Optic Neuritis is a clinical syndrome resulting from inflammation, DeMyelination, or infection of the Optic Nerve. Its diagnosis and treatment are complicated.
In 1884, Nettleship first reported 28 cases of Optic Neuritis whose clinical symptoms have been accepted up to the present without any change.
On the other hand, the development of diagnostic procedures and Steroid therapy have also altered the clinical features of Optic Neuritis.
Among several developed diagnostic procedures, the Visually Evoked Cortical Potential (VECP) has become a good tool to prove the impairment of the Optic Nerve.
In 1971, we reported a decrease of threshold intensity required to evoke VECPs in Optic Neuritis patients whose Visual Acuity was relatively well preserved.
In the same year, Halliday et al reported that Pattern VECP (PVECP) was delayed in 93% of patients with multiple sclerotis (MS) without Optic Neuritis.
Stimulated by this report, a great number of studies appeared to show the usefulness of PVECP in the diagnosis of MS.
However, few of these studies gave descriptions of Ophthalmic findings. PVECP later become known to be closely related with Ophthalmic conditions.
In the Ophthalmological field, we reported the influence of Pupillary size, accommodation power, refractive powers, eccentricity of stimulated Retinal area, Retinal luminance, contrast, wavelengths, spatial and temporal frequencies, stimulus field, etc.
On the basis of our results, we developed a television display system in 1975 and applied it clinically. In the present study, we reviewed the medical records of a total of 272 cases of Optic Neuritis who presented in our clinic between 1978 and 1999.
In the diagnostic, therapeutic point of view in relation with the data of other countries, the study was important regarding the racial differences and recent conceptions of Optic Neuritis.
The results showed that there were no racial difference in Optic Neuritis as had been thought. The development from Optic Neuritis to Multiple Sclerosis was not less than in Caucasian patients.
Regarding Steroid therapy, we found that the most effective method was sub-Tenon injection. For cases which recur and progress to Optic Atrophy, Optic Nerve transplantation will be needed.
Therefore, we have been studying the reconstruction of the Optic Nerve in Wister rats. We experimentally damaged the Ganglion Cells by causing Ischemic Retina with ligation of the Ophthalmic Artery and cutting the Optic Nerve just behind the eyeball.
To prevent the Apoptosis of Ganglion Cells, we injected various NeuroTrophic Factors such as BDNF, GDNF, and HSP 27 into the vitreous.
For effective injection of DNA, electropolation was applied and the best condition for avoiding Apoptosis was chosen. Further, in Mx-c-fox transgenic mice, we found that regeneration of Ganglion Cells was inhibited.
Based on the rescue study of the Ganglion Cells, Optic Nerve transplantation was performed using an artificial graft in which cultured Schwann Cells from the Ischiatic Nerve, BDNF, CNTF, Insulin, and Forscolin were compound and bridged to the Superior Colliculus.
The results showed a regeneration rate of the Optic Nerve Axon of 15%. This rate was much higher than in other reports.
Keratoplasty and IntraOcular Lens implantation had a relatively long history of research before achieving clinical success. We believe that Optic Nerve transplantation will one day be successful in clinical treatment in the same way.