Objective To investigate the mRNA expression of ciliary neurotrophic factor on the retina during injury and repair of optic nerves in rats. Methods Thirty-five healthy SD rats were randomly divided into 3 groups: 5 in the control group, 15 in the simply transected optic nerve group and 15 in the optic nerve-sciatic nerve anastomosis group. The simply transected and optic nerve-sciatic nerve anastomosed models were set up, and the retinal tissues of all of the rats were taken out after 3, 7 and 14 days, respectively; and the mRNA expression of CNTF in the 3 groups were observed by semiquantitative reversal transcription-polymerase chain reaction method. Results A minimum expression of CNTF mRNA was found in the retinae of the control group, and the increased rates of expression were found in the retinae of the simple transection of optic nerve group with the increase rate of 100%, 594%, and 485% on the 3rd, 7th, and 14th day respectively after the operation, while in optic nerve-sciatic nerve anastomosis group, the increase rates were found to be 258%, 752% and 515% on the 3rd, 7th, and 14th day respectively after the operation. Conclusion Retinal neurons can respond to axonal reaction of retinal ganglion cells by up-regulate endogenous CNTF after the injury of the optic nerves, which may provide a theoretic base for the application of the exogenous CNTF. (Chin J Ocul Fundus Dis，2004，20：355-357)
The optic nerve belongs to the central nervous system (CNS). Because of the lack of neurotrophic factors in the microenvironment of the CNS and the presence of myelin and glial scar-related inhibitory molecules, and the inherent low renewal potentials of CNS neurons comparing to the peripheral nerve system, it is difficult to spontaneously regenerate the optic nerve after injury. Protecting damaged retinal ganglion cells (RGCs), supplementing neurotrophic factor, antagonizing axon regeneration inhibitory factor, and regulating the inherent regeneration potential of RGCs can effectively promote the regeneration and repair of optic nerve. Basic research has made important progress, including the restoration of visual function, but there are still a lot of unsolved problems in clinical translation of these achievements, so far there is no ideal method of treatment of optic nerve injury. Therefore, it is rather urgent to strengthen the cooperation between basic and clinical research, to promote the transformation of basic research to the clinical applications as soon as possible, which will change the unsatisfactory clinical application status.
We reported 42 cases of indirect optic nerve trauma in craniofaeial injuries. Mydriasis in affected eyes was found in 30 cases with absence or diminish of direct pupillary reflex but presence of indirect pupillary reflex. Imaging examination revealed optic canal fracture in 24 eases. Seven of 9 patients in whom the diagnosis of optic trauma was comfirmed received operation of optic nerve decompression from cranial and superior orbital wall approach within 10 days following injuries ,resulting in improvement of visual loss. While the other 2 patients operated on 15 days after trauma,obtained no relieve in their visual impairemenl. And 7 of 21 presumed cases of indirect optic trauma in this series treated with steroids became blind. We suggested that pupillary examination,imaging analysis,as well as early diagnosis and operation were essential to diagnosis and management of indirect optic trauma complicating craniofacial injuries. （Chin J Ocul Fundus Dis,1994,10:210-212）
目的:探讨经鼻内窥镜下手术治疗管内段视神经损伤的围手术期护理。方法:对收治的11例视神经损伤住院患者的资料及围手术期护理过程进行分析总结。结果:行视神经减压术的11例患者中1例失访,7例有效,其中4例视力有较明显的提高。结论:经鼻内镜视神经减压术损伤小,并发症少,手术时间短,疗效满意,其中围手术期的护理是提高手术疗效的一个重要环节。
Objective To evaluate the relevant factors affecting prognosis of traumatic optic neuropathy. Methods Sixty-nine patients with traumatic optic neuropathy were enrolled. Multiple variable analysis was done to filter the risk factors to prognosis in traumatic optic neuropathy. Results At 3 months or more of followup,no light perception was found in 32 cases (46.4%); visual acuity were increased by≥1 lines in 33 cases (47.8%). The outcome of visual acuity was poorer in patients with the following conditions:no light perception after trauma （P=0.0031）, loss of consciousness （P=0.0262）, no pretreated common-dosage corticosteroids （P=0.0184）, and absence of VEP （P=0.0001）. Conclusion The initial visual acuity of no light perception, loss of consciousness, and no pretreated common-dosage corticosteroids were the risk factors to prognosis in traumatic optic neuropathy,and result of VEP was an effective prognosis indicator in traumatic optic neuropathy. (Chin J Ocul Fundus Dis, 2002, 18: 98-100)
目的:探讨颅脑损伤合并视神经损伤的发病机制及治疗.方法:对23例颅脑损伤合并视神经损伤患者的临床资料做回顾性分析。结果:经过积极治疗部分患者视力有不同程度改善。结论:治疗颅脑损伤合并视神经损伤,强调神经外科和眼科协同处理,掌握治疗时机。
ObjectiveTo observe the early ultrastructural changes of the optic nerves after the brain impact injury.MethodsEighteen 15-week-old Wistar rats were used in the air-pressure brain impact injury examination. All of the rats underwent the procedures of right-parietal-bone fenestration after abdominal cavity anesthesia with 1% sodium pentolbarbital (45 mg/kg), and then they were divided randomly into 3 groups, i.e., mild injury group (8 rats) underwent with 7 kg of air pressure in distance of 11 cm; severe injury group (8 rats) with 7 kg of airpressure in distance of 8 cm; and control group (2 rats) underwent with the parietalbone fenestration but without impact injury.The ultrastructural changes of the optic nerves were observed 1, 6, 24, and 72 hours after the injury by electron microscopy.ResultsThe difference of ultrastructural changes of optic nerve was not obvious in wild injury group and the control group, and the lanthanum nitrate was only found in the blood vessels in optic nerve. The lanthanum nitrate entered the nerve stroma 1 hour after severe and increased as time goes on. Simultaneously, displayed dilatation of endoplasmic reticulum, cavitation and tumefaction of mitochondrion, vacuolation of nerve stroma, and vacuolation of some axis-cylinder were seen in the glial cells.ConclusionThe brain impact injury may cause ultrastructural changes of the optic nerve and increase of permeability of blood vessels. (Chin J Ocul Fundus Dis, 2005,21:41-43)