Detectability of Granger causality for subsampled continuous-time neurophysiological processes (1606.08644v2)

Abstract: Granger causality is well established within the neurosciences for inference of directed functional connectivity from neurophysiological data. These data usually consist of time series which subsample a continuous-time biophysiological process. While it is well-known that subsampling can lead to imputation of spurious causal connections where none exist, here we address the equally important issue of the effects of subsampling on the ability to reliably detect causal connections which do exist. Neurophysiological processes typically feature signal propagation delays on multiple time scales; accordingly, we base our analysis on a distributed-lag, continuous-time stochastic model, and consider Granger causality in continuous time at finite prediction horizons. Via exact analytical solutions, we identify relationships among sampling frequency, underlying causal time scales and detectability of causalities. Our analysis reveals complex interactions between the time scale(s) of neural signal propagation and sampling frequency: we demonstrate that Granger causality decays exponentially as the sample time interval increases beyond causal delay times, identify detectability "black spots" and "sweet spots", and show that subsampling may sometimes improve detectability. We also demonstrate that the invariance of Granger causality under causal, invertible filtering fails at finite prediction horizons. We discuss the implications of our results for inference of Granger causality at the neural level from various neurophysiological recording modes, and emphasise that sampling rates for causal analysis of neurophysiological time series should be informed by domain-specific time scales.