No abstract

The brain is widely assumed to be a paradigmatic example of a complex, self-organizing system. As such, it should exhibit the classic hallmarks of nonlinearity, multistability, and "nondiffusivity" (large coherent fluctuations). Surprisingly, at least at the very large scale of neocortical dynamics, there is little empirical evidence to support this, and hence most computational and methodological frameworks for healthy brain activity have proceeded very reasonably from a purely linear and diffusive perspective. By studying the temporal fluctuations of power in human resting-state electroencephalograms, we show that, although these simple properties may hold true at some temporal scales, there is strong evidence for bistability and nondiffusivity in key brain rhythms. Bistability is manifest as nonclassic bursting between high-and low-amplitude modes in the alpha rhythm. Nondiffusivity is expressed through the irregular appearance of high amplitude "extremal" events in beta rhythm power fluctuations. The statistical robustness of these observations was confirmed through comparison with Gaussian-rendered phase-randomized surrogate data. Although there is a good conceptual framework for understanding bistability in cortical dynamics, the implications of the extremal events challenge existing frameworks for understanding large-scale brain systems.

Brain network hubs are both highly connected and highly inter-connected, forming a critical communication backbone for coherent neural dynamics. The mechanisms driving this organization are poorly understood. Using diffusion-weighted magnetic resonance imaging in twins, we identify a major role for genes, showing that they preferentially influence connectivity strength between network hubs of the human connectome. Using transcriptomic atlas data, we show that connected hubs demonstrate tight coupling of transcriptional activity related to metabolic and cytoarchitectonic similarity. Finally, comparing over thirteen generative models of network growth, we show that purely stochastic processes cannot explain the precise wiring patterns of hubs, and that model performance can be improved by incorporating genetic constraints. Our findings indicate that genes play a strong and preferential role in shaping the functionally valuable, metabolically costly connections between connectome hubs.