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Neurology 1999;53:177
© 1999 American Academy of Neurology
Articles

Pathologic findings in a steroid-responsive optic nerve infarct in giant-cell arteritis

J. C. Kattah, MD, L. Mejico, MD, G. A. Chrousos, MD, L. E. Zimmerman, MD and H. J. Manz, MD

From the Department of Neurology (Dr. Kattah), University of Illinois College of Medicine at Peoria, IL; and the Departments of Ophthalmology (Drs. Mejico and Chrousos) and Ophthalmology and Pathology (Drs. Zimmerman and Manz), The Center for Sight and Pathology, Georgetown University, Washington, D.C.

Address correspondence and reprint request to Dr. Jorge C. Kattah, Department of Neurology, University of Illinois College of Medicine at Peoria, Box 1649, Peoria, IL 61656-1649; e-mail: kattahj{at}uic.edu

OBJECTIVE: To investigate the pathophysiologic mechanism of optic nerve infarction in giant-cell arteritis (GCA).

BACKGROUND: Previous pathologic reports of optic nerve infarction in GCA involved patients who were blind at the time of death. The optic nerve infarcts were primarily retrolaminar in localization. Simultaneous short ciliary and ophthalmic artery vasculitis was found in all patients.

METHODS: Clinical neurologic and ophthalmologic examination, temporal artery biopsy, and neuroimaging tests were performed in a patient with an anterior ischemic optic neuropathy secondary to GCA. Pathologic examination of the viscera, eye, and brain were performed at autopsy 1 month later.

RESULTS: A prelaminar/retrolaminar infarct was found in this patient. Subsiding vasculitis was limited to the short ciliary arteries, sparing the central retinal, pial, and ophthalmic arteries.

CONCLUSIONS: The authors believe that the visual improvement observed in this patient was the result of preserved, anterior optic nerve collateral circulation, as well as the neuroprotective and anti-inflammatory effect of the corticosteroids.






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