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Disambiguating the role of blood flow and global signal with Partial Information Decomposition

By Nigel Colenbier, Frederik Van de Steen, Lucina Uddin, Russell A. Poldrack, V. D. Calhoun, Daniele Marinazzo

Posted 02 Apr 2019
bioRxiv DOI: 10.1101/596247 (published DOI: 10.3389/conf.fnins.2019.96.00045)

In resting state functional magnetic resonance imaging (rs-fMRI) a common strategy to reduce the impact of physiological noise and other artifacts on the data is to regress out the global signal using global signal regression (GSR). Yet, GSR is one of the most controversial preprocessing techniques for rs-fMRI. It effectively removes non-neuronal artifacts, but at the same time it alters correlational patterns in unpredicted ways. Furthermore the global signal includes neural BOLD signal by construction, and is consequently related to neural and behavioral function. Performing GSR taking into account the underlying physiology (mainly the blood arrival time) has been proved to be beneficial. From these observations we aimed to: 1) characterize the effect of GSR on network-level functional connectivity in a large dataset; 2) assess the complementary role of global signal and vessels; and 3) use the framework of partial information decomposition to further look into the joint dynamics of the global signal and vessels, and their respective influence on the dynamics of cortical areas. We observe that GSR affects intrinsic connectivity networks in the connectome in a non-uniform way. Furthermore, by estimating the predictive information of blood flow and the global signal using partial information decomposition, we observe that both signals are present in different amounts across intrinsic connectivity networks. Simulations showed that differences in blood arrival time can largely explain this phenomenon. With these results we confirm network-specific effects of GSR and the importance of taking blood flow into account for improve denoising methods. Using GSR but not correcting for blood flow might selectively introduce physiological artifacts across intrinsic connectivity networks that distort the functional connectivity estimates.

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