Concussion-related disruptions to hub connectivity in the default mode network are related to symptoms and cognition

Authors

Heather C. Bouchard, University of Nebraska-LincolnFollow
Kate L. Higgins, University of Nebraska-LincolnFollow
Grace Amadon, University of Nebraska - LincolnFollow
Julia M. Laing-Young, University of Nebraska-Lincoln
Arthur C. Maerlender, University of Nebraska-LincolnFollow
Seima Al-Momani, University of Nebraska-LincolnFollow
Maital Neta, University of Nebraska - LincolnFollow
Cary R. Savage, University of Nebraska - LincolnFollow
Douglas H. Schultz, University of Nebraska–LincolnFollow

ORCID IDs

Heather C. Bouchard, http://orcid.org/0000-0002-3646-6334

Kate L. Higgins, http://orcid.org/0000-0001-5340-8315

Maital Neta, http://orcid.org/0000-0001-8586-0963

Cary R. Savage, http://orcid.org/0000-0001-7997-6193

Douglas H. Schultz, http://orcid.org/0000-0003-0809-9036

Date of this Version

2023

Document Type

Article

Citation

bioRxiv preprint DOI: https://doi.org/10.1101/2023.03.07.531551

Accepted for publication in Journal of Neurotrauma (2023)

Comments

Copyright: This pre-print is available under a Creative Commons License (Attribution-NoDerivs 4.0 International), CC BY-ND 4.0

Abstract

Concussions present with a myriad of symptomatic and cognitive concerns; however, the relationship between these functional disruptions and the underlying changes in the brain are not yet well understood. Hubs, or brain regions that are connected to many different functional networks, may be specifically disrupted after concussion. Given the implications in concussion research, we quantified hub disruption within the default mode network (DMN) and between the DMN and other brain networks. We collected resting-state functional magnetic resonance imaging data from collegiate student-athletes (n = 44) at three timepoints: baseline (prior to beginning their athletic season), acute post-injury (approximately 48 hours after a diagnosed concussion), and recovery (after starting return-to-play progression, but prior to returning to contact). We used self-reported symptoms and computerized cognitive assessments collected across similar timepoints to link these functional connectivity changes to clinical outcomes.

Concussion resulted in increased connectivity between regions within the DMN compared to baseline and recovery, and this post-injury connectivity was more positively related to symptoms and more negatively related to visual memory performance compared to baseline and recovery. Further, concussion led to decreased connectivity between DMN hubs and visual network non-hubs relative to baseline and recovery, and this post-injury connectivity was more negatively related to somatic symptoms and more positively related to visual memory performance compared to baseline and recovery. Relationships between functional connectivity, symptoms, and cognition were not significantly different at baseline versus recovery.

These results highlight a unique relationship between self-reported symptoms, visual memory performance and acute functional connectivity changes involving DMN hubs after concussion in athletes. This may provide evidence for a disrupted balance of within- and between-network communication highlighting possible network inefficiencies after concussion. These results aid in our understanding of the pathophysiological disruptions after concussion and inform our understanding of the associations between disruptions in brain connectivity and specific clinical presentations acutely post-injury.