Traumatic optic neuropathy (TON): what is the best way to manage the eye pressure?

Two recent patients brought up this question. One had totaled his Tesla during a recent storm, and his airbag hit him in the left eye: he lost part of his vision instantly from traumatic optic neuropathy. 

The second was a middle aged woman, who had brain trauma many years ago during an accident but whose optic nerve’s insulation, also known as the nerve fiber layer (NFL) appeared to be thinning too quickly. 

The question came up for both of them: What is the best pressure for the previously damaged  optic nerve given the optic nerve is an extension of the brain and very sensitive to pressure fluctuations.

Traumatic optic neuropathy (TON) is damage to the optic nerve caused by trauma to the head, face, or orbit, resulting in acute visual loss. It is directly relevant to the prior discussion because a nerve already injured by TON has a reduced retinal ganglion cell (RGC) and RNFL reserve, making it more vulnerable to any additional insult — including IOP-related damage.

Definition and Classification

TON is classified into two main forms:[1][2]

- Direct TON — caused by penetrating injury (e.g., projectiles, bone fragments) directly damaging the optic nerve. This form generally causes severe, immediate, and often irreversible vision loss.

- Indirect TON — caused by transmission of forces from a distant impact site (typically a frontal or midfacial blow) to the optic nerve. This is the more common form and carries a somewhat better prognosis.

Pathophysiology

The intracanalicular segment of the optic nerve is the most commonly affected site in indirect TON, because the nerve is fixed within the bony optic canal and its dura is fused with the periosteum. This makes it uniquely susceptible to shearing forces at the proximal and distal ends of the canal.[1] The initial mechanical injury may be followed by secondary swelling within the tight canal, leading to further ischemia and potentially delayed vision loss (reported in ~10% of cases).[1] OCT studies show that RNFL thinning begins approximately two weeks after injury, while central macular thickness diminishes after four weeks.[3]

Clinical Features

The hallmark findings of TON include:[2][4]

- Decreased visual acuity (40–60% present with light perception or worse)

- Relative afferent pupillary defect (RAPD) — unless bilateral and symmetric

- Impaired color vision

- Variable visual field defects

- Normal fundus appearance acutely in posterior injuries, with optic atrophy developing after approximately 6 weeks

Epidemiology

TON is predominantly a condition of young males (84% male), with road traffic accidents as the leading cause (67%).[5] It occurs in 0.5–8% of head trauma cases, though subclinical optic nerve damage is much more common — at least half of patients with moderate-to-severe TBI demonstrate visual field defects or optic atrophy on OCT when more sensitive testing is performed.[6]

Treatment

Treatment remains controversial, with no proven effective therapy:[1][6][7]

- Corticosteroids — no clear benefit demonstrated; the CRASH trial showed increased mortality with high-dose steroids after head trauma, raising safety concerns

- Optic nerve decompression surgery — may benefit patients with optic canal fractures (53% response vs. 24% for steroids), but evidence remains limited[5]

- Observation — 20–60% of untreated patients show some spontaneous visual improvement, particularly those with better initial acuity[1]

- Early intervention (within 7 days) appears to improve outcomes for both surgical and medical approaches[5]

Link to the Prior Discussion: Why TON Makes IOP Control Critical

This is the key connection: after TON, the optic nerve has already lost a significant proportion of its RGCs and RNFL. The only known modifiable factor contributing to further RGC death is intraocular pressure.[3] This creates a clinical scenario analogous to glaucoma — a structurally compromised nerve that is more susceptible to pressure-related damage. Furthermore, the same blunt trauma that causes TON can also produce angle recession, hyphema, or lens displacement, all of which are independent risk factors for developing traumatic glaucoma (incidence ~3.4% at 6 months, up to 10% at 10 years).[8][9] This dual vulnerability — a damaged nerve combined with potential outflow pathway compromise — is precisely why maintaining stable, low IOP is clinically important in these patients, as discussed in the prior response.

Thus even though there is no direct high-quality evidence specifically addressing IOP-lowering treatment in eyes with prior TON, abnormal OCT, and early visual field changes, there is strong indirect evidence and clinical reasoning support treating such patients to maintain a low target IOP, given the already compromised optic nerve. And it is a race against time to save optic nerve tissue.

