April 2011
Volume 52, Issue 14
ARVO Annual Meeting Abstract  |   April 2011
Tuberculous Optic Neuropathy: Clinical Presentations And Visual Outcomes
Author Affiliations & Notes
  • Ellen J. Davis
    Casey Eye Institute,
    Oregon Health Sciences University, Portland, Oregon
  • William L. Hills
    Casey Eye Institute,
    Oregon Health Sciences University, Portland, Oregon
  • Kevin L. Winthrop
    Department of Medicine, Division of Infectious Diseases,
    Oregon Health Sciences University, Portland, Oregon
  • Justine R. Smith
    Casey Eye Institute,
    Oregon Health Sciences University, Portland, Oregon
  • Tuberculous Optic Neuropathy Study Group
    Oregon Health Sciences University, Portland, Oregon
  • Footnotes
    Commercial Relationships  Ellen J. Davis, None; William L. Hills, None; Kevin L. Winthrop, None; Justine R. Smith, None
  • Footnotes
    Support  Research to Prevent Blindness
Investigative Ophthalmology & Visual Science April 2011, Vol.52, 2976. doi:
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      Ellen J. Davis, William L. Hills, Kevin L. Winthrop, Justine R. Smith, Tuberculous Optic Neuropathy Study Group; Tuberculous Optic Neuropathy: Clinical Presentations And Visual Outcomes. Invest. Ophthalmol. Vis. Sci. 2011;52(14):2976.

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      © ARVO (1962-2015); The Authors (2016-present)

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Ocular tuberculosis is a common cause of blindness globally. In the world literature, reports of optic nerve involvement total only 7 individuals. We sought to describe clinical presentation and ocular outcome of tuberculous optic neuropathy in a large international cohort of patients.


Cases of tuberculous optic neuropathy were identified by web-based survey of the International Uveitis Study Group, American Uveitis Society, Association of Proctor Fellows and North American Neuro-Ophthalmology Society. Clinical data, including demographic variables, disease characteristics, management and visual outcomes were collected retrospectively.


Fifty patients with tuberculous optic neuropathy from 10 countries were identified. Tuberculosis was confirmed by identification of acid-fast bacilli in 3 cases, and presumed in 47 cases, on the basis of: positive PPD or γ-interferon release test; response to antimicrobial therapy: and/or radiological signs of pulmonary infection. For 63 affected eyes, presentation was with optic nerve edema (24%), papillitis (22%), optic neuritis (19%), optic nerve tubercles (16%), neuroretinitis (14%), compressive optic neuropathy (8%) and/or anterior ischemic optic neuropathy (3%). Other ocular manifestations included uveitis (79%), choroidal granuloma (14%), orbital apex syndrome (13%) and/or retinal detachment (6%). Initial visual acuity was ≤ 20/200 in 24 eyes (38%) and ≥ 20/50 in 29 eyes (46%). Within one year of presentation, visual acuity was ≤20/200 in 6 eyes (10%) and ≥ 20/50 in 45 eyes (71%). Visual field defects, noted in 31 eyes, recovered in 42%. For 96% of the 50 patients, treatment involved combinations of rifampin, isoniazid, pyrazinamine and ethambutol; 62% of patients also received systemic or locally injected corticosteroids. There was no significant difference in achieving visual acuity ≥ 20/50 for eyes that were treated with corticosteroid (71.9%) versus those not so treated (86.7%) (p>0.05, Fisher exact test).


In a large group of patients with tuberculous optic neuropathy, the most common signs were optic nerve edema, papillitis and optic neuritis. Visual outcomes were good, and were not impacted by the use of corticosteroid therapy.Tuberculous Optic Neuropathy Study Group Members: S-P Chee; E.T. Cunningham; E.M. Graham; Y. Guex-Crosier; A.M. Mansour; A.A. Okada; H. Petrushkin; J.A. Leavitt; S.R. Rathinam; S. Tow; I. Tugal-Tutkun

Keywords: optic nerve • bacterial disease • inflammation 

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