The optic nerve, comprised of retinal ganglion cell axons, is a specialized somatosensory nerve with a total length of approximately 40mm[13]. Anatomically, it can be divided into four segments: the intraocular segment (about 1mm), intraorbital segment (about 25mm), intracanalicular segment (5-6mm), and intracranial segment (10mm). External impact on any segment of the optic nerve can lead to severe nerve damage. The intracanalicular segment, which is the most delicate and represents the site where the optic nerve enters the cranial cavity, exhibits the highest incidence of injury at 71.4%[14–15]. On one hand, trauma can transmit external forces to the optic nerve canal, resulting in damage to the optic nerve due to the vulnerability of the bony structures surrounding the canal, such as the root of the lesser wing of the sphenoid and the base of the anterior clinoid process. On the other hand, trauma can cause optic nerve swelling and necrosis through compression of the optic nerve and its nutrient vessels due to bone fragment displacement or bleeding[16–18]. As a component of the central nervous system, the optic nerve possesses limited regenerative ability, and once the process of neuronal apoptosis begins, it becomes challenging to halt, leading to the death of numerous ganglion cells[19–20].
While various eye diseases, such as optic neuritis, retinal detachment, and ischemic optic neuropathy, can result in optic nerve damage, TON is more frequently encountered by neurosurgeons, predominantly caused by car accidents, followed by falls, blows, and fights[21]. Among our group of cases, car accidents accounted for 130 cases (63.11%), falls for 32 cases (15.53%), blows and fights for 37 cases (17.96%), and other causes for 7 cases (3.4%). Optic nerve injury mechanisms in these patients can be categorized into two types: direct injury and indirect injury[22]. Direct injury often arises from violence directly impacting the outer edge of the orbit, while indirect injury frequently occurs due to optic nerve-related blood vessel spasm resulting from violence to the supraorbital margin and nasal bone[23–24].
Following optic nerve injury, patients frequently present with clinical symptoms, such as visual field defects, impaired color vision, and potentially vision loss. In clinical practice, it is crucial to promptly identify and prioritize these symptoms, intervening early to provide treatment in order to salvage as many nerve cells as possible[25].
Once diagnosed, immediate treatment is essential for optic nerve injuries. Currently, there is no standardized treatment protocol in clinical practice[26]. The main treatment methods include high-dose steroid pulse therapy and optic nerve decompression surgery, supplemented with diuretics, vasodilators, and drugs that improve microcirculation[27–28]. Conservative treatment often involves high-dose methylprednisolone pulse therapy. In our department, we typically administer 500mg of methylprednisolone within 3–8 hours of injury, followed by a 3-day pulse treatment with a dose adjustment to 300mg. Steroids possess anti-inflammatory and antioxidant effects, reducing the formation of free radicals, alleviating edema reactions, and preventing vascular spasm. These properties inhibit nerve cell necrosis and protect the optic nerve[29]. Optic nerve decompression surgery involves surgically removing pressure on the optic nerve to facilitate self-repair. Surgical treatment is preferred for patients with noticeable bone fragments and hematomas compressing the optic nerve, which can include traditional transcranial optic nerve decompression surgery and intraorbital optic nerve decompression surgery[30–31]. Endoscopic optic nerve decompression surgery through the nasal cavity has also been utilized. Currently, there are no randomized controlled studies evaluating the therapeutic effects of different surgical techniques, so the primary criterion for selection remains the proficiency of the clinical physician[32]. Studies indicate that the combined effect of optic nerve decompression surgery and steroid therapy is superior to a single treatment plan, but more research is needed to substantiate this claim[33].
In this study, there were 63 patients with no light perception after injury, yielding an effective treatment rate of 39.68%. Additionally, 143 patients had light perception after injury, with an effective treatment rate of 74.83%. The χ2 value was 23.464, P < 0.01, demonstrating a statistically significant difference. These findings indicate that patients who retained light perception before treatment exhibited better treatment outcomes than those who did not. Patients without light perception, regardless of steroid or surgical treatment, are unlikely to experience significant vision improvement, with low degrees of improvement observed. Existing reports suggest that patients with residual vision or light perception may have intact or partially ischemic optic nerves, with a considerable number of surviving ganglion cells[34]. Conversely, patients with no light perception may have experienced severe or irreversible optic nerve transection or necrosis, with few to no surviving ganglion cells. Hence, vision restoration is possible in the former case, emphasizing the importance of timely intervention and treatment for vision recovery. However, the possibility of vision restoration is considerably lower in the latter scenario.
The selection of treatment options for TON has long been a subject of controversy[26]. Further subgroup analysis of our study reveals that for patients with residual light perception, surgical treatment may be more effective than pure steroid therapy. Conversely, for patients without light perception after injury, the effectiveness of the two treatment options does not differ significantly. Therefore, the choice of a specific treatment plan should be individualized. For patients with residual vision after injury, regardless of visual acuity level, early and timely treatment should be administered. Steroid therapy or surgical treatment should be selected based on the actual situation to maximize ganglion cell survival and provide potential for further visual recovery. In cases where patients have no light perception after injury, the appropriate treatment method should be carefully chosen, taking into account the potential risks of optic nerve injury or necrosis associated with surgical intervention.