Abstract

Brain signal variability changes across the lifespan in both health and disease, likely reflecting changes in information processing capacity related to development, aging and neurological disorders. While signal complexity, and multiscale entropy (MSE) in particular, has been proposed as a biomarker for neurological disorders, most observations of altered signal complexity have come from studies comparing patients with few to no comorbidities against healthy controls. In this study, we examined whether MSE of brain signals was distinguishable across patient groups in a large and heterogeneous set of clinical-EEG data. Using a multivariate analysis, we found unique timescale-dependent differences in MSE across various neurological disorders. We also found MSE to differentiate individuals with non-brain comorbidities, suggesting that MSE is sensitive to brain signal changes brought about by metabolic and other non-brain disorders. Such changes were not detectable in the spectral power density of brain signals. Our findings suggest that brain signal complexity may offer complementary information to spectral power about an individual’s health status and is a promising avenue for clinical biomarker development.

Highlights

  • Brain signal variability changes across the lifespan in both health and disease, likely reflecting changes in information processing capacity related to development, aging and neurological disorders

  • We examined whether brain signal complexity varied across individuals of a large and heterogeneous clinical population using a data driven approach

  • We found timescale-dependent differences in brain signal complexity for individuals who experience generalized seizures from individuals who have other brain disorders

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Summary

Introduction

Brain signal variability changes across the lifespan in both health and disease, likely reflecting changes in information processing capacity related to development, aging and neurological disorders. We found MSE to differentiate individuals with non-brain comorbidities, suggesting that MSE is sensitive to brain signal changes brought about by metabolic and other non-brain disorders. Such changes were not detectable in the spectral power density of brain signals. In most of these studies, brain signal complexity changes related to various brain diseases have been detected by comparing individuals with few to no comorbidities against matched healthy controls using data collected in highly controlled laboratory environments. We found MSE to differentiate between individuals with non-brain comorbidities and those without comorbidities

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