Traumatic optic neuropathy (TON) is a condition in which a strong blow to the forehead or frontal region, especially the eyebrow area, causes transmitted force (force that propagates rather than direct impact) to act on the optic canal, resulting in contusion of the optic nerve. Importantly, it is not necessarily associated with optic canal fracture; severe optic nerve damage can occur even in cases without fracture.
Typically, it develops after blunt trauma to the superolateral eyebrow area, so most cases show subcutaneous hemorrhage or contusion lacerations on the lateral side of the eyebrow.
Classification by pathophysiology is as follows:
TON is reported to occur in 0.5–5% of all head injuries. Common mechanisms include traffic accidents, sports injuries, and falls, with a typical pattern of blunt trauma to the superolateral brow. Only a minority of cases show optic canal deformity on plain X-ray or CT.
In the 2021 Beirut port explosion, 39 patients (48 eyes) were evaluated ophthalmologically. Orbital fractures were found in 14 eyes (29.2%), open globe injuries in 10 eyes (20.8%), and 53.8% required surgical intervention 1). Explosive trauma can also cause TON (see “Causes and Risk Factors” section for blast-induced traumatic optic neuropathy).
Traumatic optic neuropathy is a condition in which the optic nerve is damaged at the optic canal due to indirect force from blunt trauma to the brow area. In contrast, optic nerve head avulsion is a severe injury where the optic nerve is physically torn at the level of the lamina cribrosa, and the avulsion site can be seen on fundus examination immediately after injury. A key distinguishing feature is that the fundus is usually normal immediately after injury in traumatic optic neuropathy.
The main symptom is visual impairment that occurs immediately after injury.
Understanding the temporal changes after injury is important for diagnosis and management.
| Time | Fundus Findings | OCT Findings |
|---|---|---|
| Immediately after injury | Usually normal (no fundus abnormalities) | Acute changes are subtle |
| 2 weeks after injury | Optic disc changes begin to appear | GCC thickness becomes thinner and falls below normal range |
| 6–8 weeks after injury and later | Progressive optic atrophy and optic disc pallor | GCC thickness stabilizes around 30–50 days |
Relative afferent pupillary defect (RAPD) is the most important objective finding in unilateral or asymmetric bilateral cases, and is confirmed as Marcus-Gunn pupil (positive swinging flashlight test in the affected eye).
It cannot be ruled out. Immediately after injury, the fundus is often normal. Optic atrophy and optic disc pallor appear 6–8 weeks after injury, and thinning of GCC thickness on OCT is observed from about 2 weeks after injury. A normal fundus immediately after injury is not grounds for excluding the diagnosis; functional assessments such as RAPD (swinging flashlight test) are important.
Blunt trauma to the superolateral brow is the most common mechanism of injury. The impact propagates through the optic canal, causing vasogenic edema within the optic nerve parenchyma (see Pathophysiology section for details on pathophysiology).
Main causes:
Shock waves from blast overpressure propagate through ocular structures to the optic nerve, causing shear forces and stress that damage optic nerve fibers. It is characterized by the absence of penetrating injury or significant blunt trauma, and optic neuropathy can occur even without visible external signs of injury.
The most important test for diagnosing optic neuropathy is the swinging flashlight test. In the affected eye, the pupil dilates when light is shone, confirming a positive relative afferent pupillary defect (RAPD) (Marcus Gunn pupil). Even if visual acuity and fundus findings are good, this finding indicates the presence of optic nerve injury.
The following tests are used in combination for evaluation.
| Test | Main Findings | Notes |
|---|---|---|
| Swinging flashlight test | RAPD positive (most important) | False negative possible in cases with equal bilateral impairment |
| Visual acuity and visual field tests | Central scotoma, concentric narrowing, horizontal hemianopia | Other functional abnormalities may be latent even if normal |
| Plain X-ray (optic canal view) | Optic canal fracture or deformity | Still used as an adjunct even after the spread of CT |
| CT (Orbit/Head) | Optic canal fracture, bone fragment position, deformity | About 20% of fractures are missed |
| MRI (STIR sequence) | Optic nerve swelling, intra-sheath changes | Useful for excluding surgical lesions (e.g., sheath hematoma) |
| OCT | Progressive thinning of GCC thickness over time | Start monitoring 2 weeks after injury |
| VEP (Visual Evoked Potential) | Conduction delay, amplitude reduction | Objective assessment of optic nerve function |
| Spatial contrast sensitivity | Abnormal even when high-contrast visual acuity is normal | High sensitivity for detecting functional impairment |
Yes. In traumatic optic neuropathy, even if visual acuity is relatively preserved, visual field abnormalities, decreased contrast sensitivity, color vision abnormalities, and positive RAPD may be present. Evaluation using only high-contrast visual acuity risks missing the impairment. Assessment with RAPD (swinging flashlight test) is essential.
