Chapter 26 The first known written description of traumatic optic neuropathy (TON) comes from Hippocrates over 2400 years ago1: “There is a dimming of vision in those wounds which are in the brow and slightly above. In as much as the wound is more recent, they see better, but as the scar matures there is further darkening.” Traumatic optic neuropathy should be suspected with any dysfunction of afferent vision following trauma, which is not attributable to injury to the globe. Traumatic optic neuropathy can be classified by mechanism or location. Direct traumatic optic neuropathy involves injury with direct impact to the optic nerve or its sheath by a foreign body that has penetrated the globe, orbit, or cranium, or from a displaced fracture or spicule of bone in the optic canal region. Penetrating injuries are usually due to gunshot pellets or BBs, but can also be due to wood or sharp metal, for example, a knife, pencil, or tree branch. There is actual disruption of anatomic structures of the optic nerve, anywhere from the scleral canal to the chiasm. These disruptions may include lacerations, bone fragments, and may be associated with vascular ischemia or infarction, or hemorrhage into the optic nerve or its sheath. Direct TON tends to have a worse prognosis than indirect TON and generally responds less to treatment. Immediate blindness after direct traumatic optic neuropathy is usually permanent, although cases of significant visual recovery have been reported both spontaneously and following optic canal decompression.2,3 Recovery has even occurred in the case of an initial nonrecordable visual evoked response.3 Indirect traumatic optic neuropathy presents as optic nerve dysfunction, without direct disruption of anatomic structures or the surrounding associated tissues. Percussion energy is transmitted to the axons of the retinal ganglion cells causing injury and secondary necrosis of the axons. The mechanisms responsible for such injury are speculative and may include contusion or shear of the axons with disruption of axoplasmic flow; axonal compression by hemorrhage and/or swelling impeding axoplasmic flow; or vascular compromise from compression by hemorrhage or swelling, vasospasm, or vascular occlusion reducing blood flow and causing metabolic ischemia. The optic nerve originates at the lamina cribrosa within the posterior sclera. Avulsion (or evulsion) is the “forceful backward dislocation of the optic nerve from the scleral canal without any break in continuity of the adjacent coats of the globe” (Fig. 26–1).4 Most often, optic nerve avulsion is due to nonpenetrating injuries, such as a finger jabbed into the orbit, but may also occur with penetrating injuries. Complete avulsion of the optic nerve occurs when the retina and vitreous are totally separated from the optic nerve head, and the lamina cribrosa is torn from its attachments to the sclera and choroid. The retinal blood vessels may be partly or totally disrupted.5 With complete optic nerve avulsion, total blindness occurs. If only a partial avulsion, some vision may remain. In general, prognosis for visual recovery in optic nerve avulsion is poor. Although megadose systemic corticosteroids may be attempted, no form of therapy has been documented to be efficacious for optic nerve avulsion. FIGURE 26–1 Optic nerve head avulsion with hemorrhage over the optic disk. The intraorbital optic nerve is 25 mm in length and has an excess length of 7 mm, compared with the 18 mm distance from the orbital apex to the posterior globe. This excess gives the nerve its sinusoidal shape and also protects the nerve by allowing it to move away from penetrating objects or to straighten in the presence of axial proptosis, rather than stretching or tearing the axonal fibers. The orbital optic nerve receives its blood supply from the central retinal artery and the pial perforating vessels. The central retinal artery supplies only the anterior orbital optic nerve. Within the orbit, the optic nerve can be compressed by orbital or optic nerve sheath hemorrhage, causing progressive visual loss. The intracanalicular segment of the optic nerve, ~6to 10 mm in length, is the section most likely to be damaged by indirect trauma, usually closed head injury. Pressure from blunt trauma to the frontal bone may be transmitted through the sphenoid bone to the ipsilateral optic canal injuring