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Brugger, S.

Publications and source records attributed to Brugger, S..

3 recordsLinked to original sources

Delusions Emerge from Generative Model Reorganisation rather than Faulty Inference: Insights from Hybrid Predictive Coding

Predictive coding has influenced many conceptual accounts of delusions, the bizarre and distressing beliefs that accompany a range of neuropsychiatric conditions. However, these explanations remain incomplete and have rarely been tested directly using formal modelling. Here, we present a formal account of delusional beliefs based on hybrid predictive coding, which sheds light on the computational mechanisms underpinning the core features of delusions: thematic recurrence and imperviousness to contradictory evidence. In simulation experiments, we demonstrate that a combination of contextually inadequate initialisation of beliefs and excessive certainty (a hallmark of psychosis), triggers a reorganisation of the generative model relating observed events to hidden causes. This reorganisation enables the maintenance of delusional beliefs that are thematically stable, internally consistent with external inputs, and impervious to contradictory evidence, all without an increase in prediction error. Overall, our results suggest that delusions may arise not from faulty inference, as previously argued, but as an adaptive consequence of generative models learned under atypical conditions. These findings provide mechanistic insights into the computations underpinning delusions and have important implications for a novel therapeutic strategy in terms of re-training generative models.

neuroscience↗

Psychedelics and schizophrenia: Distinct alterations to Bayesian inference

Schizophrenia and states induced by certain psychotomimetic drugs may share some physiological and phenomenological properties, but they differ in fundamental ways: one is a crippling chronic mental disease, while the others are temporary, pharmacologically-induced states presently being explored as treatments for mental illnesses. Building towards a deeper understanding of these different alterations of normal consciousness, here we compare the changes in neural dynamics induced by LSD and ketamine (in healthy volunteers) against those associated with schizophrenia, as observed in resting-state M/EEG recordings. While both conditions exhibit increased neural signal diversity, our findings reveal that this is accompanied by an increased transfer entropy from the front to the back of the brain in schizophrenia, versus an overall reduction under the two drugs. Furthermore, we show that these effects can be reproduced via different alterations of standard Bayesian inference applied on a computational model based on the predictive processing framework. In particular, the effects observed under the drugs are modelled as a reduction of the precision of the priors, while the effects of schizophrenia correspond to an increased precision of sensory information. These findings shed new light on the similarities and differences between schizophrenia and two psychotomimetic drug states, and have potential implications for the study of consciousness and future mental health treatments.

neuroscience↗

Cardiac structure and function in patients with schizophrenia taking antipsychotic drugs: an MRI study

Cardiovascular disease (CVD) is a major cause of excess mortality in schizophrenia. Preclinical evidence shows antipsychotics can cause myocardial fibrosis and myocardial inflammation in murine models, but it is not known if this is the case in patients. We therefore set out to determine if there is evidence of cardiac fibrosis and/or inflammation using cardiac MRI in medicated patients with schizophrenia compared with matched healthy controls. 31 participants (14 patients and 17 controls) underwent cardiac MRI assessing myocardial markers of fibrosis/inflammation, indexed by native myocardial T1 time, and cardiac structure (left ventricular (LV) mass) and function (left/right ventricular end-diastolic and end-systolic volumes, stroke volumes, and ejection fractions). Participants were physically fit, and matched for age, gender, smoking, blood pressure, BMI, HbA1c, ethnicity, and physical activity. Compared with controls, native myocardial T1 was significantly longer in patients with schizophrenia (effect size, d=0.89; p=0.02). Patients had significantly lower LV mass, and lower left/right ventricular end-diastolic and stroke volumes (effect sizes, d=0.86-1.08; all p-values <0.05). There were no significant differences in left/right end-systolic volumes and ejection fractions between groups (p>0.05). These results suggest an early diffuse fibro-inflammatory myocardial process in patients that is independent of established CVD-risk factors and could contribute to the excess cardiovascular mortality associated with schizophrenia. Future studies are required to determine if this is due to antipsychotic treatment or is intrinsic to schizophrenia.

physiology↗