High-dose steroid therapy of traumatic optic neuropathy may fail to protect the optic nerve permanently

Citation
Z. Mariak et al., High-dose steroid therapy of traumatic optic neuropathy may fail to protect the optic nerve permanently, NEURO-OPHTH, 21(4), 1999, pp. 255-260
Citations number
16
Categorie Soggetti
Optalmology
Journal title
NEURO-OPHTHALMOLOGY
ISSN journal
01658107 → ACNP
Volume
21
Issue
4
Year of publication
1999
Pages
255 - 260
Database
ISI
SICI code
0165-8107(199906)21:4<255:HSTOTO>2.0.ZU;2-Z
Abstract
Background: The optimal treatment of traumatic optic neuropathy (TON) is st ill unresolved due to the poor understanding of the pathology involved and the relatively small number of cases in the published clinical series. It i s currently held that the results of conservative treatment with high-dose corticosteroids are similar to those obtained with surgical decompression. Purpose: To assess the late results of conservative treatment for traumatic optic neuropathy. Patients and methods: 15 patients (3 women and It men, a ge 14-64 years) who sustained a direct injury to the optic nerve as a conse quence of closed head trauma. All were treated conservatively with high-dos e dexamethasone therapy. Ten patients presented for follow-up examination 3 -11 years after the injury, on average 5.3+/-2.4 years (SD). A full ophthal mologic examination and color-coded Doppler (CCD) study of the orbital vess els was performed in all subjects. Results: Full blindness of the affected eye, persisting since the injury, was noted in six patients. Their visual a cuity did not improve in spite of vigorous treatment and their eyes remaine d without sight at the follow-up examination. The finding of an absence of flow in central retinal arteries at follow-up suggests structural damage to the nerve. Moreover, in five of these patients, distinct features of eyeba ll atrophy had evolved between the time of injury and the follow-up examina tion. Four patients, who on admission presented only with the ability to pe rceive light, responded to 2-3 weeks of steroid therapy with improvement of visual acuity to 3/50, 5/50, 5/10, and 5/7 After 4-6 years, however, the v isual acuity of all of these patients had deteriorated, resulting in nearly total blindness in one case, light perception in two, and 1/50 in the four th. Optic nerve atrophy was diagnosed in all of the affected eyes. Conclusi on: Conservative treatment of TON, even if giving transient improvement in visual function, may not be reliable in providing permanent relief from the sequelae of traumatic optic neuropathy.