the nerve. Also, rapid acceleration-deceleration movements subject the optic nerves, fixed within the optic canals of the lesser sphenoid wings, to shearing and stretching forces from the freely moving orbital and intracranial contents. Thus, major stress points for the nerve occur at the orbital apex and at the intracranial entrance to the optic canal. The intracanalicular nerve receives its blood supply from penetrating pial vessels, derived from the ophthalmic and carotid arteries, which can be sheared and avulsed by acceleration-deceleration forces. The ophthalmic artery and postganglionic sympathetic fibers can also be damaged within the canal, as they accompany the optic nerve. The intracanalicular optic nerve may also be subject to direct trauma as a potential complication of sinus surgery, due to the close relationship of the posterior ethmoid and sphenoid sinuses to the intracanalicular optic nerve.6,7 About 4% of normal persons have absence of the bony wall separating the optic nerve from the sphenoid sinus. Thus, only sinus mucosa and dura separate the optic nerve from the sinus. These people are at particular risk of inadvertent direct optic nerve trauma during sphenoid-ethmoidal sinus surgery. Indirect injury to the intracranial portion of the optic nerve is rare, because it is relatively mobile, similar to the intraorbital optic nerve. However, the intracranial optic nerve may be injured by the falciform dural fold as a result of the movement induced by forces shifting the brain during impact. Contusion hemorrhage or necrosis can be induced by frontal impact directed toward the sella by the posterior gyri recti.8 Sudden stretching of the nerve may cause tears or contusions, particularly as it exits the optic canal, due to its fixation there.8 Loss of consciousness may be present in 50 to 72% of patients with optic nerve trauma. Evaluation should be performed as soon as possible and should not be deferred. Following head trauma, ~5% of all patients show injury to some portion of the visual system.9 Indirect optic nerve trauma is much more common than direct trauma to the nerve.10 Motor vehicle accidents (45%) account for the largest single cause of traumatic optic neuropathy, whereas, falls (27%) and assault (13%) account for lesser but significant causes. Orbital and optic nerve sheath hemorrhage occur in ~10% of cases. Patients may complain of loss of vision noticed immediately after trauma or after becoming conscious. Visual loss after an interval is less common, and should suggest the possibility of intrasheath hemorrhage compressing the optic nerve. In alert and communicative patients, an effort should be made to document visual acuity with a Snellen chart and/or Rosenbaum near card using appropriate correction aids. Although visual acuity can range from 20/20 to no light perception, 50% of patients have visual acuity of light perception or worse. Color may be tested by checking for red desaturation or by using standard Ishihara pseudoisochromatic color plates. Typical visual field defects include central scotomas and/or nerve fiber bundle arcuate defects. Defects that respect the vertical midline, bitemporal defects or homonymous defects, suggest injury at the chiasm or retrochiasmal pathways. It is possible to have an associated tear or contusion of the chiasm from trauma, causing bitemporal field loss. The afferent pupillary defect is probably the most reliable sign of optic nerve injury in unilateral or asymmetric bilateral disease. Relative afferent pupillary defects can be quantified with cross-polarizing or neutral density filters. With bilaterally symmetric optic nerve injury, the pupil responses will be equal, but sluggish, and there may be light-near dissociation. The optic disc and fundus should be evaluated with a dilated exam if approved by the treating physician, using a short-acting mydriatic agent.
TRAUMATIC OPTIC NEUROPATHY
CLASSIFICATION
CLASSIFICATION BY MECHANISM
Direct Traumatic Optic Neuropathy
Indirect Traumatic Optic Neuropathy
CLASSIFICATION BY LOCATION
Optic Nerve Head
Orbital Optic Nerve
Intracanalicular Optic Nerve
Intracranial Portions of the Nerve
URGENCY OF EVALUATION
DIAGNOSIS
DEMOGRAPHICS
SYMPTOMS
SIGNS
Loss of Visual Acuity, Color Perception, or Contrast Sensitivity
Visual Field Defect
Pupils
Optic Disc and Fundus
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