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DISCUSSION
Our case series showed that 56% (n=9) responded to IVMP and had a significant improvement in VA. This is consistent with other studies which showed the success of treatment with IVMP in TON, ranging from 31% to 76% (Table 2)[4,812]. However, spontaneous improvement of VA without treatment was also reported, ranging from 20% to 67% (Table 3)[1,4,8,1113].
Another interesting observation is that patients who had poor initial VA tend to be worse than those who had better VA. Of the 7 patients who did not respond, their initial VA was at best 6/36 and majority were CF to NLP. This was not unexpected as poor initial VA may indicate a more serious injury to the optic nerve. IONTS showed similar results that initial VA is a strong predictor of the final VA[4]. However, there were 2 patients in our study whose initial VA was CF Figure 1Improvement of visual acuity with time (cumulative chart)and NLP, who responded to treatment and achieved a final VA of 6/6 and 6/24 respectively. Therefore poor initial visual acuity alone may not be the sole factor for poor visual outcome following treatment as suggested by earlier study[4,14].Table 2Visual improvement in traumatic optic neuropathy with steroid treatment（略）Table 3Visual improvement in traumatic optic neuropathy with no treatment（略）
Timing of Treatment Besides initial VA, we believe the timing in initiating treatment might play an important role in determining the prognosis. Many researchers believe that there should exist a critical period beyond which treatment will be ineffective but no studies had successfully found the correlation between the timing of initiating therapy and the final VA.
In this study, we observed that favourable response of TON to IVMP is possible within 4 days after the initial injury. The subgroup analysis showed that 75% (n=9) of those treated within 4 days of injury had favourable response while all those treated beyond 4 days of injury showed no improvement at all. Therefore, we propose that 4 days or 96 hours may be a critical time to initiate IVMP treatment for TON, beyond which the injury might be irreversible. However, very few previous studies specified when the treatment was started[1,913]. The IONTS advocated that there was no indication that the dosage or timing of corticosteroid treatment is important as the statistical difference was not significant[4]. In the IONTS, steroids was given within 7 days of injury, although majority (88%) of their patients received treatment within 2 days[4]. Given the small sample available (n=85), a small change in the number of patients through group stratification in both the timing and dosage used, may exert a considerable impact on the statistical analysis and render the results insignificant.
In practice, very often, the diagnosis of TON may be delayed as the accompanying injuries such as brain injury with loss of consciousness, and other systemic injuries make visual assessment difficult. Should timing in initiating therapy be proven vital in treating TON, this will pose a new challenge to us in managing TON because prompt diagnosis and treatment will be crucial.
Dosage of Steroids The use of steroids in treating TON was first introduced by Anderson et al in 1982 and its rationale was adopted from both NASCIS 2 and NASCIS 3 trials[5,6,15]. However, to date, there is still no recommendation in treatment of TON let alone consensus on the safe and effective dosage of steroids used.
On the other hand, there is increasing concern over the possible harmful effects of megadose steroids on the optic nerve[1618]. Recent nonclinical studies in rats by Ohlsson et al[19] showed that megadose corticosteroids might be harmful to the injured optic nerve. In 2000, Steinsapir et al[20] showed that for IVMP above 30mg/kg, there was a dosedependent decline in neurons with increasing dose of IVMP. Evidence of this harmful effect on human optic nerve in a similar manner is still lacking and yet to be determined. A smaller dose of IVMP may not be neurotoxic and is believed to reduce swelling of the optic nerve hence limiting the injury[18].
The dosage of IVMP used in our study is a moderate dose of 1g IVMP in a single dose or divided doses depending on individual consultants preference. A moderate dose was chosen to avoid the side effects and possible neurotoxicity of megadose IVMP[18].
Limitation of the Study This is a retrospective case series with a small number of patients and lacking a control group. Some of these patients have concurrent head injuries which had either been dealt with or managed concurrently with the neurosurgical team. Therefore, with this small sample, we are unable to demonstrate statistically significant results. Thus, some of these observations may even arise by chance. Patients with serious injury requiring intensive care and acute neurosurgical intervention were not included in the study as the records of eye assessment of these patients were not standardized.
The regime of steroids used was not standardized. Although the dosage of steroids used in our unit is similar, ie 1g/day, the actual regime used is dependent on each individual consultants preference, ranging from 1g IVMP once a day, 500mg IVMP twice a day or 250mg IVMP four times a day for 3 days. Different regimes of IVMP may in itself cause different outcomes.
In conclusion, traumatic optic neuropathy, although uncommon, is an important cause of visual morbidity especially in the productive young group of patients. Previous studies did not provide us with enough information to formulate the best treatment for this condition. At present, the treatment should be tailored to each individual patient based on physicians experiences.
Based on our observation of this case series, we propose that if treatment is initiated within 4 days of injury, a moderate dose of IVMP, for example, 1g IVMP once a day for three days followed by tapering dose of oral prednisolone may be beneficial. A large randomized control trial is needed to guide us further. Future larger studies should consider looking into the timing and dosage of treatment for traumatic optic neuropathy.
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