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Mild traumatic brain injury (mTBI) accounts for approximately 75% of all TBI cases, and the mechanisms are still poorly understood, in part due to limitations of current diagnostic tools. Yet, there is a critical need to detect the presence of mTBI to mitigate risk of further injury. In this study, we explore the potential of collagen hybridizing peptides (CHPs), which selectively bind to damaged collagen, to detect damage in the pia-arachnoid complex (PAC), a major load-transferring interface during head trauma. To generate damage, porcine PAC samples underwent peel tests. Peak force to failure and CHP fluorescence were measured in three regions of the brain at multiple post-mortem times. The peak force of PAC failure was region-specific, with increasing failure forces moving anterior to posterior (frontal: 20.91 ± 38.77 mN; parietal: 64.72 ± 33.31 mN; occipital: 86.68 ± 43.46 mN) and significantly different between frontal and occipital regions (p = 0.034). CHP fluorescence was significantly different between control and peeled PAC samples in mean pixel intensity (MPI; p = 0.031), median pixel intensity (MedPI; p = 0.009), and percent pixels above a defined threshold (PP; p = 0.014). Each of these CHP fluorescence metrics were significantly and positively correlated with peak force at failure (MPI: p = 0.049; MedPI: p = 0.026; PP: p = 0.002). These data suggest CHP is a viable solution to detecting the presence and severity of damage at the brain-skull interface, and may be a useful tool for quantifying damage in vivo. 

Abstract Traumatic brain injury (TBI) is a common injury modality affecting a diverse patient population. Axonal injury occurs when the brain experiences excessive deformation as a result of head impact. Previous studies have shown that the arachnoid trabeculae (AT) in the subarachnoid space significantly influence the magnitude and distribution of brain deformation during impact. However, the quantity and spatial distribution of cranial AT in humans is unknown. Quantification of these microstructural features will improve understanding of force transfer during TBI, and may be a valuable dataset for microneurosurgical procedures. In this study, we quantify the spatial distribution of cranial AT in seven post‐mortem human subjects. Optical coherence tomography (OCT) was used to conduct in situ imaging of AT microstructure across the surface of the human brain. OCT images were segmented to quantify the relative amounts of trabecular structures through a volume fraction (VF) measurement. The average VF for each brain ranged from 22.0% to 29.2%. Across all brains, there was a positive spatial correlation, with VF significantly greater by 12% near the superior aspect of the brain (p < .005), and significantly greater by 5%−10% in the frontal lobes (p < .005). These findings suggest that the distribution of AT between the brain and skull is heterogeneous, region‐dependent, and likely contributes to brain deformation patterns. This study is the first to image and quantify human AT across the cerebrum and identify region‐dependencies. Incorporation of this spatial heterogeneity may improve the accuracy of computational models of human TBI and enhance understanding of brain dynamics.