Excerpt from Traumatic Optic Neuropathy
Synonyms, Key Words, and Related Terms: traumatic optic neuropathy, optic neuropathy, optic nerve injury, vision loss, trauma, frontal trauma, orbital trauma, optic nerve avulsion, optic nerve transection, diffuse orbital hemorrhage, localized orbital hemorrhage, optic nerve sheath hematoma, orbital emphysema, TON
Traumatic optic neuropathy (TON) refers to an acute injury of the optic nerve secondary to trauma. The optic nerve axons may be damaged either directly or indirectly and the visual loss may be partial or complete. An indirect injury to the optic nerve typically occurs from the transmission of forces to the optic canal from blunt head trauma. This is in contrast to direct TON, which results from an anatomical disruption of the optic nerve fibers from penetrating orbital trauma, bone fragments within the optic canal, or nerve sheath hematomas.
Problem
Patients with TON can present with a variable degree of vision loss (decreased visual acuity, visual field abnormalities, or loss of color vision). Most cases (up to 60%) present with severe vision loss of light perception (LP) or worse. In the acute phase, the optic nerve usually appears normal on funduscopic examination, but optic nerve atrophy is often seen 3-6 weeks after the injury.
Frequency
The incidence of TON in the setting of a closed traumatic head injury in various studies ranges from 0.5-5%. The vast majority of TON cases are seen in males (up to 85%), with a mean age of 34 years. Motor vehicle and bicycle accidents account for the majority of causes, followed by falls and assaults. TON has also been associated with penetrating orbital trauma (eg, stab wounds, pellet and gunshot wounds, foreign bodies) and recreational sports (eg, paint ball injury).
Pathophysiology
The pathophysiology of TON is thought to be multifactorial, and some researchers have also postulated a primary and secondary mechanism of injury. In indirect TON cases, the injury to the axons is thought to be induced by shearing forces that are transmitted to the fibers or to the vascular supply of the nerve. Studies have shown that forces applied to the frontal bone and malar eminences are transferred and concentrated in the area near the optic canal. The tight adherence of the optic nerve’s dural sheath to the periosteum within the optic canal is also thought to contribute to this segment of the nerve being extremely susceptible to the deformative stresses of the skull bones. Such injury leads to ischemic injury to the retinal ganglion cells within the optic canal.
A secondary mechanism can result in optic nerve swelling after the occurrence the acute injury. The optic nerve swelling can exacerbate retinal ganglion cell degeneration by further compromising the vascular blood supply, either through a rise in intraluminal pressure or reactive vasospasm. These secondary mechanisms, in theory, form the rationale for optic canal decompression via medical (ie, steroids) or surgical means (ie, bony decompression). Finally, the intracranial segment of the optic nerve may be damaged by forces delivered to the axons by the shifting of the brain following head trauma. With this mechanism, the nerve fibers may be injured against the falciform dural fold or through a shearing force where the nerve becomes fixed as it enters the intracranial opening of the optic foramen.
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