Optic nerve head avulsion

Key points at a glance

Key points of this condition

• Optic nerve head avulsion is a rare condition in which trauma separates the optic nerve from the eye at the level of the lamina cribrosa.
• It is a type of traumatic optic neuropathy (TON) and is classified as an anterior traumatic optic neuropathy.
• With complete avulsion, there is no light perception (NLP), and the impact on vision can be devastating.
• There is no established effective treatment, so early diagnosis and avoiding unnecessary treatment are important.
• When vitreous hemorrhage makes it impossible to view the fundus, B-mode ultrasound and CT are useful for diagnosis.
• In traumatic optic neuropathy with an optic canal fracture, optic canal decompression surgery may help improve vision.
• From 6 to 8 weeks after injury, progressive optic atrophy develops and the optic disc becomes pale.

1. What is optic nerve head avulsion?

Optic nerve head avulsion (ONA) is a condition in which trauma causes the optic nerve to separate from the eyeball at the level of the lamina cribrosa. It is not accompanied by rupture of the optic nerve dural sheath or the adjacent sclera¹⁾. optic nerve evulsion and optic nerve avulsion refer to the same condition, but they are distinguished by their etymology.

Optic nerve head avulsion is a type of traumatic optic neuropathy (traumatic optic neuropathy; TON) and is classified as anterior traumatic optic neuropathy¹⁾. Traumatic optic neuropathy overall occurs in 0.5 to 5% of head injuries⁵⁾, and optic nerve head avulsion is a rare condition among them²⁾. The degree can range from partial avulsion to complete avulsion, and the impact on visual function can be devastating¹⁾.

The most common sites of avulsion are the optic nerve head (most common), the orbital apex, and the optic chiasm¹⁾. The leading cause is traffic accidents, and sports injuries, falls, and assaults can also cause it. In a meta-analysis by Buchwald et al., small blunt objects or fingers accounted for 49% of the causes¹⁾.

Q What is the difference between optic nerve head avulsion and traumatic optic neuropathy (TON)?

A

Optic nerve head avulsion is a type of traumatic optic neuropathy and refers to physical separation at the level of the lamina cribrosa. Traumatic optic neuropathy is a concept that includes a wide spectrum from contusion to complete transection, and optic nerve head avulsion is positioned as one of the most severe types¹⁾.

2. Main symptoms and clinical findings

Mahjoub A, Sellem I, Mahjoub A, et al. Optic nerve avulsion: Case report. Ann Med Surg (Lond). 2021;68:102554. Figure 1. PMCID: PMC8278239. License: CC BY.

Initial fundus photograph and ocular ultrasound showing hemorrhage around the optic disc after trauma. The paired images help explain how optic nerve head avulsion can appear at first presentation.

Symptoms

• Acute severe vision loss: In complete rupture, there is no light perception (NLP). In partial rupture, some visual function may remain.
• Sudden vision loss: A rapid drop in vision immediately after the injury is typical³⁾.
• Eye pain: Eye pain may occur along with the trauma at the time of injury³⁾.

Clinical findings

The main findings confirmed by the doctor are listed below.

• Relative afferent pupillary defect (RAPD): Detected in the affected eye. This is a characteristic finding of traumatic optic neuropathy¹⁾³⁾⁴⁾.
• Fundus findings (optic disc): If the media are clear, abnormally deep cupping of the optic disc is seen. This is due to a cavity formed as the optic nerve retracts within the dural sheath. It is frequently accompanied by vitreous hemorrhage or peripapillary hemorrhage¹⁾.
• Normal fundus immediately after injury: Right after the injury, no abnormality may be seen in the fundus. From about 6 to 8 weeks after the injury, optic atrophy gradually progresses and the optic disc becomes pale.
• Complication of central retinal artery occlusion: This may occur in severe cases.
• Critical flicker fusion frequency (CFF): Markedly decreased or unmeasurable.

Partial avulsion

Visual acuity: Some visual function may remain.

OCT findings: A deep cavity can be seen in the optic disc. RNFL thinning has been reported (46 μm temporal, 91 μm superotemporal, and 60 μm superonasal)¹⁾.

