Computational psychiatry (Cambridge, Mass.)最新文献

Background: Hazardous drinking is associated with maladaptive alcohol-related decision-making. Existing studies have often focused on how participants learn to exploit familiar cues based on prior reinforcement, but little is known about the mechanisms that drive hazardous drinkers to explore novel alcohol cues when their value is not known.

Methods: We investigated exploration of novel alcohol and non-alcohol cues in hazardous drinkers (N = 27) and control participants (N = 26) during electroencephalography (EEG). A normative computational model with two free parameters was fit to estimate participants' weighting of the future value of exploration and immediate value of exploitation.

Results: Hazardous drinkers demonstrated increased exploration of novel alcohol cues, and conversely, increased probability of exploiting familiar alternatives instead of exploring novel non-alcohol cues. The motivation to explore novel alcohol stimuli in hazardous drinkers was driven by an elevated relative future valuation of uncertain alcohol cues. P3a predicted more exploratory decision policies driven by an enhanced relative future valuation of novel alcohol cues. P3b did not predict choice behavior, but computational parameter estimates suggested that hazardous drinkers with enhanced P3b to alcohol cues were likely to learn to exploit their immediate expected value.

Conclusions: Hazardous drinkers did not display atypical choice behavior, different P3a/P3b amplitudes, or computational estimates to novel non-alcohol cues-diverging from previous studies in addiction showing atypical generalized explore-exploit decisions with non-drug-related cues. These findings reveal that cue-specific neural computations may drive aberrant alcohol-related decision-making in hazardous drinkers-highlighting the importance of drug-relevant cues in studies of decision-making in addiction.

Functional connectivity (FC) and neural excitability may interact to affect symptoms of autism spectrum disorder (ASD). We tested this hypothesis with neural network simulations, and applied it with functional magnetic resonance imaging (fMRI). A hierarchical recurrent neural network embodying predictive processing theory was subjected to a facial emotion recognition task. Neural network simulations examined the effects of FC and neural excitability on changes in neural representations by developmental learning, and eventually on ASD-like performance. Next, by mapping each neural network condition to subject subgroups on the basis of fMRI parameters, the association between ASD-like performance in the simulation and ASD diagnosis in the corresponding subject subgroup was examined. In the neural network simulation, the more homogeneous the neural excitability of the lower-level network, the more ASD-like the performance (reduced generalization and emotion recognition capability). In addition, in homogeneous networks, the higher the FC, the more ASD-like performance, while in heterogeneous networks, the higher the FC, the less ASD-like performance, demonstrating that FC and neural excitability interact. As an underlying mechanism, neural excitability determines the generalization capability of top-down prediction, and FC determines whether the model's information processing will be top-down prediction-dependent or bottom-up sensory-input dependent. In fMRI datasets, ASD was actually more prevalent in subject subgroups corresponding to the network condition showing ASD-like performance. The current study suggests an interaction between FC and neural excitability, and presents a novel framework for computational modeling and biological application of a developmental learning process underlying cognitive alterations in ASD.

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 self-report 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.

Background: Behavioral activation is an evidence-based treatment for depression. Theoretical considerations suggest that treatment response depends on reinforcement learning mechanisms. However, which reinforcement learning mechanisms are engaged by and mediate the therapeutic effect of behavioral activation remains only partially understood, and there are no procedures to measure such mechanisms.

Objective: To perform a pilot study to examine whether reinforcement learning processes measured through tasks or self-report are related to treatment response to behavioral activation.

Method: The pilot study enrolled 13 outpatients (12 completers) with major depressive disorder, from July of 2018 through February of 2019, into a nine-week trial with BA. Psychiatric evaluations, decision-making tests and self-reported reward experience and anticipations were acquired before, during and after the treatment. Task and self-report data were analysed by using reinforcement-learning models. Inferred parameters were related to measures of depression severity through linear mixed effects models.

Results: Treatment effects during different phases of the therapy were captured by specific decision-making processes in the task. During the weeks focusing on the active pursuit of reward, treatment effects were more pronounced amongst those individuals who showed an increase in Pavlovian appetitive influence. During the weeks focusing on the avoidance of punishments, treatment responses were more pronounced in those individuals who showed an increase in Pavlovian avoidance. Self-reported anticipation of reinforcement changed according to formal RL rules. Individual differences in the extent to which learning followed RL rules related to changes in anhedonia.

Conclusions: In this pilot study both task- and self-report-derived measures of reinforcement learning captured individual differences in treatment response to behavioral activation. Appetitive and aversive Pavlovian reflexive processes appeared to be modulated by separate psychotherapeutic interventions, and the modulation strength covaried with response to specific interventions. Self-reported changes in reinforcement expectations are also related to treatment response.

Trial registry name: Set Your Goal: Engaging in GO/No-Go Active Learning, #NCT03538535, http://www.clinicaltrials.gov.

Exposure therapy - exposure to a feared stimulus without harmful consequences - can reduce fear responses in many mental disorders. However, such relief is often partial and temporary: fear can return after the therapy has ended. Conditioning research has identified three mechanisms for the return of fear, viz. change in physical context (renewal), the passage of time (spontaneous recovery), and an encounter with the fear-producing unconditioned stimulus (reinstatement). To understand why fear returns and thereby develop more effective therapies, we develop mathematical learning models based on that of Rescorla and Wagner. According to this model, context cues present during extinction become conditioned inhibitors (i.e. safety signals) which prevent total erasure of the threat association. Adding various mechanisms to the model allows it to explain different facets of the return of fear. Among these mechanisms is decay of inhibitory associations, which provides a novel explanation for spontaneous recovery. To make the benefits of exposure robust and permanent, one must minimize the degree to which the extinction context becomes inhibitory in order to maximize unlearning. We simulate several experimental paradigms that reduce the return of fear and explain them according to this principle.

