Trauma-induced kinking of the optic nerve: A rare manifestation of optic neuropathy

INTRODUCTION

Traumatic optic neuropathy (TON) is an acute injury to the optic nerve caused by trauma, resulting in vision loss that can range from partial deficits to complete blindness. It is classified by injury location – such as the optic nerve head, intraorbital, intracanalicular (most common), or intracranial segments – or by mechanism, including direct (penetrating or compressive) versus indirect (blunt force transmission).^[1] Severity spans minor contusions to optic nerve avulsion or associated optic canal fractures, with an incidence of 0.7–2.5% in head or midface trauma cases. Most patients are young adult males in their early 30’s, often involved in high-impact events like motor vehicle accidents.^[2]

CASE REPORT

A 26-year-old male presented to the outpatient department with a history of self-reported fall from a motorcycle 1 week prior, after which he sustained significant injury to the left eye. He complained of diminished vision, pain, and redness in the left eye. Examination revealed visual acuity of 6/6 in the right eye and 6/12 in the left eye. Slit-lamp biomicroscopy showed subconjunctival hemorrhage with a grade 2 relative afferent pupillary defect in the left eye, indicating optic nerve dysfunction. Dilated fundus examination demonstrated normal optic disc and macula in both eyes at initial presentation, with no evidence of retinal hemorrhages, exudates, or macular edema to suggest alternative diagnoses like traumatic retinopathy or commotio retinae; however, the absence of early disc swelling or peripapillary changes did not rule out intraorbital or intracanalicular optic nerve injury.

Magnetic resonance imaging (MRI) revealed a tortuous intraocular optic nerve with a focal kink [Figure 1], suggestive of traumatic stretching or deformation consistent with indirect TON, potentially from transmitted blunt force during the fall. The neurologist recommended against surgical intervention due to the absence of compressive hematoma or entrapment. We initiated a trial of systemic corticosteroids, starting with pulse methylprednisolone therapy (e.g., 1 g/day intravenous for 3 days) followed by oral prednisone taper, aiming to reduce optic nerve edema and inflammation. Oral and maxillofacial surgery evaluation confirmed a left lateral orbital wall fracture involving the zygomatic bone and greater wing of the sphenoid, without optic canal involvement, further supporting a non-surgical approach.

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Figure 1: Magnetic resonance imaging showing kinked left optic nerve (arrow).

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At 6-week follow-up, the patient’s left eye visual acuity had stabilized at 6/24, reflecting partial recovery but persistent deficit from axonal damage. Repeat dilated funduscopy now showed temporal pallor of the left optic disc [Figure 2] – a classic late sign of optic atrophy in TON, resulting from retinal ganglion cell loss and axonal degeneration following the initial trauma; the pallor was sector-specific temporally, aligning with preserved nasal field function and correlating with the focal MRI kink, while the macula remained uninvolved [Figure 3a and 3b].

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Figure 2: At 6 weeks, (a) fundus of right eye showing normal disc and macula, (b) fundus of left eye showing temporal pallor.

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Figure 3a: Humphrey field analyzer, 30-2 of the right eye, normal.

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Figure 3b: Humphrey field analyzer, 30-2 of the left eye, showing superior hemifield loss.

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DISCUSSION

TON is commonly seen in young adult males. The most common etiology is road traffic accidents (RTAs) similar to our case. The common mode of TON is indirect injury to the optic nerve by transmitted shock from an orbital impact.^[3] Other modes of TON direct injury to the optic nerve by optic canal fracture, optic nerve sheath hematoma, are both known for poor prognosis.^[4] In our patient, imaging confirmed no evidence of optic canal fracture; however, there was kinking of the retrobulbar optic nerve, a finding that, to our knowledge, has not been previously reported. Loss of consciousness, no improvement in vision after 48 hours (h) despite steroid treatment, carries a poor visual prognosis. There was no history of loss of consciousness in our case but late presentation led to poor vision. Furthermore, the international optic nerve trauma study confirmed no added benefits with a high dose of steroid beyond 48 h.^[5]

CONCLUSION

In all RTA patients, especially those with craniofacial trauma, the possibility of TON should be assessed bedside upon presentation using visual acuity, pupillary response, and color vision testing to enable early detection even before imaging. Loss of consciousness and poor patient compliance often limit timely intervention, as altered mental status hinders reliable neuro-ophthalmic evaluation in acute settings.^[6,7]

High-resolution imaging is mandatory in all head injury cases, with thin-section (1 mm) axial and coronal computed tomography scans essential to detect subtle optic canal fractures, orbital disruptions, or bone fragments impinging the optic nerve – serving as the gold standard for confirming injury site and guiding management despite variable prognostic value. Multispecialty collaboration among neurologists, ophthalmologists, and oral/maxillofacial surgeons is crucial to optimize vision outcomes, as timely integration addresses concomitant traumatic brain injury, fractures, and inflammation for better recovery rates.^[8]