Course: Glial proliferation gradually covers the avulsion cavity. It becomes prominent after 1 month¹⁾.

Complete avulsion

Visual acuity: No light perception (NLP).

Fundus: The optic nerve retracts within the dural sheath, forming a deep cavity.

Prognosis: Recovery of visual function is unlikely. Structural damage is irreversible⁴⁾.

Over time on OCT, GCC thickness thins from 2 weeks after injury, falls below the normal range, and stabilizes around 30 to 50 days. Fluorescein fundus angiography may show branch vein occlusion and microvascular remodeling¹⁾.

Q How is it diagnosed when vitreous hemorrhage makes the fundus impossible to see?

A

B-mode ultrasonography is useful. It can detect a hypoechoic area corresponding to the avulsed site¹⁾. CT and MRI are also used as adjuncts. See the section on Diagnosis and Examination Methods for details.

3. Causes and Risk Factors

• Blunt trauma: This is the most common mechanism of onset¹⁾. A small blunt object or a finger enters between the eyeball and the orbital wall.
• Penetrating trauma: Relatively rare, but it does occur. There have been reports of penetrating injuries from branches in ATV accidents → globe luxation + optic nerve transection²⁾.
• High-risk groups: Men, victims of traffic accidents, accidental eye injuries during sports, and head and facial trauma from falls.
• ATV accidents: These are open, high-speed vehicles without protective devices, so the risk of facial and eye injuries is high²⁾.

Prevention and daily care

• Please use appropriate eye protection during sports.
• When riding an ATV (all-terrain vehicle), wear a helmet, goggles, and a seat belt.
• After an eye injury, see an ophthalmologist promptly. Do not overlook decreased vision or changes in the way you see light.

4. Diagnosis and examination methods

The characteristics of each imaging test are shown below.

Examination	Main use	Points to note
CT (thin slices)	Detection of fractures and optic nerve head avulsion	Thin slices of 0.75-1 mm are essential
MRI (STIR/DWI)	Detection of optic nerve swelling and transection	Contraindicated when metallic foreign bodies are present
B-mode ultrasound	Diagnosis in cases of vitreous hemorrhage	Can be performed noninvasively and quickly

• Fundus examination (ophthalmoscopy): If the ocular media are clear, a diagnosis can be made directly. An abnormally deep optic disc cup is seen.
• B-mode ultrasonography: Useful when the optic disc cannot be seen because of vitreous hemorrhage. It detects a hypoechoic area at the avulsion site ¹⁾.
• CT: The first-line imaging test for orbital trauma. Thin-slice CT (0.75-1 mm) is essential, and 3 mm slices may miss optic canal fractures and Onodi cell hemorrhage ⁸⁾. Reports say that 20% of optic canal fractures are missed on CT. A defect in the scleral wall may be seen.
• MRI: STIR sequences can detect swelling and high signal in the optic nerve ⁴⁾. DWI (diffusion-weighted imaging) can also detect restricted diffusion in the optic nerve ⁴⁾. In cases of optic nerve rupture, fluid signal is seen at the canal-intracranial junction ⁴⁾. As a first-line test after trauma, it is contraindicated when there may be metallic foreign bodies.
• OCT: It is often not useful in the early stage because of opacity of the intervening transparent tissues. If the media are clear, changes in the ONH and macula can be recorded ¹⁾.

5. Standard treatment

Treatment for optic nerve head avulsion

No effective treatment has been established for optic nerve head avulsion. It is important to make an early diagnosis and avoid unnecessary treatment. High-dose intravenous steroids have not shown benefit and may instead carry a risk of harm ¹⁾.

Treatment of traumatic optic neuropathy in general

The following may be considered for traumatic optic neuropathy in general, including types other than optic nerve head avulsion.

• IONTS (International Optic Nerve Trauma Study): Neither steroid therapy nor optic canal decompression surgery has shown clear superiority over observation. Treatment should be decided individually ³⁾⁷⁾.
• Conservative treatment: Early administration of hyperosmotic fluids and steroids may be used.
• Optic canal decompression surgery: Vision improvement may be expected when there is an optic canal fracture. It can be performed in a minimally invasive way using an endoscopic transnasal approach (ETOND) ⁶⁾. Early surgery (within 24 to 48 hours after injury) is associated with a better prognosis ⁵⁾. When preoperative vision is hand motion or better, the postoperative improvement rate is higher ⁵⁾.

