Objective To evaluate the treatment of surgery and high-dose corticosteroid relevant factors to prognosis in traumatic optic neuropathy. Methods Forty patients(40 eyes) with traumatic optic neuropathy were enrolled.Optic nerve decompression using transcranial approaches,sinus endoscopy and orbital-ethmoidal sinus rout were performed in 14 patients.Eleven patients were treated with high-dose corticosteroids (5 cases with 1 mg/kg dexamethasone,6 cases with 30 mg/kg methylprednisolone) and 15 patients received nonspecific management chose by themselves.The outcomes of visual acuity in short term and final stage were compared between surgery,high-dose corticosteroid and nonspecific treatment.Multiple variable analysis was done to determine the factors affecting the outcome of visual acuity. Results No light perception were found in 19 cases (19 out of 44 cases,47.5%),whereas visual acuity was light perception to 0.02 in 12 cases (30.0%) and 0.05 or better in 9 cases (22.5%).The odds ratio of high-dose corticosteroid to nonspecific therapy was 2.96 (P=0.0125).The final visual acuity in patients treated with high-dose corticosteroid were better than other two groups (P=0.005,P=0.023,respectively).The short term (within 3 days) effective rate was higher in corticosteroid therapy group than operated group (P=0.024).No light perception following optic nerve trauma appeared to be more danger as 2.14 folds (P=0.0349) than those with light perception or better in term of final visual acuity outcome. Conclusions High-dose corticosteroid may be benefit to traumatic optic neuropathy.The treatment in traumatic optic neuropathy using optic nerve decompression needs to be determined.No light perception at initial is an important risk factor in the outcome. (Chin J Ocul Fundus Dis,2000,16:75-77)
Objective To investigate the survivability of ret inal ganglion cells (RGC) after optic nerve crush with intraocular injection of schwann cells(SC) derived neurotrophic (SCNA) in vivo． Methods Schwann cells of 3～5 day newborn mice were cultured,conditioned media without serum was collected,ultraspeed centrifugalized,and frozen-dry.SD rats were divided into normal contrl,crush control,medium treatment and SCNA treatment groups,and 20 eyes in every group.RGC of adult rats were labelled with flu orogold.Seven days later,the optic nerve was intraorbitally crushed and SCNA was injected into the vitreous on the 5th,7th,21th and 28th day after crush,the number of RGC were counted respectively. Results The densities of RGC began to decrease on the 7th day after injury,the number of RGC was 70.2% and 40.5% of normal controls on the 14th and 28th day,respectively .In the group with SCNA injection,RGC densities decreased on the 7th day,but RGC densities were much higher then that of controls on the 14th,21th,and 28th day after injury (Plt;0.01). Conclusions SCNA administered intraocularly at the time of crush of optic nerve can protect RGC from injury and death of the cells. (Chin J Ocul Fundus Dis，2000，16：1-70)
Objective To observe in vitro the protective effect of cranial nerve growthine (CNG) on the optic nerve injured by acute ocular hypertension. Methods Thirty white rabbits were divided into five groups,and 6 in each.The acute ocular hypertension(50 mm Hg) models were established by forcing perfusion of normal saline solution into the anterior chamber sustained for 6 h in one eye,and the contral ateral eye of each rabbit was regard as control.Three rabbits in each group were then treated by CNG 0.2 ml intramuscularly every day.The optic nerve and retina was surgically removed at five different time points (lst,3rd,7th,15th and 30th day) after operation.With the HRP orthograde tracing technique and transmitted electron microscope,the effect of CNG on the optic nerve was observed by the changes of axonal transport and ultrastructure of optic nerve. Results Compare with experimental control groups (25.17plusmn;1.03),HRP reactive products of treated groups (39.79plusmn;2.29) markedly increased after seven days (Plt;0.01).The degeneration of axons in treated groups was relatively lighter after fifteen days and some axons recovered after thirty days. Conclusion CNG might improve the axonal transport and the recovery of axons after the optic nerve injured by acute ocular hypertension. (Chin J Ocul Fundus Dis,2000,16:88-90)