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Traumatic Optic Neuropathies

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Abstract

Deceleration injury directed to the ipsilateral forehead or to the midface region from motor vehicle and bicycle accidents is the most common cause of traumatic optic neuropathy. Optic nerve injuries are usually classified as being direct or indirect injuries. Direct injuries involve an external object penetrating the optic nerve, whereas indirect injuries occur when the force of collision is transferred to the skull and partially absorbed by the optic nerve. The most common optic nerve injuries involve indirect injury to the posterior or intracanalicular portion of the optic nerve. In addition to head trauma, traumatic optic neuropathy can also be a complication of ocular or endoscopic sinus surgical procedures.

Decreased best corrected visual acuity and a relative afferent pupillary defect (RAPD), without other ocular pathology that could account for the visual loss, would support the diagnosis of traumatic optic neuropathy affecting the posterior orbital, intracanalicular, or intracranial portion of the optic nerve. Optical coherence tomography is able to assess and monitor axonal loss after traumatic optic neuropathy. If the patient is unconscious or if the RAPD is absent in bilateral cases, visual evoked potentials may help in confirming the suspicion of traumatic optic neuropathy, especially in comatose patients. Neuroimaging may also help in localizing the site of optic nerve injury.

There is a relatively high rate of spontaneous visual recovery in traumatic optic neuropathy. No convincing data yet supports that high-dose methylprednisolone nor optic nerve sheath decompression provides any additional visual benefit over observation alone. Corticosteroids may also inhibit inherent neuroprotective processes. The management of each case needs to be assessed on an individual basis.

Strategies for optic nerve rescue and regeneration include peripheral nerve grafts and stem cell transplantation into the retina, which requires the creation of an environment permissive to axon regrowth and the promotion of axon regrowth with nerve growth factors. These transplanted cells then need to form functional synapses with retinal interneurons and their target neurons in the brain, preserving the retinotopic organization of the visual pathway. Neuroprotective agents can also enhance retinal ganglion cell survival.

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Chan, J.W. (2014). Traumatic Optic Neuropathies. In: Chan, J. (eds) Optic Nerve Disorders. Springer, New York, NY. https://doi.org/10.1007/978-1-4614-0691-4_5

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