ProfG and Dr Kappoor did a neuroprotection of a sodium channel blocker called neuroprotection and it suggested that the nervous system was protected from damage. In the study below it looks like this study was being repeated. However, disaster struck and there was a seeming drug-induced adverse event that led the trial to be stopped.
One person developed Stevens–Johnson syndrome (SJS), This is a type of severe skin reaction. The most common cause is certain medications such as lamotrigine and carbamazepine (which are sodium changel blockers like phenytonin. But it occurs with other sodium channel blockers. In East Asian populations studied , carbamazepine– and phenytoin-induced SJS is strongly associated with HLA-B*1502 (HLA-B75), an HLA-B serotype of the broader serotype HLA-B15.
In the this study the plan was to get people on drugs within 14 days just like the london study, which used the fellow eye as the control. This was in part used because of the variability of response
Effect of phenytoin on retinal ganglion cells in acute isolated optic neuritis. Yadegari S, Gholizade A, Ghahvehchian H, Aghsaei Fard M.Neurol Sci. 2020 Mar 24. doi: 10.1007/s10072-020-04360-2. [Epub ahead of print]
OBJECTIVE: Phenytoin has been shown to reduce the peripapillary retinal nerve fiber layer (pRNFL) loss in optic neuritis (ON). We evaluated the effects of phenytoin on retinal ganglion layers and visual outcomes of newly diagnosed acute ON.
METHODS:A randomized, placebo-controlled trial was conducted in a tertiary referral eye hospital and patients with the first episode of typical demyelinating ON, without any history of multiple sclerosis were randomly assigned to phenytoin or placebo. The thickness of ganglion cell-inner plexiform layer (GCIPL) measured by optical coherence tomography (OCT) was considered as the primary outcome.
RESULTS: One patient in the phenytoin group developed severe cutaneous rashes that progressed to Stevens-Johnson syndrome (SJS)/toxic epidermal necrosis (TEN), and further allocation of patients to the phenytoin group was stopped, and finally fifteen participants were included in the phenytoin group. Fifty-one patients were enrolled to the placebo group, from which four were excluded. Both visual acuity and field were not significantly different between the control and phenytoin groups after 1 and 6 months. Mean 3- and 6-mm macular GCIPL thicknesses decreased after 6 months to 73.6 ± 14.1 and 57.9 ± 7.5 μm, respectively, in the phenytoin group and to 71.6 ± 15.7 and 55.6 ± 6.6 μm, respectively, in the placebo group with no significant differences between the two groups (P = 0.77 and P = 0.26, respectively.
CONCLUSION:Phenytoin is not probably safe and effective as neuroprotection after acute ON. Further investigation with other sodium channel inhibitors could be considered.