Although evidence suggests that antidepressants are effective at treating depression, the mechanisms behind antidepressant action remain unclear, especially at the cognitive/computational level. In recent years, reinforcement learning (RL) models have increasingly been used to characterise the roles of neurotransmitters and to probe the computations that might be altered in psychiatric disorders like depression. Hence, RL models might present an opportunity for us to better understand the computational mechanisms underlying antidepressant effects. Moreover, RL models may also help us shed light on how these computations may be implemented in the brain (e.g., in midbrain, striatal, and prefrontal regions) and how these neural mechanisms may be altered in depression and remediated by antidepressant treatments. In this paper, we evaluate the ability of RL models to help us understand the processes underlying antidepressant action. To do this, we review the preclinical literature on the roles of dopamine and serotonin in RL, draw links between these findings and clinical work investigating computations altered in depression, and appraise the evidence linking modification of RL processes to antidepressant function. Overall, while there is no shortage of promising ideas about the computational mechanisms underlying antidepressant effects, there is insufficient evidence directly implicating these mechanisms in the response of depressed patients to antidepressant treatment. Consequently, future studies should investigate these mechanisms in samples of depressed patients and assess whether modifications in RL processes mediate the clinical effect of antidepressant treatments.

Gambling disorder is a behavioral addiction that negatively impacts personal finances, work, relationships and mental health. In this pre-registered study (https://osf.io/5ptz9/) we investigated the impact of real-life gambling environments on two computational markers of addiction, temporal discounting and model-based reinforcement learning. Gambling disorder is associated with increased temporal discounting and reduced model-based learning. Regular gamblers (n = 30, DSM-5 score range 3-9) performed both tasks in a neutral (café) and a gambling-related environment (slot-machine venue) in counterbalanced order. Data were modeled using drift diffusion models for temporal discounting and reinforcement learning via hierarchical Bayesian estimation. Replicating previous findings, gamblers discounted rewards more steeply in the gambling-related context. This effect was positively correlated with gambling related cognitive distortions (pre-registered analysis). In contrast to our pre-registered hypothesis, model-based reinforcement learning was improved in the gambling context. Here we show that temporal discounting and model-based reinforcement learning are modulated in opposite ways by real-life gambling cue exposure. Results challenge aspects of habit theories of addiction, and reveal that laboratory-based computational markers of psychopathology are under substantial contextual control.

Computational modelling is a promising approach to parse dysfunctional cognitive processes in substance use disorders (SUDs), but it is unclear how much these processes change during the recovery period. We assessed 1-year follow-up data on a sample of treatment-seeking individuals with one or more SUDs (alcohol, cannabis, sedatives, stimulants, hallucinogens, and/or opioids; N = 83) that were previously assessed at baseline within a prior computational modelling study. Relative to healthy controls (HCs; N = 48), these participants were found at baseline to show altered learning rates and less precise action selection while completing an explore-exploit decision-making task. Here we replicated these analyses when these individuals returned and re-performed the task 1 year later to assess the stability of baseline differences. We also examined whether baseline modelling measures could predict symptoms at follow-up. Bayesian and frequentist analyses indicated that: (a) group differences in learning rates were stable over time (posterior probability = 1); and (b) intra-class correlations (ICCs) between model parameters at baseline and follow-up were significant and ranged from small to moderate (.25 ≤ ICCs ≤ .54). Exploratory analyses also suggested that learning rates and/or information-seeking values at baseline were associated with substance use severity at 1-year follow-up in stimulant and opioid users (.36 ≤ rs ≤ .43). These findings suggest that learning dysfunctions are moderately stable during recovery and could correspond to trait-like vulnerability factors. In addition, computational measures at baseline had some predictive value for changes in substance use severity over time and could be clinically informative.

Computational models of decision making have identified a relationship between obsessive-compulsive symptoms (OCS), both in the general population and in patients, and impairments in perceptual evidence accumulation. Some studies have interpreted these deficits to reflect global disease traits which give rise to clusters of OCS. Such assumptions are not uncommon, even if implicit, in computational psychiatry more broadly. However, it is well established that state- and trait-symptom scores are often correlated (e.g., state and trait anxiety), and the extent to which perceptual deficits are actually explained by state-based symptoms is unclear. State-based symptoms may give rise to information processing differences in a number of ways, including the mechanistically less interesting possibility of tying up working memory and attentional resources for off-task processing. In a general population sample (N = 150), we investigated the extent to which previously identified impairments in perceptual evidence accumulation were related to trait vs stated-based OCS. In addition, we tested whether differences in working memory capacity moderated state-based impairments, such that impairments were worse in individuals with lower working memory capacity. We replicated previous work demonstrating a negative relationship between the rate of evidence accumulation and trait-based OCS when state-based symptoms were unaccounted for. When state-based effects were included in the model, they captured a significant degree of impairment while trait-based effects were attenuated, although they did not disappear completely. We did not find evidence that working memory capacity moderated the state-based effects. Our work suggests that investigating the relationship between information processing and state-based symptoms may be important more generally in computational psychiatry beyond this specific context.