I finished yesterday emotionally burnt-out; “broken and useless, no longer working or effective” or “kaput” as the Germans would say. I did an all-day clinic with my registrar off sick; it was hard and brutal.
On my way home I wondered to myself if I should change the name of my MS clinic to the ‘Smouldering MS Clinic’. Virtually all of my patients had smouldering MS or as some of you would prefer me to call it PIRA (progression independent of relapses).
With our aggressive campaigns of treat-early-and-effectively, treat-2-target, zero-tolerance, NEDA (no evident disease activity) I think we have exposed the real MS, i.e. smouldering disease. Almost all my follow-up patients were NEDA yesterday and doing ‘well’. However, when I interrogated them almost all of them had subtle symptoms and signs of disease worsening. Worsening fatigue, cognitive slowing, reduced walking distance, dropped feet on exertion, nocturia, sexual dysfunction, numbness and clumsiness of the hand, subtle unsteadiness of gait, poor balance in the dark and when tired, increased leg spasms at night, reduced auditory discrimination, problems with night vision, etc.
The new norm is smouldering MS or more likely the realisation that MS is smouldering MS. Our anti-inflammatory DMTs are doing what we say they should do, i.e. they are stopping focal inflammatory lesions and relapses, but are they getting to the core of the disease, ‘smouldering MS’? I suspect not.
I have argued several times before on this blog that focal inflammation is not MS and that the real disease is what is driving the immune system to produce the focal inflammatory events. I suspect that effective DMTs are simply converting relapsing-forms of MS into what we used to call primary progressive MS.
If you have MS this post will be very depressing, but as soon as the MS community faces up to the above the better. We would then start directing our limited resources to tackle smouldering MS.
I would encourage the funders (government, charitable, private and pharma) to start to divert their R&D spend to addressing smouldering MS. What needs to be done? I would encourage out-of-the-box thinking and support alternative hypotheses of MS. We need deep phenotyping and biomarker studies. More trials on drugs targeting CNS B-cells and plasma cells, microglia inhibitors or activators (both need to be tested), drugs that target astrocyte and oligodendrocyte biology, antiviral trials and trials targeting ageing mechanisms. I would also include systems biology and the impact of diet, etc. on smouldering disease. We need a “Smouldering MS March of Dimes” event to raise the money to get on top of the real MS.
I would like to thank you all for helping out with our grant naming survey. It is clear that from a scientific perspective PIRA (progression independent of relapses) won out. However, smouldering MS came a close second and most commentators prefer this name to describe PIRA to people with MS and their families, i.e. smouldering MS is a lay-term for PIRA. I, therefore, suggest we keep both names in the MS lexicon and use them interchangeably when discussing the real MS.
Don’t be fooled into a false sense of security that because you are NEDA that your MS is under control. We clearly need to go beyond NEDA to tackle MS.
60 thoughts on “My ‘Smouldering MS Clinic’”
Yes, yes, yes, yes, yes!
What about more research into hidden inflammation? We know it’s there. Just because it doesn’t show up on an MRI doesn’t mean there’s no inflammation and that has to be a factor in progression.
What you just described was my husband’s life before HSCT – all those worsening symptoms but nothing showing in the MRI. He was rapidly worsening SPMS
Last week he had his 3 year follow up at King’s – no new lesions (T1 or T2) but then, why would there be – but more importantly, no progression and no smouldering MS. His MS has been frozen.
It sounds incredibly tough. However, without what you’ve done for them, your patients would have had relapses to contend with too. It’s one battle at least part won, surely?
Re: “It’s one battle at least part won, surely?”
Yes, definitely. The base of the pyramid is in place. However, saying this there are still many academics who don’t buy into combination therapies.
I have early onset, slow PPMS, have had it nearly 20 years now, and have never had any treatment other than physiotherapy. It is of course very disappointing that DMTs are not controlling the true disease, but from my perspective it is also very heartening to hear of a shift towards treating the real McCoy, finally.
For the keen readers of this blog – what has changed over less than 11 months from (“If I had MS if you seriously consider HSCT”), followed by lines along the lines of “Alemtuzumab is second best after HSCT on reducing BVL” to the very depressing “I suspect that effective DMTs are simply converting relapsing-forms of MS into what we used to call primary progressive MS.”
Re: ” “Alemtuzumab is second best after HSCT on reducing BVL”
One good news story yesterday was a patient who came back to see me 48 months into alemtuzumab treatment (two courses 2016 and 2017) with no complaints and NEDA. In fact, this patient had improved. So the early IRT (immune reconstitution therapy) experiment needs to run its course. Unfortunately, it may take a further 10-15 years to get an answer.
