ProfG has been banging-on about “Treat early and effectively to save brain”, until he is blue in the face….So much so, that he has turned into a Smurf
Sadly there are still many of his colleagues that don’t buy into this… and follow the mantra of “There….There, we’ll get ya a nice wheel chair”

The vast majority of neuros and pharma bods still cling-on to the notion that single drug treatment is the only way to go.
The therapeutic pyramid has not been built in the minds of the masses.

Why do I say this?
Look at all the clinical trials that academics do…MS-“NOT SO” SMART is a good example. Three neuroprotectives against placebo and doing nothing about the inflammatory component….It failed so it was not so smart…STAT-2 follows STAT MS and looks at a neuroprotective but not on top of a disease modifying treatment. What will happen if MS-SMART-2 comes along?….Combination or more of the same I suspect. We can blame those people for making the wrong choice of drug to justify another go, but god forbid if we have the wrong type of trial design. If it is it fails each time and we have not learned for past mistakes
However, time is running out. The progressive MS space is getting filled with DMT and neuroprotectives/remyelination agents will have to go on top of these. I say great and about time.
However ProfG has also been making the case that MS is one disease and it is not relapsing MS on one day and the next day it is progressive M.
Nerve loss and damage occurs at the begining to the end of MS. Therefore we should consider a neuroprotectant at the beginning of MS as well as the end. OK the problem is I can’t say definitively which agent, but we have to make a start before ProfG turns into Papa Smurf.

