Traumatic optic neuropathy (TON) is a major cause of irreversible vision loss following blunt cranial trauma, yet the absence of clinically relevant large animal models that faithfully recapitulate human TON has significantly impeded translational research. Current rodent models do not reproduce optic canal fracture, a key injury mechanism in many patients with TON. Here, we combined high-fidelity finite element analysis (FEA) with iterative engineering to establish a reproducible goat model of TON. We first built a high-resolution human-head finite element model to characterize force transmission to the optic nerve. Across clinically relevant periorbital impacts, stress preferentially concentrated in the intracanalicular segment, reaching a peak force density of approximately 500 N/m² at 50.6 ms, about fivefold higher than in the intraorbital segment. Simulations further showed that direct optic canal impact reproduced comparable intracanalicular stress with a markedly lower input force: 195 N, compared with 3900 N for periorbital impact. Guided by these insights, we developed transnasal endoscopic impact systems capable of inducing optic canal fractures in goats. TON was confirmed within 24 hours by a characteristic relative afferent pupillary defect (RAPD), and at 1 month post-injury goats (n = 14) exhibited a 10%–20% reduction in ganglion cell complex (GCC) thickness and 40%–65% reductions in flash visual evoked potential (FVEP) and pattern electroretinogram (PERG) amplitude ratios (all P ≤ 0.001), with structural and functional preservation of the fellow eye. This study presents a robust, standardized, and clinically relevant large-animal platform for investigating TON pathophysiology.
Zhonghao et al. (Thu,) studied this question.
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