A Cold Fire Burning inside
A Smoky Stench, neither Burning nor being put out
My clinic days they test me a say, are you taking meds?
You look pretty good.
I pulled myself together to get there.
I perform for the Doctor, Trying to do my Best
Or they won’t like me
Or they would feel a failure
Or they’ll give up on me.
My Adult side knows they care for me.
My Child side is scared of what a Doctor I worked with called “The Dwindles”.
You’re on the right track, Dr. G
Thank you for making the effort.
“I finished yesterday emotionally burnt-out; “broken and useless, no longer working or effective” or “kaput” as the Germans would say. I did an all-day clinic with my registrar off sick; it was hard and brutal.”
Slightly OTT. At least you can go for a run, have a brisk walk round the park, or look forward to a well earned retirement where you can travel…. What you describe, is what MSers feel like most days… we don’t get a day off, just the knowledge things will get worse!
Your post leaves me with mixed emotions. Firstly, annoyed that after decades or research, trials, lots of therapies, a focus on achieving NEDA… that it looks like MS researchers have been barking up the wrong tree. I took the risks attached to my highly effective induction therapy and am now being told all I’ve done is covert myself (at 45) to PPMS! Pixxed off doesn’t really capture how I feel. Where do I apply for a refund / compensation given that the expert advice I received was dud? Perhaps at ECTRIMS 2020 there should be a one minute silence so the researchers can reflect on all the patients they have let down?
At least you have the courage to put your hands up! However, please don’t create another 20 years of MS research projects. I’ve had enough of the every expanding industry which is MS research.
What we need is focused effort on what drives progression (smouldering MS) and identifying drugs to stop it (not just slow it down). I thought there was an international alliance looking at progression which was set up a few years ago. No doubt little has been achieved.
This is a very depressing post for anyone with MS today. I wonder if it’s time to ditch your wretched treatment pyramid given the new insights? Time to ditch the tube map? All we needed was one treatment to stop smouldering MS in its tracks. Looks like all we got over the last 25 years were expensive sticking plasters. I’m looking forward to meeting my neuro in November for my annual check-up. He’s an MSologist, and I hope he’s read this post. It’s been clear for years that progression carries on regardless whatever current treatment you are offered. Once again, thank you for stating what other neuros must see in their clinic but have chosen to ignore.
Re: “Slightly OTT. At least you can go for a run, have a brisk walk round the park, or look forward to a well-earned retirement where you can travel…. What you describe, is what MSers feel like most days… we don’t get a day off, just the knowledge things will get worse!”
Unfortunately, life is a lottery and I may have my expectation of a well-earned retirement thwarted by who knows; developing bowel, prostate or renal cancer, or having a myocardial infarction. I think we all have to learn to reflect on what we have and try an do today what needs to be done and hopefully, the longterm goals will materialise. I think this applies to living with MS, which is why I encourage all my patients to practice mindfulness.
Re: “I wonder if it’s time to ditch your wretched treatment pyramid given the new insights?”
I think we the new insights support the treatment pyramid. It is not that we don’t need anti-inflammatory DMTs, but the add-on treatments to stop smouldering MS.
Thanks for your honest opinion and honest self reflection. I wish your “blinded” colleagues would support your viewpoint publicly.
It has been clear for quite some time that the treatment pyramid is incorrect and evidence is mounting to support this. Tysabri and Gilenya with their “field effect” is just one example as you have so eloquently pointed out on this blog.
For many years now, it should have been neuroinflammation that is studied concurrently with neurodegeneration, remyelination and neurorestoration products.
Neuroinflammation means INNATE immunity caused by a virus, possibly EBV controlled memory B-cell clusters, with associated hot microglia, A1 astrocytes, oligodendrocyte changes or neuronal death and NOT adaptive peripheral immunity, which is only a downstream effect, that should be the focus.
It is too bad most MS patients are now no better off clinically, socially and economically than if they took no drug at all. Hey but at least Pharma has made 20+ billion per year off of drugs they knew didn’t work with purposeful faulty endpoints in their trials (relapse rates, Gd+MRI) instead on long term disability as Dr. Ebers pointed out.
I cannot wait to hopefully meet you in the New Year Gavin. I have my appointment booked. I know you cannot comment on personal patients but need to get this off my thoughts. I had Venoplasty in 2012 I have lost so many symptoms by having this done. I have gone from PPMS backwards. I understand what you mean by smouldering M/S. I am smouldering but don’t know where it is coming from. The messages are there to walk but they need a kick up the bum to make them more stronger. Confused because I am. What part of the pie do I fit into please ? x
Dear Professor G,
You are doing a brilliant job. Nothing depressing at all because this is something we patients new but no one would listen . Happy to hear something is moving , someone is thinking outside the box . If everybody acknowledges this something will be able to be changed, property solutions to be found .
