Optic disc morphology after arteritic anterior ischemic optic neuropathy

Citation
Ss. Hayreh et Jb. Jonas, Optic disc morphology after arteritic anterior ischemic optic neuropathy, OPHTHALMOL, 108(9), 2001, pp. 1586-1594
Citations number
75
Categorie Soggetti
Optalmology,"da verificare
Journal title
OPHTHALMOLOGY
ISSN journal
01616420 → ACNP
Volume
108
Issue
9
Year of publication
2001
Pages
1586 - 1594
Database
ISI
SICI code
0161-6420(200109)108:9<1586:ODMAAA>2.0.ZU;2-1
Abstract
Objective: To evaluate the appearance of the nerve head inpatients after gi ant cell arteritis-induced arteritic anterior ischemic optic neuropathy (A- AION). Design: Noncomparative clinical case series. Patients: The study comprised 29 patients who presented with unilateral A-A ION and temporal artery biopsy-proven giant cell arteritis. Stereoscopic op tic disc photographs, taken of both the affected and unaffected eyes at the onset of the disease and after a follow-up period of 20.10 +/- 25.36 month s (median, 11 months; range, 2-102 months), were morphometrically evaluated . Main Outcome Measures: Size and shape of the optic disc, neuroretinal rim, optic cup, and alpha and beta zones of parapapillary atrophy. Results: In t he eyes after A-AION, at the end of the study, the neuroretinal rim was sig nificantly (P = 0.002) smaller, and the optic disc cup area was significant ly (P = 0.001) larger than those of the contralateral unaffected eyes. Alph a zone and beta zone of parapapillary atrophy did not vary significantly (P > 0.50). Conclusions: A-AION, like glaucomatous optic neuropathy, results in neurore tinal rim loss and optic disc cupping. However, in contrast to glaucoma, A- AION is not associated with an enlargement of parapapillary atrophy. The re asons and mechanisms responsible for these similarities and dissimilarities are discussed. Marked clinical, morphologic, and histopathologic similarit ies in optic disc cupping and loss of neuroretinal rim between A-AION and g laucomatous optic neuropathy are highly suggestive of a common mechanism fo r the development of the two diseases (i.e., ischemia of the optic nerve he ad). The subject is discussed at length. (C) 2001 by the American Academy o f Ophthalmology.