Matsuzaki H, Kunita M, Kawai K
Jpn J Ophthalmol. 1982;26(4):447-61.
A total of 33 cases with optic nerve damage due to blunt head trauma were followed for 6 months to one year with the average follow-up period of 9 months. Eleven cases were treated by surgical decompression of the optic canal and 22 cases were followed by medical treatment. The optic canal fracture was documented in 51% of the cases, and the incidence was not significantly different between both groups. When the visual acuity was zero at the time of the first examination, no visual improvement could be obtained. Omitting these cases, visual improvement was seen in 42.8% of patients treated by surgery and in 58.8% of patients with medical treatment, which consisted of a combined use of prednisolone, mannitol, urokinase and vitamin B12. The percentage of visual improvement did not differ between cases with and without optic canal fracture. In the Japanese monkey, the optic nerve was exposed and various insults were given, including traction, ligation and small optic sheath resection. After traction and ligation, the visually evoked response (VEP) became extinguished or reduced, but after release from the insult, a tendency of recovery was found in the VEP. The threshold to elicit the VEP by localized light stimulus was increased by optic nerve ligation, but after its release the threshold tended to decrease. The effects of the optic nerve sheath resection were slight, and the increase in the threshold recovered after 4 weeks. It was thought that the optic nerve is resistant to indirect insults. From the clinical and experimental studies, it was concluded that the mechanism of the optic nerve damage due to blunt head trauma is multiple, and that the cases should be treated by intensive medical treatment rather than by surgical intervention.
共有33例因钝性头部外伤导致视神经损伤的患者接受了6个月至1年的随访，平均随访期为9个月。11例患者接受了视神经管减压手术治疗，22例患者接受了药物治疗。51%的病例记录有视神经管骨折，两组之间的发生率无显著差异。初次检查时视力为零的患者，视力无改善。排除这些病例后，手术治疗的患者中有42.8%视力得到改善，药物治疗的患者中有58.8%视力得到改善，药物治疗包括联合使用泼尼松龙、甘露醇、尿激酶和维生素B12。视神经管骨折患者和无骨折患者的视力改善百分比无差异。在日本猕猴中，暴露视神经并给予各种损伤，包括牵拉、结扎和小范围视神经鞘切除。牵拉和结扎后，视觉诱发电位（VEP）消失或降低，但损伤解除后，VEP有恢复趋势。视神经结扎会使局部光刺激诱发VEP的阈值升高，但解除结扎后阈值有降低趋势。视神经鞘切除的影响较小，4周后阈值升高恢复。认为视神经对间接损伤有抵抗力。从临床和实验研究得出结论，钝性头部外伤导致视神经损伤的机制是多方面的，这些病例应采用强化药物治疗而非手术干预。
