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August 1990

The Management of Traumatic Optic Neuropathy

Author Affiliations

Baltimore, Md

Arch Ophthalmol. 1990;108(8):1086-1087. doi:10.1001/archopht.1990.01070100042030

In 1963, Walsh and Lindenberg1 microsurgically examined 140 optic nerves from 70 patients who had died after head trauma. These investigators classified changes in the intraorbital, intracanalicular, and intracranial portions of the nerves as primary or secondary lesions. Primary lesions occur at the instant of the blow to the head and consist of the following: (1) hemorrhages in the optic nerve, the dura, and the vaginal sheaths; (2) tears in the nerve, usually in the intracranial segment but occasionally affecting the entire nerve; and (3) contusion necrosis from direct trauma. Secondary lesions can develop seconds, minutes, or even hours after the initial trauma and are basically circulatory in origin. These lesions include edema and necrosis of the optic nerve from systemic and localized circulatory insufficiency, such as that resulting from vasospasm, primary vaso-occlusion, and external compression of vessels. In view of the many factors that may play a role in

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