Fukumasa et al. (2024) reported a 10-year-old boy with traumatic optic neuropathy due to an optic canal fracture who underwent optic canal decompression surgery 6 hours after injury and received postoperative prednisolone 25 mg/kg/day. His preoperative hand motion vision improved to 20/30 after 12 days and was maintained at 9 months ⁵⁾. Vision improvement has been reported in about 80% of pediatric traumatic optic neuropathy cases.

Tachibana et al. (2024) performed endoscopic optic canal decompression after pulse methylprednisolone 1 g/day for traumatic optic neuropathy in a 70-year-old man. VA improved from 0.2 to 0.8 (after 6 months)⁷⁾.

When submacular hemorrhage is present: pneumatic displacement using SF6 gas + rtPA 25 μg/0.1 mL intravitreal injection may be effective. There are reports of successful submacular movement of the hemorrhage with prone positioning for 3 days¹⁾.

Points to note during treatment

• If the structural damage is irreversible, such as complete avulsion or optic nerve transection, there is no surgical indication⁴⁾.
• Risks of steroid therapy complications include gastrointestinal bleeding, infection, and adverse effects in patients with traumatic brain injury⁴⁾.
• There is no effective treatment for optic nerve head avulsion itself, and unnecessary invasive treatment should be avoided under an appropriate diagnosis.

Q Is surgery effective for optic nerve head avulsion?

A

There is no established effective treatment for optic nerve head avulsion itself. However, in traumatic optic neuropathy with an optic canal fracture, optic canal decompression may help improve vision⁵⁾. If there is irreversible structural damage such as complete avulsion, surgery is not indicated⁴⁾.

6. Pathophysiology and detailed mechanisms of onset

The main mechanisms of optic nerve head avulsion are classified into indirect injury and direct injury.

• Lamina cribrosa fragility: Optic nerve axons lose their myelin and supporting connective tissue at the lamina cribrosa. This area is the most vulnerable to injury, and most cases occur at the junction between the optic nerve head and the globe. After the unmyelinated nerve is torn, it moves backward within the nerve sheath.
• Bell phenomenon (indirect injury): During trauma, a protective reflex that rotates the eyeball upward and outward adds rotational strain to the optic nerve¹⁾.
• Sudden rise in intraocular pressure (indirect injury): A proposed mechanism in nonpenetrating blunt trauma is that a sudden rise in intraocular pressure pushes the optic nerve out. Computer modeling by Cirovic et al. showed that intraocular pressure can reach as high as about 300 mmHg¹⁾.
• Sudden globe displacement: Shearing occurs when the eye is rapidly displaced forward or the optic nerve is pushed backward (retropulsion).
• Direct injury: Direct injury to the optic nerve head from penetrating trauma (relatively rare).
• Intraorbital avulsion: Avulsion farther posteriorly has also been reported. Histopathologic findings showing no neural tissue within the dural sheath have been reported as proof of disrupted continuity within the orbit²⁾.
• Glial response: In partial avulsion, glial tissue covers the avulsion cavity. Glial proliferation becomes prominent after 1 month¹⁾.
• Vascular injury: Changes in peripapillary vessels near the avulsion site may impair retinal perfusion¹⁾.

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7. Latest Research and Future Prospects (Reports at the Research Stage)

For patients: Please read carefully

The following information is still in the research stage or under clinical trials and is not standard treatment available at general hospitals. It is reference information for specialists on future medical advances.

Blood flow assessment by LSCI (Laser Speckle Contrast Imaging)

LSCI (Laser Speckle Contrast Imaging) is a technique that noninvasively and quantitatively evaluates optic nerve head blood flow in traumatic optic neuropathy.

Jallow et al. (2025) detected a lower Peak BFVi (blood flow velocity index) on LSCI in a 15-year-old boy with direct posterior traumatic optic neuropathy: 13.4 a.u. in the affected eye versus 20.5 a.u. in the healthy eye at 3 weeks⁹⁾. The difference persisted at 6 months, with 13.7 a.u. in the affected eye versus 15.1 a.u. in the healthy eye. This may be useful for evaluating acute trauma.

