) and again after 5-9 months (n = 22). We also describe single session data for a larger sample (n = 157) to provide better population-level estimates of task performance variance. Replicating previous findings, threat of shock improved distractor accuracy and slowed target reaction time on our task. Critically, both within-subject self-report measures of anxiety (ICC = 0.66) and threat-potentiated task performance (ICC = 0.58) showed clinically useful test-retest reliability. Threat-potentiated task performance may therefore hold promise as a non-subjective measure of individual anxious responding.},
	language = {eng},
	journal = {Scientific Reports},
	author = {Aylward, Jessica and Robinson, Oliver J.},
	month = jan,
	year = {2017},
	pmid = {28071668},
	pmcid = {PMC5223119},
	keywords = {Adolescent, Adult, Anxiety, Diagnostic Tests, Routine, Female, Healthy Volunteers, Humans, Male, Retrospective Studies, Stress, Psychological, Young Adult},
	pages = {40094},
}

Response to stress or external threats is a key factor in mood and anxiety disorder aetiology. Current measures of anxious responding to threats are limited because they largely rely on retrospective self-report. Objectively quantifying individual differences in threat response would be a valuable step towards improving our understanding of anxiety disorder vulnerability. Our goal is to therefore develop a reliable, objective, within-subject 'stress-test' of anxious responding. To this end, we examined threat-potentiated performance on an inhibitory control task from baseline to 2-4 weeks (n = 50) and again after 5-9 months (n = 22). We also describe single session data for a larger sample (n = 157) to provide better population-level estimates of task performance variance. Replicating previous findings, threat of shock improved distractor accuracy and slowed target reaction time on our task. Critically, both within-subject self-report measures of anxiety (ICC = 0.66) and threat-potentiated task performance (ICC = 0.58) showed clinically useful test-retest reliability. Threat-potentiated task performance may therefore hold promise as a non-subjective measure of individual anxious responding.

@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{charpentier_anxiety_2016,
	title = {Anxiety promotes memory for mood-congruent faces but does not alter loss aversion},
	volume = {6},
	issn = {2045-2322},
	doi = {10.1038/srep24746},
	abstract = {Pathological anxiety is associated with disrupted cognitive processing, including working memory and decision-making. In healthy individuals, experimentally-induced state anxiety or high trait anxiety often results in the deployment of adaptive harm-avoidant behaviours. However, how these processes affect cognition is largely unknown. To investigate this question, we implemented a translational within-subjects anxiety induction, threat of shock, in healthy participants reporting a wide range of trait anxiety scores. Participants completed a gambling task, embedded within an emotional working memory task, with some blocks under unpredictable threat and others safe from shock. Relative to the safe condition, threat of shock improved recall of threat-congruent (fearful) face location, especially in highly trait anxious participants. This suggests that threat boosts working memory for mood-congruent stimuli in vulnerable individuals, mirroring memory biases in clinical anxiety. By contrast, Bayesian analysis indicated that gambling decisions were better explained by models that did not include threat or treat anxiety, suggesting that: (i) higher-level executive functions are robust to these anxiety manipulations; and (ii) decreased risk-taking may be specific to pathological anxiety. These findings provide insight into the complex interactions between trait anxiety, acute state anxiety and cognition, and may help understand the cognitive mechanisms underlying adaptive anxiety.},
	language = {eng},
	journal = {Scientific Reports},
	author = {Charpentier, Caroline J. and Hindocha, Chandni and Roiser, Jonathan P. and Robinson, Oliver J.},
	month = apr,
	year = {2016},
	pmid = {27098489},
	pmcid = {PMC4838853},
	keywords = {Adult, Affect, Anxiety, Anxiety Disorders, Cognition, Decision Making, Emotions, Facial Expression, Female, Gambling, Humans, Male, Memory, Memory, Short-Term, Quantitative Trait, Heritable, Reaction Time, Stress, Psychological, Surveys and Questionnaires, Young Adult},
	pages = {24746},
}

Pathological anxiety is associated with disrupted cognitive processing, including working memory and decision-making. In healthy individuals, experimentally-induced state anxiety or high trait anxiety often results in the deployment of adaptive harm-avoidant behaviours. However, how these processes affect cognition is largely unknown. To investigate this question, we implemented a translational within-subjects anxiety induction, threat of shock, in healthy participants reporting a wide range of trait anxiety scores. Participants completed a gambling task, embedded within an emotional working memory task, with some blocks under unpredictable threat and others safe from shock. Relative to the safe condition, threat of shock improved recall of threat-congruent (fearful) face location, especially in highly trait anxious participants. This suggests that threat boosts working memory for mood-congruent stimuli in vulnerable individuals, mirroring memory biases in clinical anxiety. By contrast, Bayesian analysis indicated that gambling decisions were better explained by models that did not include threat or treat anxiety, suggesting that: (i) higher-level executive functions are robust to these anxiety manipulations; and (ii) decreased risk-taking may be specific to pathological anxiety. These findings provide insight into the complex interactions between trait anxiety, acute state anxiety and cognition, and may help understand the cognitive mechanisms underlying adaptive anxiety.

@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{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{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{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{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},
}