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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. 

Traumatic brain injury poses a major public health challenge with significant immediate and long-term effects. Repetitive head trauma is an ongoing area of research, and little is known about the response of cerebral blood vessels to such loading. This study investigated the mechanical response of cerebral arteries to repetitive overstretch, hypothesizing that repeated overstretch leads to cumulative damage. To test this hypothesis, middle cerebral artery segments from twelve piglets were subjected to sub-yield, high-rate overstretch of varying severities, with up to 10 repetitions. The stress-stretch behavior of the vessels revealed that repetitive overstretch caused progressive softening that increased with both overstretch magnitude and number of exposures. This softening was notably limited to the toe region, with no changes occurring in the higher-stress, linear portion of the repeated overstretch curves. Mild-to-moderate overstretches resulted in gradual softening, while severe overstretches caused dramatic softening with the first exposure and little further change with subsequent overstretches. Mildly damaged vessels displayed a small amount of recovery with time, but the magnitude of this recovery was minimal and declined with increasing repetitions and severity. No clear relationship was observed between collagen denaturation and the magnitude and number of overstretches. These findings provide important insights into the mechanics of cerebral vessels under repetitive loading, suggesting that vascular damage from repeated trauma accumulates, potentially exacerbating existing injury. These results increase understanding of soft tissue damage and inform the development of constitutive damage models for cerebral arteries, a critical tool needed to improve predictions of traumatic brain injury progression. STATEMENT OF SIGNIFICANCE: This study investigates the mechanical response of cerebral arteries to repetitive overstretch, revealing cumulative softening effects. Unlike previous studies focusing on single overstretch events, our research is the first to explore repetitive exposures in cerebral arteries and to report softening as a function of both overstretch magnitude and number of exposures. Given the role of cerebral vessels in maintaining a healthy brain and their contributions to the structural response of the brain in TBI events, progressive vessel softening in repetitive TBI may lead to increased vulnerability with the potential to exacerbate existing injury. These findings enhance understanding of soft tissue damage mechanisms, providing critical insights for developing constitutive damage models and improving injury predictions in repeated TBI. 

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.