Treatment for Optic Neuritis Holds Promise
The American Academy of Neurology (AAN) is meeting this week and of course we are particularly interested in the Multiple Sclerosis part of the proceedings. If you follow the advances in MS research then you know most ‘new’ discoveries are timed to be announced with these big conventions. This week will be no exception.
The news is already out that we can expect to hear more about promising trial results on the treatment of optic neuritis, an inflammatory problem of demyelination of the optic nerve that often results in permanent damage and loss of vision of some degree, up to partial and sometimes total blindness.
A team of researchers from England proposed a while back that neuroprotection of the nerves during an MS relapse was possible using commonly available drugs, and after successfully testing their ideas on mice, they have now demonstrated that their approach looks promising by testing a small population of people with MS having an attack of optic neuritis. Of course this is excellent news, but even better is the drug that might be the answer to halting demyelination and slowing secondary and primary progressive forms of MS is a drug already used by humans. That means it’s safety profile has already been studied and proven. The protection and regeneration of lost pathways came by using a commonly prescribed epilepsy drug – phenytoin, a sodium channel blocker. You may know it by the trade name Dilantin.
The study due to be presented this Friday at AAN was conducted by Dr. Raj Kapoor, of University College London Hospital and others. People who were at the onset of an optic neuritis attack – within 14 days of their first symptoms – were randomized into either a placebo group or received phenytoin. The timing for this intervention is critical and catching optic neuritis early is important to minimize damage.
Of the people who received the drug there was a 30% reduction in axonal loss. Any advantage that can be gained by stopping this loss is significant. Unlike the brain which has lots of ways it can rework around damaged pathways, there are few routes for the signals between our brain and eyes to travel, and there is little room for demyelination before the sight is impacted in meaningful ways.
One of the researchers who did much preliminary work looking at sodium channel blockers is Dr. Gavin Giovannoni. He and a team of other academic researchers at Barts and the London School of Medicine and Dentistry, are also working in their lab to develop a version of a sodium channel blocker that looks to be even more effective than phenytoin. Dr. Giovannoni runs one of the widest read multiple sclerosis blogs on the web – Multiple Sclerosis Research – and does a thorough job of explaining the results of their work to date. You can read his complete update at AAN 2015: Embargo lifted early on optic neuritis trial.
The use of sodium channel blockers as a neuroprotective drug has been looked at before and from what I read, there must be many labs around the world looking at formulating a version specifically for MS. Dr. Giovannoni writes that he and his team began their work on sodium channel blockers over 15 years ago. The use of this type of drug offers the hope that even though they were looking at optics neuritis, the slowing of neurodegeneration could be meaningful for people with SPMS and PPMS, and there might even be hope for repair and regeneration of damaged myelin. What works to stop the inflammation of the optic nerves should very well also work on the nerves in the spine that are causing the progression of this disease for so many of us.
It’s estimated that at least 50% of people with MS experience Optic Neuritis at least once. Watch for the big headlines on Friday about this important finding – here’s hoping this one pans out and further studies back these initial findings.
Wishing you well,
This article represents the opinions, thoughts, and experiences of the author; none of this content has been paid for by any advertiser. The MultipleSclerosis.net team does not recommend or endorse any products or treatments discussed herein. Learn more about how we maintain editorial integrity here.