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Gillan, C. M.

Publications and source records attributed to Gillan, C. M..

5 recordsLinked to original sources

Neural dynamics of covert habit activation and control in humans

The neuroscience of habits in humans presumes a competition between two systems: stimulus-response and goal-directed. But lacking strong causal manipulations for inducing habits in humans, researchers have struggled to understand the brain mechanisms supporting the development of stimulus-response associations over time and their interaction with goal-directed processes. To address this, we conducted a preregistered electroencephalography (EEG) study with 14 days of stimulus-response training and used tight temporal controls to isolate the functioning of each system. In line with our preregistered hypothesis, we found that the lateralized readiness potential (LRP) tracked covert activation of habitual responses, detectable on trials where inappropriate habits are overcome and behavior is classed as goal-directed. In exploratory analyses, the strength of this covert habitual activation was associated with the degree of inappropriate habit expression on separate trials where response preparation time was limited. Further, exploratory analyses suggested that frontal midline theta (FM{theta}) power was selectively elevated when extensively trained habits needed to be overridden, and that this elevation scaled with individual differences in habit expression. These data provide evidence consistent with a dual systems account in which habit expression reflects competition between distinct neural subsystems and offer a new window into the formation and override of habits.

neuroscience↗

Model-based learning deficits in compulsivity are linked to faulty representations of task structure

Individuals with higher levels of compulsivity exhibit poorer performance on tasks that require model-based planning but the underlying causes have yet to be established. Here, we sought to determine whether these deficits stem from impoverished action-outcome relational knowledge (i.e. issues building an accurate model of the world) and/or an inability to translate models into action. 192 participants performed a two-step reinforcement learning task with concurrent EEG recordings. We found that representations of task-relevant action-outcome associations reflected in reaction time and parietal-occipital alpha-band power were stronger in individuals whose decisions were more model-based, and critically, were weaker in those high in compulsivity. At the time of choice, mid-frontal theta power, a general marker of cognitive control, was also negatively associated with compulsivity, but not model-based planning. These data suggest that model-based planning deficits in compulsive individuals may arise from failures in building an accurate model of the world.

neuroscience↗

Null results from a dimensional study of error-related negativity (ERN) and self-reported psychiatric symptoms

Alterations in error processing are implicated in a range of DSM-defined psychiatric disorders. For instance, obsessive-compulsive disorder (OCD) and generalised anxiety disorder show enhanced electrophysiological responses to errors - i.e. error-related negativity (ERN) - while others like schizophrenia have an attenuated ERN. However, as diagnostic categories in psychiatry are heterogeneous and also highly intercorrelated, the precise mapping of ERN enhancements and impairments is unclear. To address this, we recorded electroencephalograms (EEG) from 196 participants who performed the Flanker task and collected scores on 9 questionnaires assessing psychiatric symptoms to test if a dimensional framework could reveal specific transdiagnostic clinical manifestations of error processing dysfunctions. Contrary to our hypothesis, we found no association between ERN amplitude and symptom severity of OCD, trait anxiety, depression, social anxiety, impulsivity, eating disorders, alcohol addiction, schizotypy or apathy. A transdiagnostic approach did nothing to improve signal; there was no association between three transdiagnostic dimensions (anxious-depression, compulsive behaviour and intrusive thought and social withdrawal) and ERN magnitude. In these same individuals, we replicated a previously published transdiagnostic association between goal-directed learning and compulsive behaviour and intrusive thought. Associations between the ERN and psychopathology might be smaller than previously assumed and/or dependent on a greater level of symptom severity than other transdiagnostic cognitive biomarkers.

neuroscience↗

Experimentally-induced and real-world acute anxiety have no effect on goal-directed behaviour.

Compulsivity is associated with failures in goal-directed control, an important cognitive faculty that protects against developing habits. But might this effect be explained by co-occurring anxiety? Previous studies have found goal-directed deficits in other anxiety disorders, and to some extent when healthy individuals are stressed, suggesting this is plausible. We carried out a causal test of this hypothesis in two experiments (between-subject N=88; within-subject N=50) that used the inhalation of hypercapnic gas (7.5% CO2) to induce an acute state of anxiety in healthy volunteers. In both experiments, we successfully induced anxiety, assessed physiologically and psychologically, but this did not affect goal-directed performance. In a third experiment (N=1413), we used a correlational design to test if real-life anxiety-provoking events (panic attacks, stressful events) impair goal-directed control. While small effects were observed, none survived controlling for individual differences in compulsivity. These data suggest that anxiety has no meaningful impact on goal-directed control.

animal behavior and cognition↗

Excessive deliberation in social anxiety

A goal of computational psychiatry is to ground symptoms in more fundamental computational mechanisms. Theory suggests that rumination and other symptoms in mood disorders reflect dysregulated mental simulation, a process that normally serves to evaluate candidate actions. If so, these covert symptoms should have observable consequences: excessively deliberative choices, specifically about options related to the content of rumination. In two large general population samples, we examined how symptoms of social anxiety disorder (SAD) predict choices in a socially framed reinforcement learning task, the Patent Race game. Using a computational learning model to assess learning strategy, we found that self-reported social anxiety was indeed associated with an increase in deliberative evaluation. The effect was specific to learning from a particular (\"upward counterfactual\") subset of feedback, broadly matching the biased content of rumination in SAD. It was also robust to controlling for other psychiatric symptoms. These results ground the symptoms of SAD, such as overthinking and paralysis in social interactions, in well characterized neuro-computational mechanisms and offer a rare example of enhanced function in disease

animal behavior and cognition↗