Objective To observe the ocular manifestations and therapeutic effect of multiple sclerosis (MS) and neuromyelitis optica (NMO) with ocular symptoms.Methods The clinical data of 107 patients who was diagnosed with MS and NMO with ocular symptoms in our hospital were retrospectively analyzed, including 81 MS patients and 26 NMO patients.The counting of erythocytes and leukocyte，protein content and oligoclonal bands were detected by MRI and cerebrospinal fluid (CSF) in order to ensure the clinical diagnosis with MS and NMO. All the patients had undergone regular ophthalmologic examination of visual acuity，slit lamp microscope and fundus examination.In addition，visual field and visual evoked potential (VEP) examination were performed to analyze the clinical characteristics of ocular manifestations.The patients were received therapy with large dose methylprednisolone or activating blood and dissolving stasis and trophic nerve by chinese medicine. The effects of three methods on ocular manifestations were analyzed. All the patients were followed up for one month to five years. Results Among 81 MS patients，retrobulbar neuritis occurred in 24 patients (29.6%), the other common symptoms included paralytic strabismus and diplopia（30.3%）. Among 26 NMO patients，acute papillitis occurred in 12（46.2%），while retrobulbar neuritis occurred in 14 (53.8%). The most common symptom of both MS and NMO was impaired vision and high abnormal rate. The results of MRI showed that demyelinating lesions beside ventricle was the most performance in MS patients，while abnormalities in spinal cord were found in NMO patients.The results of CSF showed that the positive oligoclonal bands was 75.3% and 19.2% in MS and NMO patients respectively. The potential time delay and (or) amplitude declination were observed by VEP. Large dose methylprednisolone can improve vision and diplopia in a short period.Conclusion The abnormal ocular manifestations of MS and NMO patients are common and complicated. Ocular symptoms has important reference value in the early diagnosis of MS and NMO.
ObjectiveTo observe the concentration of plasma endothelin (ET-1) in patients with nonarteritic anterior ischemic optic neuropathy(NAION) and investigate the relationship between ET-1 and NAION.MethodsThe plasma levels of ET-1 in 41 patients with NAION and 15 age-matched normal control subjects were measured by radioimmuoassay (RIA). The patients with NAION were divided into high papilloedema group, light papilloedema group, and recovery group according to the degree of papilloedema; and were divided into group1 (within 14 days), 2 (within 15-30 days), 3 (within 31-60 days), and 4 (within 61-180 days) according to the disease course. The plasma levels of ET-1 in different groups were detected and compared.ResultsThe plasma level of ET-1 in patients with NAION was significantly higher than that in the normal subjects (t=5.02，P＜0.05）and there was no obvious difference in NAION patients with different genders.There were significant differences of the plasma level among the groups with different degree of papilloedema（F=4.65，P＜0.05）. ET-1 plasma level gradually decreased as the disease course increased, and there were significant differences among the groups with different disease course（F=4.29，P＜0.05）. The difference of plasma level of ET-1 between Group 13 with corresponding disease courses and the control group was significant respectively(t1=5.92，t2=3.47，t3=2.18， P1lt;0.01, P2lt;0.05, P3lt;0.05)ConclusionThe plasma level of ET-1 in patients with NAION may be related to the degree of papilloedema lesion and disease courses. (Chin J Ocul Fundus Dis, 2005,21:156-158)
Ras homolog family (Rho)/ Rho-associated coiled-coil kinase (ROCK) signaling pathway widely exists in human and mammal cells, which is closely related to inhibition of repair after optic nerve damage. The expression level of Rho/ROCK signaling pathway-related proteins is up-regulated in glaucoma, and related with the death of retinal ganglionic cell (RGC) and the axon activity. ROCK inhibitors can protect the surviving RGC and promote axon extension with a dose-dependent manner. ROCK inhibitors also can inhibit glial scar formation, lower intraocular pressure and inhibit inflammatory response to some degrees. Rho/ROCK signaling pathway correlates with the optic nerve disease progression, and ROCK inhibitors hope to become a new therapeutic drug.