DTI (diffusion tensor imaging)

Diffusion tensor imaging (DTI) can quantify microstructural changes in the optic nerve and may be useful for predicting prognosis⁴⁾.

Quantitative GVF evaluation (KSM-GVF program)

This is a quantification method using an ImageJ macro on Goldmann perimetry, allowing changes in isopter area to be tracked over time⁷⁾. It is being applied to evaluate visual field changes in traumatic optic neuropathy.

Neuroprotective and regenerative therapies

Experimental approaches such as erythropoietin, BDNF (brain-derived neurotrophic factor), and stem cell therapy are expected to support future optic nerve repair⁴⁾.

Q What is LSCI, and how might it help diagnose traumatic optic neuropathy?

A

LSCI is short for laser speckle contrast imaging, a noninvasive technique for quantitatively evaluating blood flow in the retina and optic disc. It has been shown to detect reduced blood flow in the affected eye compared with the healthy eye in traumatic optic neuropathy⁹⁾, and its use as an objective indicator for acute trauma is being studied.

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8. References

1. Bayram-Suverza M, Rosano-Barragán M, Ramírez-Estudillo J. Long-term follow-up of a patient with partial optic nerve avulsion associated with submacular hemorrhage who underwent pneumatic displacement. Am J Ophthalmol Case Rep. 2024;35. PMCID:PMC11152889.

2. Omari A, Carniciu AL, Desai M, Schimmel O, Schlachter DM, Folberg R, et al. Globe dislocation and optic nerve avulsion following all-terrain vehicle accidents. American journal of ophthalmology case reports. 2022;27:101621. doi:10.1016/j.ajoc.2022.101621. PMID:35782169; PMCID:PMC9243039.

3. Tenewitz JE, Chen EJ, Cartwright MJ. A rare presentation of direct traumatic optic neuropathy in a patient poked in the eye by an antenna. Cureus. 2021;13(9):e18244. doi:10.7759/cureus.18244.

4. Naik SN, Nayak DV. Unravelling the Unseen: A Case Series Exploring the Enigmas of Traumatic Optic Neuropathy. Cureus. 2024;16(12):e75546. doi:10.7759/cureus.75546. PMID:39803156; PMCID:PMC11722660.

5. Fukumasa H, Yamaga Y, Miyaoka R, Kobayashi M, Nishiyama K. Successful Combination Therapy of Optic Canal Decompression and Steroid Administration for Traumatic Optic Neuropathy in a 10-Year-Old Boy. Cureus. 2024;16(9):e70124. doi:10.7759/cureus.70124. PMID:39449917; PMCID:PMC11501498.

6. Okui T, Sakamoto T, Morikura I, Okui T, Ayasaka K, Okuma S, et al. Feasibility of navigation-assisted endoscopic transnasal optic nerve decompression for the treatment of traumatic optic neuropathy in patients with midfacial fractures. Journal of the Korean Association of Oral and Maxillofacial Surgeons. 2024;50(5):273-284. doi:10.5125/jkaoms.2024.50.5.273. PMID:39482103; PMCID:PMC11535127.

7. Tachibana M, Kanno J, Hashimoto M, Hosokawa Y, Sawada M, Nishiyama-Ota Y, et al. Quantification of Goldmann Visual Fields During Resolution of Traumatic Optic Neuropathy. Case reports in ophthalmological medicine. 2024;2024:5560696. doi:10.1155/2024/5560696. PMID:39583778; PMCID:PMC11585370.

8. Mehta A, Rathod R, Ahuja C, Singh M, Virk RS. Hemorrhage in Onodi Cell Leading to Traumatic Optic Neuropathy. Craniomaxillofacial trauma & reconstruction. 2021;14(1):70-73. doi:10.1177/1943387520922021. PMID:33613839; PMCID:PMC7868511.

9. Jallow MA, Gholap RS, Asanad S, et al. Laser speckle contrast imaging detects relative blood flow reduction in traumatic optic neuropathy. Am J Ophthalmol Case Rep. 2025;38:102326. doi:10.1016/j.ajoc.2025.102326.