Why IOP control matters in this setting

An optic nerve that has already sustained structural damage from trauma has a reduced reserve of retinal ganglion cells (RGCs) and retinal nerve fiber layer (RNFL). The glaucoma literature consistently demonstrates that eyes with pre-existing optic nerve damage are more vulnerable to further IOP-related injury:

- Each 1 mmHg higher mean IOP is associated with 0.05 µm/year faster RNFL loss, and this effect is amplified in eyes already showing progression.[1]

- Eyes maintained below their target IOP had significantly slower RNFL thinning (−0.44 vs −0.71 µm/year) compared to those above target.[2]

- The AAO Preferred Practice Pattern for POAG states that the greater the pre-existing optic nerve damage, the lower the target IOP should be set, and that a reduction of at least 25% from baseline has been shown to slow progression.[3]

Applying glaucoma principles to post-TON eyes

Although the initial insult was traumatic rather than glaucomatous, the downstream concern is the same: an optic nerve with diminished structural reserve (abnormal OCT/RNFL thinning) and early functional loss (visual field changes) is at heightened risk for further deterioration from even "normal" IOP levels. This parallels the concept of normal-tension glaucoma, where damage occurs at statistically normal pressures in susceptible nerves. The Collaborative Normal-Tension Glaucoma Study demonstrated that IOP lowering slows visual field progression even in eyes with physiologic IOP levels.[4][5]

Additionally, ocular trauma itself can cause angle recession, trabecular pigmentation, or other outflow pathway damage that predisposes to traumatic glaucoma — a well-recognized entity that may develop months to years after injury.[6] Gonioscopy should be performed to evaluate for angle recession or other structural changes.

Key considerations for management

- Confirm the etiology of the OCT and visual field changes. Determine whether the findings represent stable post-traumatic atrophy or progressive loss. Serial OCT and visual fields over time are essential — if the RNFL is thinning progressively or visual fields are worsening, this strongly supports IOP-lowering treatment.

- Set a low target IOP. Given the already compromised nerve, a target IOP in the low-to-mid teens (or lower) is reasonable, analogous to managing moderate-to-advanced glaucoma.[3]

- Evaluate for traumatic glaucoma. Perform gonioscopy to assess for angle recession, trabecular pigmentation, or cyclodialysis, as these findings carry significant risk for chronic IOP elevation.[6][7]

- Monitor closely. The AAO recommends periodic reassessment of target IOP by comparing optic nerve status (disc appearance, RNFL, and ganglion cell layer on OCT) and visual fields with prior examinations.[3]

In summary, while no randomized trial has specifically studied IOP-lowering in post-TON eyes with structural and functional loss, the weight of glaucoma evidence strongly supports maintaining a low, stable IOP in any eye with a compromised optic nerve and early visual field changes. The damaged nerve has less capacity to tolerate pressure-related stress, making proactive IOP management a prudent clinical approach.

Would you like to explore the specific gonioscopic findings and long-term risk of traumatic glaucoma development after closed globe injury?

References

1. Impact of Intraocular Pressure Control on Rates of Retinal Nerve Fiber Layer Loss in a Large Clinical Population. Jammal AA, Thompson AC, Mariottoni EB, et al. Ophthalmology. 2021;128(1):48-57. doi:10.1016/j.ophtha.2020.06.027.
2. The Impact of Achieving Target Intraocular Pressure on Glaucomatous Retinal Nerve Fiber Layer Thinning in a Treated Clinical Population. Pham AT, Bradley C, Hou K, et al. American Journal of Ophthalmology. 2024;262:213-221. doi:10.1016/j.ajo.2023.11.019.
3. Primary Open-Angle Glaucoma Preferred Practice Pattern®. Gedde SJ, Bowden EC, Challa P, et al. Ophthalmology. 2026;133(4):P1-P103. doi:10.1016/j.ophtha.2025.12.029.
4. Glaucoma in Adults—Screening, Diagnosis, and Management. Stein JD, Khawaja AP, Weizer JS. JAMA. 2021;325(2):164-174. doi:10.1001/jama.2020.21899.
5. Influence of Intraocular Pressure on Clinical Decision-Making in Glaucoma Management. Polski A, Brintz BJ, Hess R, et al. JAMA Ophthalmology. 2026;:2843764. doi:10.1001/jamaophthalmol.2025.5593.
6. Pathophysiology and Management of Glaucoma and Ocular Hypertension Related to Trauma. Razeghinejad R, Lin MM, Lee D, Katz LJ, Myers JS. Survey of Ophthalmology. 2020 Sep - Oct;65(5):530-547. doi:10.1016/j.survophthal.2020.02.003.
7. Early Predictors of Traumatic Glaucoma After Closed Globe Injury: Trabecular Pigmentation, Widened Angle Recess, and Higher Baseline Intraocular Pressure. Sihota R, Kumar S, Gupta V, et al. Archives of Ophthalmology (Chicago, Ill. : 1960). 2008;126(7):921-6. doi:10.1001/archopht.126.7.921.