Important information on the structure of complex systems can be obtained by measuring to what extent the individual components exchange information among each other. The linear Granger approach, to detect cause-effect relationships between time series, has emerged in recent years as a leading statistical technique to accomplish this task. Here we generalize Granger causality to the nonlinear case using the theory of reproducing kernel Hilbert spaces. Our method performs linear Granger causality in the feature space of suitable kernel functions, assuming arbitrary degree of nonlinearity. We develop a new strategy to cope with the problem of overfitting, based on the geometry of reproducing kernel Hilbert spaces. Applications to coupled chaotic maps and physiological data sets are presented.

A growing number of studies approach the brain as a complex network, the so-called ‘connectome’. Adopting this framework, we examine what types or extent of damage the brain can withstand—referred to as network ‘robustness’—and conversely, which kind of distortions can be expected after brain lesions. To this end, we review computational lesion studies and empirical studies investigating network alterations in brain tumour, stroke and traumatic brain injury patients. Common to these three types of focal injury is that there is no unequivocal relationship between the anatomical lesion site and its topological characteristics within the brain network. Furthermore, large-scale network effects of these focal lesions are compared to those of a widely studied multifocal neurodegenerative disorder, Alzheimer’s disease, in which central parts of the connectome are preferentially affected. Results indicate that human brain networks are remarkably resilient to different types of lesions, compared to other types of complex networks such as random or scale-free networks. However, lesion effects have been found to depend critically on the topological position of the lesion. In particular, damage to network hub regions—and especially those connecting different subnetworks—was found to cause the largest disturbances in network organization. Regardless of lesion location, evidence from empirical and computational lesion studies shows that lesions cause significant alterations in global network topology. The direction of these changes though remains to be elucidated. Encouragingly, both empirical and modelling studies have indicated that after focal damage, the connectome carries the potential to recover at least to some extent, with normalization of graph metrics being related to improved behavioural and cognitive functioning. To conclude, we highlight possible clinical implications of these findings, point out several methodological limitations that pertain to the study of brain diseases adopting a network approach, and provide suggestions for future research.

We review the theory and algorithms of electrophysiological brain connectivity analysis. This tutorial is aimed at providing an introduction to brain functional connectivity from electrophysiological signals, including electroencephalography, magnetoencephalography, electrocorticography, and stereoelectroencephalography. Various connectivity estimators are discussed, and algorithms introduced. Important issues for estimating and mapping brain functional connectivity with electrophysiology are discussed.