1,987 publications from this institution
Typically, people perform actions in a valenced—positive or negative—way, depending on their attitudes or desires. These forms of action are named vitality forms (VFs). While it is well established that action goals are mediated by a parieto-frontal network, less is known about the processing of VFs. Recent fMRI studies suggest that the insula (INS)—and its connections with the parieto-frontal circuit—plays a crucial role in VFs processing. However, a key question remains: How does our internal affective state shape our motor behavior? To explore this issue, we conducted an fMRI study. Participants were required to perform two sequential tasks: 1) to evoke either a positive (enthusiastic) or a negative (angry) affective state (feeling task); 2) to execute an action while maintaining these affective states (execution task). Univariate analysis revealed activation of the INS and dorsolateral prefrontal cortex (PFC) during the feeling task, which extended to the premotor (PM) and parietal areas during the execution task. To determine the directionality of information flow among these nodes, we employed dynamic causal modeling. Bayesian model comparison showed that, during the feeling task, affect generation involves INS, which, together with the PFC, modulates the activity of PM. In contrast, during execution, motor commands emerge from PM and influence activity in the INS and PFC. These findings indicate that while the internal states crucially imply the INS, their regulation is mediated by PFC. The PM cortex plays a crucial role in the selection of the corresponding action VFs.
We recently described a dynamic causal model of a COVID-19 outbreak within a single region. Here, we combine several of these (epidemic) models to create a (pandemic) model of viral spread among regions. Our focus is on a second wave of new cases that may result from loss of immunity--and the exchange of people between regions--and how mortality rates can be ameliorated under different strategic responses. In particular, we consider hard or soft social distancing strategies predicated on national (Federal) or regional (State) estimates of the prevalence of infection in the population. The modelling is demonstrated using timeseries of new cases and deaths from the United States to estimate the parameters of a factorial (compartmental) epidemiological model of each State and, crucially, coupling between States. Using Bayesian model reduction, we identify the effective connectivity between States that best explains the initial phases of the outbreak in the United States. Using the ensuing posterior parameter estimates, we then evaluate the likely outcomes of different policies in terms of mortality, working days lost due to lockdown and demands upon critical care. The provisional results of this modelling suggest that social distancing and loss of immunity are the two key factors that underwrite a return to endemic equilibrium.
Abstract Sequential experimental paradigms are fundamental to cognitive neuroscience, yet standard event-related response analysis struggles with the temporal variability inherent to these designs. Conventional epoching treats each event within a sequence as an independent response, discarding the temporal dependencies between successive events and obscuring systematic changes in neural state that accumulate across the sequence. In order to generate responses that capture the entire sequence, it necessitates alignment across trials to correct for the inherent temporal jitter that would otherwise blur averaged responses and obscure the true sequential dynamics. Existing temporal alignment methods warp observed signals directly, making them vulnerable to correlated noise and potentially disrupting multichannel temporal relationships essential for connectivity and causal analyses. Event-Related Warping (ERW) addresses these limitations by aligning template functions encoding experimental event structure rather than neural signals themselves. Templates constructed from event onsets and durations undergo smooth monotonic warping via gradient-based optimisation, then estimated trajectories are applied uniformly across all channels, preserving inter-channel timing relationships and causal structure. This design-level alignment exploits experimentally observable jitter whilst maintaining signal integrity. Simulations with known ground truth incorporating Gaussian jitter, skewed latencies, amplitude-latency coupling, and multi-parameter dependencies yielded standardised root-mean-square errors (sRMSE) of 0.27-0.38. Distance-weighted averaging, emphasising temporally consistent trials, provided 5-13% improvement when jitter exceeded 100 ms, with maximal benefit (≈13% reduction) under quadratic amplitude-latency coupling. Empirical validation using an auditory go/no-go dataset with cue-to-target intervals of 1.5-4.1 seconds demonstrated that ERW recovers jittered target-locked responses with comparable fidelity (sRMSE 0.24-0.51) to conventional epoching of time-locked events, whilst preserving inter-channel lag relationships (cross-covariance sRMSE 0.63-0.82). ERW thus extends standard trial averaging to scenarios where temporal variability would otherwise preclude coherent response recovery, supporting investigation of temporally extended processing in ecologically valid paradigms whilst maintaining compatibility with established ERP frameworks and downstream connectivity analyses.
This paper develops a Bayesian mechanics for adaptive systems. Firstly, we model the interface between a system and its environment with a Markov blanket. This affords conditions under which states internal to the blanket encode information about external states. Second, we introduce dynamics and represent adaptive systems as Markov blankets at steady state. This allows us to identify a wide class of systems whose internal states appear to infer external states, consistent with variational inference in Bayesian statistics and theoretical neuroscience. Finally, we partition the blanket into sensory and active states. It follows that active states can be seen as performing active inference and well-known forms of stochastic control (such as PID control), which are prominent formulations of adaptive behaviour in theoretical biology and engineering.
Abstract This report describes a dynamic causal model that could be used to address questions about the rollout and efficacy of vaccines in the United Kingdom. For example, is suppression of community transmission a realistic aspiration? And, if not, what kind of endemic equilibrium might be achieved? What percentage of the population needs to be vaccinated? And over what timescale? It focuses on the synergies among (i) vaccination , (ii) the supported isolation of contacts of confirmed cases and (iii) restrictions on contact rates (i.e., lockdown and social distancing). To model these mitigations, we used a dynamic causal model that embeds an epidemiological model into agent-based behavioural model. The model structure and parameters were optimised to best explain responses—to the first and subsequent waves—enabling predictions over the forthcoming year under counterfactual scenarios. Illustrative analyses suggest that the full potential of vaccination is realised by increasing the efficacy of contact tracing: for example, under idealised (best case) assumptions—of an effective vaccine and efficient isolation of infected pre-symptomatic cases— suppression of community transmission would require 50% herd immunity by vaccinating 22% by the end of 2021; i.e., 15 million people or about 50,000 per day. With no change in the isolation of contacts, 36% would require vaccination, i.e., 25 million people. These figures should not be read as estimates of the actual number of people requiring vaccination; however, they illustrate the potential of this kind of model to quantify interactions among public health interventions. We anticipate using this model in a few months—to estimate the average effectiveness of vaccines when more data become available.
This technical report describes a dynamic causal model of the spread of coronavirus through a population. The model is based upon ensemble or population dynamics that generate outcomes, like new cases and deaths over time. The purpose of this model is to quantify the uncertainty that attends predictions of relevant outcomes. By assuming suitable conditional dependencies, one can model the effects of interventions (e.g., social distancing) and differences among populations (e.g., herd immunity) to predict what might happen in different circumstances. Technically, this model leverages state-of-the-art variational (Bayesian) model inversion and comparison procedures, originally developed to characterise the responses of neuronal ensembles to perturbations. Here, this modelling is applied to epidemiological populations-to illustrate the kind of inferences that are supported and how the model