4.7 Article

Adiabatic dynamic causal modelling

Journal

NEUROIMAGE
Volume 238, Issue -, Pages -

Publisher

ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.neuroimage.2021.118243

Keywords

Dynamic causal modelling; Cross spectral density; Phase transition; Adiabatic approximation; Bayesian model selection; Bayesian model reduction

Funding

  1. Wellcome [203147/Z/16/Z]
  2. Worshipful Company of Pewterers

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Adiabatic dynamic causal modelling is a method for inferring slow changes in biophysical parameters controlling fast neuronal fluctuations. It relies on established neural mass models and an adiabatic approximation to summarize fast neuronal states using second order statistics. The method introduces a circular causality involving synaptic parameters and neuronal activity, and is validated through simulations and an illustrative application to seizure activity in an animal model.
This technical note introduces adiabatic dynamic causal modelling, a method for inferring slow changes in biophysical parameters that control fluctuations of fast neuronal states. The application domain we have in mind is inferring slow changes in variables (e.g., extracellular ion concentrations or synaptic efficacy) that underlie phase transitions in brain activity (e.g., paroxysmal seizure activity). The scheme is efficient and yet retains a biophysical interpretation, in virtue of being based on established neural mass models that are equipped with a slow dynamic on the parameters (such as synaptic rate constants or effective connectivity). In brief, we use an adiabatic approximation to summarise fast fluctuations in hidden neuronal states (and their expression in sensors) in terms of their second order statistics; namely, their complex cross spectra. This allows one to specify and compare models of slowly changing parameters (using Bayesian model reduction) that generate a sequence of empirical cross spectra of electrophysiological recordings. Crucially, we use the slow fluctuations in the spectral power of neuronal activity as empirical priors on changes in synaptic parameters. This introduces a circular causality, in which synaptic parameters underwrite fast neuronal activity that, in turn, induces activity-dependent plasticity in synaptic parameters. In this foundational paper, we describe the underlying model, establish its face validity using simulations and provide an illustrative application to a chemoconvulsant animal model of seizure activity.

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