A couple of years ago Dr Raj Kappoor and ProfG did a trial in optic neuritis and tested a sodium channel blocker to see if it could save nerves in the eye after optic neuritis. This was based on studies that MD1, 2, 3 & 4 had done in the beasties.
The trial worked and it saved loss of nerves by about 30%, but then what?….Yep Nothing.
I said to the neuros..”You have done a trial and it worked. Why not do a follow up?. Why is there no change in clinical practise?”. Surely anyone in relapse or sub-clinical relapse (new lesion) should at least get or be offered, sodium channel blockers to protect against the “inflammatory penumbra” (damage associated with the generation of an inflammatory lesions) that occurs when lesions occur.
I remember when I asked Dr Kappor, why was there no follow-on study? The answer was because there was no clinical effect, people were not loosing sight, so why do it?…..I thought duh.
A lost nerve is a lost nerve. You only get clinical problems when you have lost sufficient nerves to exhaust your reserve….Diabetes occurs when you have lost 80% of your pancreatic beta cells, Parkinsons disease occurs when you have lost lots of dopaminergic cells . How can you happily burn your reserve away. How can you happily allow other people to burn their reserve away…
However the softly, softly brigade do it, in my opinion, with the use of CRAB drugs that do not get disease under effective control for most people.
Now OK, I am not treating people and maybe the neuros are considering the balance as sodium channel blockers are not without side effects, but Dr Kapoor and to some extent profG, by their inactivity in trying to change clinical practise have contributed to people losing their sight reserve and probably brain reserve. Now profG may argue he has done something, but change clinical practise? Has that occurred?.
ProfKappoor did this studyafter we revived the idea after prof Smith and Kapoor messed up by doing a trial with outcome that was no good and chose a drug and dose that caused side effects and stopped people taking their treatment. NDG saved the day otherwise this would be a dead duck.
I know getting funding to do the same study is very difficult. But surely there is no point in undertaking trials unless there is a plan to do something with the information if it is positive. I do not think academics think enough about this.
How long is it since MS-STAT before MS-STAT2 ? No forward planning from the PIs and funders. Wasting so much time. As an academic we are judged on impact but as a scientist we are powerless to make things happen. If ideas stall because of ineffective trial design or clinical activity. If you see improvement in walking speed would that convince you something is happening…two studies .
Normal Visual Recovery after Optic Neuritis Despite Significant Loss of Retinal Ganglion Cells in Patients with Multiple Sclerosis.Sherif M, Bergin C, Borruat FX. Klin Monbl Augenheilkd. 2019 Apr;236(4):425-428
BACKGROUND:Optic neuritis (ON) is a frequent manifestation of demyelinating attack in multiple sclerosis (MS). Initial visual loss can vary from minimal to complete. Visual improvement occurs in about 95% of patients, some of them recovering to normal [visual acuity (VA), color vision, visual field (VF)]. We analyzed retinal ganglion cell layer (RGCL) thickness in MS patients who recovered their normal vision after ON to determine whether a relative preservation of RGCL existed in these patients.
MATERIALS AND METHODS: We conducted a retrospective study of all patients with MS and ON examined by one of us (F. X. B.) between 2013 and 2018. Inclusion criteria were strictly unilateral ON, full recovery of vision, computerized visual field, and OCT examinations. Full recovery of vision was defined as VA ≥ 10/10, Ishihara ≥ 11/13, and VF mean defect (MD) ≤ 2.6 dB. Evaluation of RGCL was obtained with spectral domain optical coherence tomography (SD-OCT). The normal fellow eye of all patients served as the control group. Relative thinning of RGCL, expressed as percentage, was calculated by comparing results from the affected eye to the fellow eye of the same patient.
RESULTS:Twenty-one patients (21 affected eyes – Group 1, 21 normal fellow eyes – Group 2) satisfying the inclusion criteria were retrieved from our database. All patients exhibited the relapsing-remitting form of MS. There were 16 women and 5 men. Mean age was 39.3 years old. There were no statistically significant differences between Group 1 and Group 2 for either VA (p = 0.3934) or Ishihara (p = 0.140), but a significant difference was found for VF MD (p = 0.0405). A markedly significant difference for RGCL thickness (p = 0.0001) was found, without any correlation with the degree of visual recovery. A subgroup of patients (n = 14) was examined at the time of initial visual loss. We correlated their results of visual function to the final RGCL thickness, and a correlation was found between either the initial VA loss or the initial VF loss and the final loss of RGCL (R2 = 0.4075 and R2 = 0.00739, respectively).
CONCLUSIONS: In our study, all patients with ON lost a significant amount of RGCL despite a full recovery of vision, as defined by our criteria. The percentage of RGCL loss varied from 5 - 27% and could not be correlated with any final visual indices. However, a correlation was found with the degree of initial visual loss. Despite sometimes marked RGCL loss after ON, patients with MS can recover normal visual function, according to standard clinical tests.
So with one attack of optic neuritis you have lost 5-27% of your visual reserve Wouldn’t you want to save it?