Objective: In this study, we investigate the preoperative and postoperative computed tomography (CT) scores in severe traumatic brain injury (TBI) patients undergoing decompressive craniectomy (DC) and compare their predictive accuracy. Methods: Univariate and multivariate logistic regression analyses were used to determine the relationship between CT score (preoperative and postoperative) and mortality at 30 days after injury. The discriminatory power of preoperative and postoperative CT score was assessed by the area under the receiver operating characteristic curve (AUC). Results: Multivariate logistic regression analysis adjusted for the established predictors of TBI outcomes showed that preoperative Rotterdam CT score (odds ratio [OR], 3.60; 95% confidence interval [CI], 1.13–11.50; P = 0.030), postoperative Rotterdam CT score (OR, 4.17; 95% CI, 1.63–10.66; P = 0.003), preoperative Stockholm CT score (OR, 3.41; 95% CI, 1.42–8.18; P = 0.006), postoperative Stockholm CT score (OR, 4.50; 95% CI, 1.60–12.64; P = 0.004), preoperative Helsinki CT score (OR, 1.44; 95% CI, 1.03–2.02; P = 0.031), and postoperative Helsinki CT score (OR, 2.55; 95% CI, 1.32–4.95; P = 0.005) were significantly associated with mortality. The performance of the postoperative Rotterdam CT score was superior to the preoperative Rotterdam CT score (AUC, 0.82–0.97 vs 0.71–0.91). The postoperative Stockholm CT score was superior to the preoperative Stockholm CT score (AUC, 0.76–0.94 vs 0.72–0.92). The postoperative Helsinki CT score was superior to the preoperative Helsinki CT score (AUC, 0.88–0.99 vs 0.65–0.87). Conclusions: In conclusion, assessing the CT score before and after DC may be more precise and efficient for predicting early mortality in severe TBI patients who undergo DC.

Background: Traumatic optic nerve injury is a leading cause of irreversible blindness across the world and causes progressive visual impairment attributed to the dysfunction and death of retinal ganglion cells (RGCs). To date, neither pharmacological nor surgical interventions are sufficient to halt or reverse the progress of visual loss. Axon regeneration is critical for functional recovery of vision following optic nerve injury. After optic nerve injury, RGC axons usually fail to regrow and die, leading to the death of the RGCs and subsequently inducing the functional loss of vision. However, the detailed molecular mechanisms underlying axon regeneration after optic nerve injury remain poorly understood. Methods: Research content related to the detailed molecular mechanisms underlying axon regeneration after optic nerve injury have been reviewed. Results: The present review provides an overview of regarding potential strategies for axonal regeneration of RGCs and optic nerve repair, focusing on the role of cytokines and their downstream signaling pathways involved in intrinsic growth program and the inhibitory environment together with axon guidance cues for correct axon guidance. A more complete understanding of the factors limiting axonal regeneration will provide a rational basis, which contributes to develop improved treatments for optic nerve regeneration. These findings are encouraging and open the possibility that clinically meaningful regeneration may become achievable in the future. Conclusion: Combination of treatments towards overcoming growth-inhibitory molecules and enhancing intrinsic growth capacity combined with correct guidance using axon guidance cues is crucial for developing promising therapies to promote axon regeneration and functional recovery after ON injury.