title: Modeling distinct imaging hemodynamics early after TBI: the relationship between signal amplitude and connectivity.
abstract: Over the past decade, fMRI studies of cognitive change following traumatic brain injury (TBI) have investigated blood oxygen level dependent (BOLD) activity during working memory (WM) performance in individuals in early and chronic phases of recovery. Recently, BOLD fMRI work has largely shifted to focus on WM and resting functional connectivity following TBI. However, fundamental questions in WM remain. Specifically, the effects of injury on the basic relationships between local and interregional functional neuroimaging signals during WM processing early following moderate to severe TBI have not been examined. This study employs a mixed effects model to examine prefrontal cortex and parietal lobe signal change during a WM task, the n-back, and whether there is covariance between regions of high amplitude signal change, (synchrony of elicited activity (SEA) very early following TBI. We also examined whether signal change and SEA differentially predict performance during WM. Overall, percent signal change in the right prefrontal cortex (rPFC) was and important predictor of both reaction time (RT) and SEA in early TBI and matched controls. Right prefrontal cortex (rPFC) percent signal change positively predicted SEA within and between persons regardless of injury status, suggesting that the link between these neurodynamic processes in WM-activated regions remains unaffected even very early after TBI. Additionally, rPFC activity was positively related to RT within and between persons in both groups. Right parietal (rPAR) activity was negatively related to RT within subjects in both groups. Thus, the local signal intensity of the rPFC in TBI appears to be a critical property of network functioning and performance in WM processing and may be a precursor to recruitment observed in chronic samples. The present results suggest that as much research moves toward large scale functional connectivity modeling, it will be essential to develop integrated models of how local and distant neurodynamics promote WM performance after TBI.
authors.affiliation: Psychology Department, Pennsylvania State University, State College, 313 Moore Building, University Park, PA, 16802, USA.
authors.forename: John D
authors.initials: JD
authors.lastname: Medaglia
authors.forename: Andrew A
authors.initials: AA
authors.lastname: McAleavey
authors.forename: Sohayla
authors.initials: S
authors.lastname: Rostami
authors.forename: Julia
authors.initials: J
authors.lastname: Slocomb
authors.forename: Frank G
authors.initials: FG
authors.lastname: Hillary
mesh_terms: D000328:Adult; D001921:Brain / Q000098:blood supply / Q000503:physiopathology*; D001930:Brain Injuries / Q000503:physiopathology*; D001931:Brain Mapping / Q000379:methods; D002560:Cerebrovascular Circulation / Q000502:physiology*; D005260:Female; D006439:Hemodynamics / Q000502:physiology*; D006801:Humans; D008279:Magnetic Resonance Imaging / Q000379:methods; D008297:Male; D008570:Memory, Short-Term / Q000502:physiology*; D008959:Models, Neurological; D009434:Neural Pathways / Q000098:blood supply / Q000503:physiopathology; D009483:Neuropsychological Tests; D011930:Reaction Time