No abstract available.
Optic Nerve Injuries* ; Optic Nerve*

No abstract available.
Optic Nerve Injuries* ; Orbit*

No abstract available.
Gadolinium* ; Optic Nerve Diseases ; Optic Nerve Injuries*

No abstract available.
Gadolinium* ; Optic Nerve Diseases ; Optic Nerve Injuries*

Traumatic optic neuropathy (TON) refers to optic nerve injury resulting from direct and indirect head and facial trauma. The pathogenesis of indirect TON has not been fully elucidated, and the management of TON remains controversial. In this review article, I review the recent literature regarding TON and discuss how to manage indirect TON.
Head ; Optic Nerve ; Optic Nerve Injuries*

We performed full field pattern reversal VEP using UTAS-E 2000, in 87 eyes of the 70 patients with amblyopia(14 eyes) and optic nerve diseases; optic neuritis(21 eyes), optic nerve atrophy(23 eyes), toxic optic neuropathy(15 eyes) and optic nerve injury(14 eyes) from December 1993 to July 1994. This study was carried out to evaluate the relationship of the visual acuity with P1 amplitude, P1 latency, and to compare the latency of P1, and P1-N2 amplitude to each disease group and the normal groups. There was no correlation between the visual acuity and P1 latency, but significant correlation between the visual acuity and P1 amplitude(p<0.01). In the P1 implicit time, optic neuritis, optic nerve atrophy and toxic optic neuropathy patients presented marked delay and amblyopia patients presented moderate delay, but there was no other significant difference in each disease group. Over 50% of each disease group except amblyopia presented P1 destruction. Therefore, the authers concluded that P1 amplitude might not be good parameter in diagnosis of the optic nerve disease because of its variability to the visual acuity, but P1 latency and P1 destruction could be good parameter.
Amblyopia* ; Atrophy ; Diagnosis ; Humans ; Optic Nerve Diseases* ; Optic Nerve Injuries ; Optic Nerve* ; Optic Neuritis ; Visual Acuity

We investigated the efficacy of high dose corticosteroid therapy in the treatment of traumatic optic-neuropathy. We experimentally damaged the optic nerves of six white rabbits with a Hartman mosquito. Three of the rabbits were intravenously injected with 0.25mg/kg dexamethasone every six hours for a 48 hour period. The others were used as controls. In both groups, the optic nerves were removed after one month and stained with Hematoxyline-eosin, then examined microscopically. No histological differences were found in either the control or the experimental group.
Culicidae ; Dexamethasone ; Optic Nerve ; Optic Nerve Injuries* ; Rabbits

We compared the result of 6 patients[group A]treated with high dose steroid only with the result of 14 patients[group B]treated with optic canal decompression after at least 24 hours of high dose steroid therapy without improvement. 4 of 6 patients[66%]in group A and 7 of 14 patients[50%]in group B improved in visual acuity.But 1 of 6 patients[17%] in group A and 6 of 14 patients[43%]in group B had marked improvement in visual function[above 0.02].Of 5 patients with optic canal fracture in orbit CT in group B, all had improved visual function and 4 had marked improvement in visual function. If CT demonstrates bony fragments impinging on intracanalicular optic nerve, or if vision deteriorates or fails to improve during the first 24 hours of high dose steroid and initial visual acuity is no light perception, optic canal decompression is considered effective and valid treatment modality in TON.
Decompression* ; Humans ; Optic Nerve ; Optic Nerve Injuries* ; Orbit ; Visual Acuity

PURPOSE: To evaluate the effect of high dose corticosteroid and optic canal decompression on the traumatic optic nerve injury. METHODS: Twenty six patients who were diagnosed to have traumatic optic nerve injury, were divided into two groups in which one group received corticosteroid therapy while the other group underwent optic canal decompression combined with corticosteroid therapy. RESULTS: Visual acuity increased by > OR =3 lines of LogMAR scale in 47% of the corticosteroid group, in 28% of operation and steroid group, and in 42% of overall cases. But the degree of visual acuity improvement had no difference between two groups(p=0.72). As the patients were divided into two groups based on initial visual acuity such as no light perception and light perception or better, the initial visual acuity did not have influence on the final visual outcome in both corticosteroid group and operation and steroid group(p=0.78, p=0.33). CONCLUSIONS: This result suggest that effect of high dose corticosteroid and optic canal decompression on traumatic optic nerve injury is not different.
Decompression* ; Humans ; Optic Nerve Injuries* ; Optic Nerve* ; Visual Acuity

In order to investigate causative mechanisms of optic neuropathy, retrospective clinical studies including ophthalmologic examination, imaging study, and molecular biologic analyses were performed on 322 patients with optic neuropathy. The causes include hereditary optic neuropathy(71 patients, 22.1%), optic neuritis(66 patients, 20.5%), traumatic optic neuropathy(40 patients, 12.5%), ischemic optic neuropathy(35 patients, 10.9%), compressive optic neuropathy(31 patients, 9.6%), toxic optic neuropathy(23 patients, 7.1%), etc. In 29 patients of bilateral optic atrophy and 18 patients of unilateral optic atrophy, the causative mechanism was not clear. In conclusion, hereditary optic neuropathy was the most common causative mechanism of optic neuropathy in this study. The importance of meticulous history taking and molecular biologic test should be stressed in differential diagnosis of optic neuropathy.
Diagnosis, Differential ; Humans ; Optic Atrophy ; Optic Nerve Diseases* ; Optic Nerve Injuries ; Optic Neuritis ; Retrospective Studies