The phenyton optic neuritis trial indicated benefit from early treatment with a neuroprotective, but it never went anywhere and clinical practise has not changed. But maybe you do need protection and repair agents all the way through MS and certainly at the beginning when there is something to save. Indeed it is most important right at the beginning.
Why? Because this is when you have what we call “neurological reserve”. You can afford to loose a few nerves before you notice anything, but once you reach that point every nerve that is lost can be important.People with PPMS have used up their reserve quickly.
It is not just MS. You can lose about 80% of your pancreas before you notice type 1 diabetes.
Currently you can’t grow a brain so best not to lose it.
What more do you need?…..Evidence?….How much more do you need?
Axonal Degeneration Independent of Inflammatory Activity: Is It More Intense in the Early Stages of Relapsing-Remitting Multiple Sclerosis Disease? Cilingir V, Batur M.Eur Neurol. 2020 Sep 21:1-9. doi: 10.1159/000510116. Online ahead of print.
Background: This study aimed to investigate whether there are differences in the axonal degeneration rate between patients in the early years of relapsing-remitting multiple sclerosis (RRMS) disease and RRMS patients in their later years.
Methods: The early-stage RRMS patients (EMS) group had 65 patients whose duration of disease was within 3 years from the date of the first attack. The late-stage RRMS patients (LMS) group had 69 patients whose duration of disease was within the range of 3-10 years from the date of the first attack. In addition, a control group was composed of 32 healthy subjects. Peripapillary retinal nerve fiber layer (RNFL) thickness was monitored with spectral-domain OCT in all included patients for approximately 3 years.
Results: The annual RNFL atrophy rate (aRNFLr) in the EMS group was -1.246 ± 0.778 μm/year, the aRNFLr in the LMS group was -0.898 ± 0.536 μm/year, and the aRNFLr was -0.234 ± 0.154 μm/year in the control group (p < 0.001). The aRNFLr in the EMS group was significantly higher than the aRNFLr in the LMS group (p = 0.01). The aRNFLr was not associated with MRI activity or the condition of having an attack. There was a correlation between Expanded Disability Status Scale (EDSS) progression and aRNFLr in both the EMS and LMS patient groups (r = -0.471, p < 0.001, and r = -0.567, p < 0.001, respectively).
Conclusion: The axonal degeneration rate is faster in RRMS patients in the first years of the disease than in later years. In addition, axonal degeneration occurs independently of inflammatory activity. Axonal degeneration is correlated with disability progression, but not with inflammatory findings, such as clinical episodes and MRI activity.
Now the visual pathway is affected early in MS and could account for this phenomenon…you know that is not the real point..Rest assurred more evidence is on the way. However we need evidence for the right therapeutics to use. As for correlations of R=0.04-0.5…as seen here….is meaning less.
My experience of talking to a consultant neuropsychiatrist and their neuropsychiatry registrar was they were both unaware of the treat MS early and effectively campaign/ school of thought.
🙁
Perhaps targeting neuropsychiatrists and making them aware might be a good idea? It may affect how they treat and understand MS patients. The impression I got from them is they understand MS is a slow, gradual burn even in RRMS and there is no rush or priority needed.
Perhaps Barts MS could collaborate with a neuropsychiatrist on something, to start getting the message out there?
Fully agree with this.
Suppose you had complete freedom to assemble an (experimental) treatment protocol (preferably out of already available drugs), how would it look like?
How do we force our care teams to take notice of this. Too many of us are being left by the wayside (obv not by you guys) – how do we create pressure for neurologists to change the habits of a lifetime? After all, we’re just patients, they’re the doctors, the experts, have spent years of their lives studying blah, blah, blah. What can we do to make them listen?
PwMS need to be insistent, this can be done in a polite, non-aggressive way. If that fails then consider changing MS Consultant. If you have a neurology consultant that is not an MS specialist consultant, consider finding one. The hospital may not be forthcoming in this suggestion, so being proactive if you can is a must.
I changed my neuro after several years of polite, non-agressive requests to escalate my DMT were ignored/dismissed. MRI remained stable, but walking getting worse plus new symptoms.. Now under a new pro-active neuro… and just finished Ocrevus infusion. Yes, it was a hassle and time-consuming to switch, but so pleased I did. Brought terrific piece of mind knowing I am doing all I can.
Rachel
I also have been “banging on” about this to my neurologist & MS nurse who are based at a “Centre of Excellence” – like talking to a brick wall.
Since diagnosis 10 years ago I have had one mri & one physical examination which was limited to the soles of my feet & that was after weeks of telephone calls when I was experiencing a relapse.
I truely don’t think this is good enough.
CoE yep why has uptake of the knowledge been so slow
Education and persistence
MD, a question abut neuroprotectants – i have read a number of previous posts about gaba drugs / baclofen having neuroprotective qualities. Maybe i am being stupid but i couldnt work out definitively whether gabapentin was considered to fall in this category. I have just obtained a prescription (for symptomatic reasons) so in the absense of clinical trials, we are left to try our own……
Gabapentin (despite its name) doesn’t act at GABA receptors.
Thanks for the reply MD. I was never any good at science but i did better at in English so i will rephrase the question…..do you consider gabapentin to have neuroprotective qualities?
If Prof G cant convince is colleagues who will?
It is not just MS. You can lose about 80% of your pancreas before you notice type 1 diabetes.
Parkinson also
“The discovery of brain-first Parkinson’s is a bigger challenge. This variant of the disease is probably relatively symptom-free until the movement disorder symptoms appear and the patient is diagnosed with Parkinson’s. By then the patient has already lost more than half of the dopamine system, and it will therefore be more difficult to find patients early enough to be able to slow the disease,” says Per Borghammer.
How do I say this without risking potential skepticism? I’ve met with for years. Aside from finding the perfect Neuroprotectant Nerve Healing Anti Inflammatory Cocktail (bound to cost mightily), can you ever find a better way to evaluate pwMS level of Nerve Inflammation and Destruction than MRI with Gadolinium Contrast that is known to accumulate in our brains? I’m talking about Daily Wearable Monitor combined with daily self assessment, diary, testing. Activity level, sleep, pain. Hopeful for a miracle including Doctors who are Dreamers of the impossible. 😎
Fortunately my neuro holds the view to hit it hard and early.