Traumatic Optic Neuropathy Workup

Neuroimaging studies (computed tomography [CT] scanning or magnetic resonance imaging [MRI]) are an important part of the assessment when traumatic optic neuropathy (TON) is suspected. In the post-trauma setting, CT scanning is the preferred modality for demonstrating the presence of an optic canal fracture, a displaced bony fragment impinging upon the optic nerve, a metallic foreign body in the orbit, orbital emphysema, or an optic nerve sheath hematoma. A brain and orbit MRI may be useful in certain settings to delineate the extent of hemorrhage involving the neurovascular structures at the orbital apex or to rule out inflammatory or infiltrative causes for an optic neuropathy. The vast majority of patients with TON suffer an indirect injury to the optic nerve within the optic canal, and neuroimaging studies typically demonstrate no abnormalities of the anterior visual pathways, although a fracture in the region of the optic canal may be seen.

A retrospective study by Bodanapally et al indicated that, using diffusion-weighted imaging (DWI), hyperintensity of the optic nerve resulting from diffusion restriction can aid in the diagnosis of TON. ^[3]

A retrospective study by Reddy et al indicated that in patients with TON, CT scan findings of intraconal hematoma and hematoma along the optic nerve are risk factors for poor visual acuity at hospital admission. ^[4]

See the list below:

• Visual field perimetry

  • Automated perimetry can be obtained only in patients who retain adequate vision/acuity. Patients with poor visual acuity (worse than 20/200) may be assessed with Goldmann perimetry or with confrontational visual field testing.

  • No visual field loss pattern is pathognomonic for traumatic optic neuropathy (TON), although a dense central scotoma is characteristic. Recovery of optic nerve function may be documented via serial visual field testing.

• Visual evoked potential (VEP)

  • VEP can be helpful to document the presence of TON in unresponsive patients or in cases with concomitant ocular injuries. Patients can also be followed with serial VEP examinations to document recovery of function when clinical parameters are equivocal.

  • VEP is not considered essential in making the diagnosis of TON, and logistically, the ability to perform a neurophysiological evaluation is often hindered by the inability to transport the trauma patient to the neurophysiology laboratory.

  • In unilateral cases of TON, a flash VEP amplitude ratio (affected side/normal side) greater than 0.5 appears predictive of a favorable, long-term visual outcome. Visual recovery is considered unlikely when VEP amplitudes are nonrecordable.

• Retinal nerve fiber layer (NFL) imaging: Scanning laser polarimetry and optical coherence tomography can be used to assess and monitor retinal NFL axonal loss during the period of follow-up.

Traumatic optic neuropathy (TON) is based on a clinical diagnosis of optic nerve dysfunction supported by a recent history of trauma to the head. In an acute setting following trauma, the diagnosis may be delayed if the patient is unconscious and a formal visual acuity assessment cannot be performed. In a conscious, cooperative patient, the diagnosis of TON should be verified by testing the patient for an abnormal visual acuity, an ipsilateral afferent pupillary defect (APD), impairment of color vision, and a visual field defect on formal perimetry.

Visual acuity

Even in an acute trauma setting, patients should have a visual acuity assessment as soon as possible. This can be performed with a Snellen eye chart (which measures distance vision) or a near vision card. If the patient cannot read the top letter on the eye chart, the visual acuity may be recorded with the following nomenclature (in order of decreasing visual acuity): counting fingers vision, hand motion perception, light perception (LP), or no light perception (NLP).

Pupil examination

The pupil examination assesses the size of both pupils, the response of the pupils to light and near stimulation, and an evaluation for a relative afferent pupillary defect or APD (swinging-flashlight test). The swinging-flashlight test compares the pupillary reaction to light between the two eyes; normally, both pupils should constrict equally to light, and the constriction should be maintained as the light is rapidly switched between the two pupils. An eye with a unilateral optic nerve injury will demonstrate an APD, verifying the presence of TON. In the rare case of a bilateral TON, a relative APD may not be seen if the injury is symmetric between the 2 sides, and both pupils may be dilated and nonreactive to light if the injury is profound.

Funduscopic examination

The funduscopic examination can be performed with the use of a direct ophthalmoscope, indirect ophthalmoscope, or the slit-lamp biomicroscope. Because the location of the injury in most TON cases is within the posterior orbit or the optic canal, the optic disc typically appears normal on funduscopic examination on initial diagnosis. Optic nerve atrophy usually appears 3-4 weeks after the traumatic event, and the disc acquires a diffuse pallor. Rarely, optic nerve changes can be seen with direct injuries to the retrobulbar section of the optic nerve, presenting as an avulsed optic nerve head or optic disc swelling with surrounding hemorrhage.

Cadaver studies have not demonstrated consistent histopathologic findings in traumatic optic neuropathy, suggesting multiple mechanisms of injury in patients with TON. Gross pathologic changes that have been reported include hematomas within the optic nerve sheath and occasionally areas of visible necrosis. Microscopic findings include interstitial hemorrhage, fibrosis of the pial septa, and a chronic inflammatory infiltrate by lymphocytes, plasma cells, and iron-laden macrophages. One case demonstrated degeneration of axons with loss of myelin in a triangular section consistent with damage to the penetrating vessels supplying the infracted region.

With time, loss of astrocyte support appears to occur within the optic nerve in TON injuries, followed by replacement of the axons with microglia. Based on the histopathologic findings in TON, axonal loss appears to occur either through shearing forces, hemorrhagic infarction, direct compression of the nerve fibers from an extrinsic nerve sheath hematoma, or a combination of these mechanisms.