Abstract

Indirect traumatic optic neuropathy (ITON) is a condition that is often associated with traumatic brain injury and can result in significant vision loss due to degeneration of retinal ganglion cell (RGC) axons at the time of injury or within the ensuing weeks. We used a mouse model of eye-directed air-blast exposure to characterize the histopathology of blast-induced ITON. This injury caused a transient elevation of intraocular pressure with subsequent RGC death and axon degeneration that was similar throughout the length of the optic nerve (ON). Deficits in active anterograde axon transport to the superior colliculus accompanied axon degeneration and first appeared in peripheral representations of the retina. Glial area in the ON increased early after injury and involved a later period of additional expansion. The increase in area involved a transient change in astrocyte organization independent of axon degeneration. While levels of many cytokines and chemokines did not change, IL-1α and IL-1β increased in both the ON and retina. In contrast, glaucoma shows distal to proximal axon degeneration with astrocyte remodeling and increases in many cytokines and chemokines. Further, direct traumatic optic neuropathies have a clear site of injury with rapid, progressive axon degeneration and cell death. These data show that blast-induced ITON is a distinct neuropathology from other optic neuropathies.

Highlights

  • Indirect traumatic optic neuropathy (ITON) is a condition in which the optic nerve (ON) degenerates in the absence of a penetrating injury

  • We have developed a model of ITON in which an air-blast is directed at the eye to avoid causing a traumatic brain injury (TBI) and associated cortical visual system damage that could confound results (Hines-Beard et al, 2012; Bernardo-Colon et al, 2018)

  • The goal of this study was to examine the pathophysiology of axon degeneration after blast-induced ITON in order to better inform the development of treatment strategies

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Summary

Introduction

Indirect traumatic optic neuropathy (ITON) is a condition in which the optic nerve (ON) degenerates in the absence of a penetrating injury. It is a rare condition in the general U.S population but occurs in 0.5–5.0% of patients with a traumatic brain injury (TBI) (Steinsapir and Goldberg, 1994; Sarkies, 2004). Four to six weeks after injury the optic disk typically develops pallor, indicative of atrophy (Agrawal et al, 2013). During this time approximately 10% of ITON patients exhibit further vision loss (Yu-WaiMan, 2015). There are no therapies that have been shown to be more effective than observation alone

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