Objective:

Traumatic brain injury (TBI) patients report chronic cognitive difficulties after the injury. By using simultaneous EEG-fNIRS assessment under cognitive strain in TBI patients, we aimed to examine distinct neural and hemodynamic signatures that could potentially explain the experienced decline.

Background:

TBI affects approximately 2.8 million Americans annually, with veterans of the US armed forces experiencing disproportionately high rates. Despite long-term cognitive complaints, conventional imaging is often normal, leaving neurophysiological mechanisms driving persistent cognitive decline elusive. While EEG and fNIRS independently demonstrate sensitivity to TBI-related dysfunction, simultaneous recording enables direct examination of the coordination between neural activity and cerebral blood flow, an effect described as neurovascular coupling.

Design/Methods:

Thirteen individuals (aged 45.7±10.5) with history of combat-related mild TBI and without dementia underwent simultaneous 16-16 channel EEG-fNIRS recording during an n-back working memory task. All TBI participants passed standard cognitive screening (MOCA: 26±1.6); however, a comprehensive cognition battery using NIH Toolbox revealed two distinct subgroups: cognitively under-performing (score=31.57±5.71; n=6) and maintained (score=56.17±9.36; n=7). We paired our dataset with age-matched healthy controls (n=5). Hemodynamic responses, spectral power, event-related potentials, and functional connectivity between modalities were analyzed.

Results:

Cognitively underperforming TBI patients demonstrated significantly reduced prefrontal hemodynamic responses during working memory compared to unimpaired TBI patients and controls, despite preserved spatial activation patterns. EEG analyses revealed characteristic TBI signatures: reduced alpha power, elevated slow-wave activity, and altered event-related potential amplitudes consistent with established literature. EEG-fNIRS correlation patterns revealed a significant decrease in functional connectivity in the cognitively underperforming group, implying a dissociation in neurovascular coupling.

Conclusions:

Simultaneous EEG-fNIRS detected neurovascular coupling abnormalities in TBI patients who passed conventional screening, with reduced hemodynamic efficiency and altered neural oscillations correlating with cognitive underperformance. This multimodal approach offers potential biomarkers for detecting subtle TBI-related dysfunction and identifying candidates for targeted cognitive rehabilitation.