Interacting systems are prevalent in nature, from dynamical systems in physics to complex societ al dynamics. The interplay of components can give rise to complex behavior, which can often be explained using a simple model of the system's constituent parts. In this work, we introduce the neural relational inference (NRI) model: an unsupervised model that learns to infer interactions while simultaneously learning the dynamics purely from observational data. Our model takes the form of a variational auto-encoder, in which the latent code represents the underlying interaction graph and the reconstruction is based on graph neural networks. In experiments on simulated physical systems, we show that our NRI model can accurately recover ground-truth interactions in an unsupervised manner. We further demonstrate that we can find an interpretable structure and predict complex dynamics in real motion capture and sports tracking data.
An alternative approach to inferring interactions is Granger causality @cite_9 . Granger causality however assumes a linear dynamical model and only tries to infer the existence of a causal relation and not to infer relation types.
@cite_9
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Multi-electrode neurophysiological recordings produce massive quantities of data. Multivariate time series analysis provides the basic framework for analyzing the patterns of neural interactions in these data. It has long been recognized that neural interactions are directional. Being able to assess the directionality of neuronal interactions is thus a highly desired capability for understanding the cooperative nature of neural computation. Research over the last few years has shown that Granger causality is a key technique to furnish this capability. The main goal of this article is to provide an expository introduction to the concept of Granger causality. Mathematical frameworks for both bivariate Granger causality and conditional Granger causality are developed in detail with particular emphasis on their spectral representations. The technique is demonstrated in numerical examples where the exact answers of causal influences are known. It is then applied to analyze multichannel local field potentials recorded from monkeys performing a visuomotor task. Our results are shown to be physiologically interpretable and yield new insights into the dynamical organization of large-scale oscillatory cortical networks. Hawkes (1971) introduced a powerful multivariate point process model of mutually exciting processes to explain causal structure in data. In this paper it is shown that the Granger causality structure of such processes is fully encoded in the corresponding link functions of the model. A new nonparametric estimator of the link functions based on a time-discretized version of the point process is introduced by using an infinite order autoregression. Consistency of the new estimator is derived. The estimator is applied to simulated data and to neural spike train data from the spinal dorsal horn of a rat. We introduce a measure of causality that captures the functional dependencies in dynamical systems and subsequently, define a new type of graphical model, functional dependency graph, to encode such dependencies. We study the relationship between this type of graphical model and other graphical models such as directed information graphs and linear dynamical graphs that have been proposed to capture causal influences in dynamical systems. We show that functional dependency graphs are a generalization of these previously introduced graphical models and learn the functional dependencies in a larger class of models. We also establish sufficient conditions under which the functional dependency graph defined through our measure is equivalent to the directed information graphs. Some simulation results on linear and nonlinear dynamics are provided. We consider the question of evaluating causal relations among neurobiological signals. In particular, we study the relation between the directed transfer function (DTF) and the well-accepted Granger causality, and show that DTF can be interpreted within the framework of Granger causality. In addition, we propose a method to assess the significance of causality measures. Finally, we demonstrate the applications of these measures to simulated data and actual neurobiological recordings.