A diagnosis of traumatic brain injury (TBI) is typically based upon patient medical history, clinical exam and imaging tests. Elevated plasma levels of glial fibrillary acidic protein (GFAP), ubiquitin c-terminal hydrolase L1 (UCH-L1) and neurofilament light chain (NF-L) have been observed in numerous studies of TBI patients. It is reasonable to view traumatic optic neuropathy (TON) as a focal form of TBI. The purpose of this study was to assess if circulating GFAP, UCH-L1, and NF-L are also elevated in a porcine model of TON. Serum levels of GFAP, UCH-L1, and NF-L were measured immediately before optic nerve crush and one hour post-injury in ten Yucatan minipigs. Severity of optic nerve crush was confirmed by visual inspection of the optic nerve at time of injury, loss of visual function as measured by flash visual evoked potential (fVEP) at 7 and 14 days and histological analysis of axonal transport of cholera toxin-β (CT-β) within the optic nerve. Post-crush concentrations of GFAP, UCH-L1, and NF-L were all significantly elevated compared to pre-crush concentrations (p<0.01, p=0.01 and p<0.01, respectively). The largest increase was observed for GFAP with the post-injury median concentration increasing nearly seven-fold. The use of these TBI biomarkers for diagnosing and managing TON may be helpful for non-ophthalmologists in particular in diagnosing this condition. In addition, the potential utility of these biomarkers for diagnosing other optic nerve and/or retinal pathologies should also be evaluated.

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