Early diagnosis (within 24–48 hours after injury) and prompt and appropriate reduction of optic nerve parenchymal edema significantly affect prognosis.
Pharmacotherapy
Steroid pulse therapy: Intravenous administration of prednisone equivalent 1,000 mg/day for 2–3 days is a standard option.
High-dose steroid therapy: Systemic administration of prednisolone equivalent 80–100 mg/day. Used as an alternative similar to pulse therapy.
Hyperosmotic agents: Intravenous infusion of Glycerol® or D-mannitol 300–500 mL for 3–7 days to reduce optic nerve parenchymal edema.
Tapering: Gradually reduce steroids while monitoring visual progress.
Surgical Treatment
Optic canal decompression: There is much controversy regarding the indications for open surgery. Many believe that reducing edema within the optic nerve parenchyma is difficult to achieve surgically, except in cases where the optic nerve is clearly compromised due to marked deformation of the optic canal or significant displacement of bone fragments.
Transnasal endoscopic approach: In recent years, a minimally invasive transnasal endoscopic approach has become feasible.
Limited indications: Cases with marked deformation of the optic canal or significant displacement of bone fragments are considered appropriate for surgery.
The IONTS compared steroid therapy, optic canal decompression, and observation, and none showed a significant advantage over the others 2). Treatment selection should be individualized based on the patient’s general condition, severity of injury, and presence of fractures.
In the IONTS (International Optic Nerve Trauma Study), none of steroid therapy, optic canal decompression, or observation showed a significant advantage. Severe cases where loss of light perception does not recover quickly after injury tend to have poor treatment response. Steroid pulse therapy is performed to reduce edema within the optic nerve parenchyma, but its effectiveness varies greatly among individuals, and the indication should be determined by comprehensively considering the patient’s general condition, mechanism of injury, and severity.
The main cause of optic nerve damage is thought to be vasogenic edema within the optic nerve parenchyma (tissue corresponding to the white matter of the brain) caused by blunt trauma. This is similar to brain edema after head trauma, and direct damage to optic nerve fibers in the optic canal due to hematoma or bone fragments is relatively rare.
This vasogenic edema compresses the optic nerve within the bony optic canal, leading to impaired blood flow, ischemia, and axonal damage through a mechanism similar to compartment syndrome.
Shock waves generated by blast overpressure propagate through ocular structures, causing shear stress on optic nerve fibers. This leads to traumatic axonal injury, progressing to neuroinflammation and functional impairment. While macroscopic damage is absent, axonal injury, gliosis, and inflammation occur at the tissue level.
Animal models (Rex et al.) have confirmed the following:
Glaucoma
Direction of axonal degeneration: distal to proximal degeneration.
Tissue changes: astrocyte remodeling occurs.
Inflammation: multiple cytokines are elevated.
Direct Traumatic Optic Neuropathy
Site of injury: A clear site of injury exists.
Progression: Rapid and progressive axonal degeneration and cell death.
Mechanism: Direct mechanical compression and shearing are the main causes.
Blast-Induced TON
Site of injury: No macroscopic injury. Widespread effects due to shock wave.
Inflammation: Elevation pattern limited to IL-1α and IL-1β.
Characteristics: Shows a unique neuropathology different from glaucoma and direct traumatic optic neuropathy.
Research-stage treatment candidates are shown below.
| Treatment | Research Status | Remarks |
|---|---|---|
| Erythropoietin (EPO) | Pilot study | Improved outcomes reported in patients with traumatic optic neuropathy (Kashkouli et al.) |
| Caspase-2 siRNA | Animal models | Under investigation in air blast-induced ocular trauma model (Thomas et al.) |
| Neuroprotective factors (e.g., BDNF) | Basic research stage | Research targeting suppression of neurodegeneration and inflammatory factors is ongoing |
| Intravitreal injection | Animal models | Administration one day after injury may increase degenerating axons (Naguib et al.). Caution needed for acute phase administration |
In a pilot study by Kashkouli et al., administration of EPO to patients with traumatic optic neuropathy was reported to improve visual outcomes. Direct application to blast-induced cases requires further research.
Research targeting enhancement of neuroprotective and neuroregenerative factors, and suppression of neurodegeneration and inflammatory factors is currently ongoing, and future clinical application is expected.