We really do not know, when does MS start? The brain reserve could hide a lot of invisible damage, and of course when DMDs switch of the inflammation a lot of (visible and invisible has done). So finally added with annage related BVL the sympthoms are growing…
What about the remarkable effect of Alemtizumab? As I know it’s efficacy correlated (esp BVL) with the stability of the disease.
Re: “What about the remarkable effect of Alemtuzumab? As I know it’s efficacy correlated (esp BVL) with the stability of the disease.”
You are right. Alemtuzumab data is extraordinary, but the population treated in the trials were very early in the course of their disease and it is still too early to be confident that they don’t have smouldering MS. Even if it doesn’t reverse or switch off smouldering MS it is definitely delaying its manifestations.
I will stress again it is all about treating early and effectively. Waiting too long to treat and delaying escalating to more effective DMTs almost certainly comes at a price down the road.
Would anti-inflammatory drugs perhaps not be rendered unnecessary with an effective treatment for the real disease?
Re: “Would anti-inflammatory drugs perhaps not be rendered unnecessary with an effective treatment for the real disease?”
Possibly. If MS proves to be due to a virus then all that will be required to treat, and hopefully cure the disease, is an antiviral. If on the other hand it is autoimmune then you will need the anti-inflammatories at least the IRTs to get on top of the inflammation.
For clarity – are you saying that there’s no point taking a DMT (induction or maintenance) as they won’t have any impact on smouldering MS or disease progression.
I had very aggressive MS with disabling relapses (one relapse put me in a wheelchair for a bit). Lemtrada stopped any more relapses and I have been stable (relapses, MRI and EDSS for the last 7 years). So the treatment was a lifesaver for me. I don’t know if I have any smouldering MS or have converted to PPMS, but I feel that Lemtrada has given me 7 good years and that must be worth something. I know someone with rapidly progressing PPMS and they are in a terrible situation. I’m glad I started with RRMS as it helped me get my head around the disease.
Re: “For clarity – are you saying that there’s no point taking a DMT (induction or maintenance) as they won’t have any impact on smouldering MS or disease progression.”
No, not at all. You have to have an anti-inflammatory (base of the treatment pyramid)m, but that is not enough. You then need an add-on therapy to address the other pathology.
But you do not know if anti-inflammatories would still be necessary, depending on the “other” therapies mode of action / efficacy. The inflammation is the body’s reaction to damage. Not the root of the damage.
Is it no surprise that EAE steered the understanding of MS from its trust source (viral / smouldering inflammation) to one where it was an inflammatory disease focused on myelin. EAE was a very poor model for a number of reasons, but the recent insights show how useless it was and treatments to stop progression / smouldering MS were never going to come from EAE.
Prof Hauser also is onboard with the thinking about PIRA / silent progression:
Can’t you team up with Hauser and a couple of likeminded researchers to tackle smouldering MS? Too many research teams work in silos without genuine collaboration. Too focused on winning funding, working for pharma or getting a trophy from ECTRIMS than cracking the real MS.
Re: “Too focused on winning funding, working for pharma or getting a trophy from ECTRIMS than cracking the real MS.”
Without funding, we can’t do the necessary research and without Pharma, we can’t do clinical trials. The one thing we can do without are trophies 😉
PIRA – thanks for explaining what that means prof G. That was written on many lampposts and walls where I grew up near Belfast. Only now do I find out that it means (progression independent of relapses)
Nothing to do with the Provisional Irish Republican Army 😉 But I could draw some analogies.
This is not a depressing post this is a dose of realism. I’ve had MS for nearly 50 years. It has never done anything more than to get very slowly worse and worse for nearly 50 years. Picked up and identified quite by chance. Only ever had a few relapses that come and go instantly. Never eligible for any sort of a drug. Nw definitely Sp#MS with more problems than you can shake a stick at
At last my MS has a description, it smoulders, it is recognised. Next step is to get drugs for it. Researchers eyes are being refocused. Yes, there is treatment for aggressive MS such as HSCT but mine just slowly meanders along like the Ganges. OK it is now SPMS but it is continually getting worse.
Yes drugs are being trialled for neuroprotection and possibly rebuilding the myelin sheath. Lets hope something positive comes our of this cos surely that is a step towards dousing the embers of smouldering MS whether you were diagnosed yesterday or 50 years ago
If anyone can tackle the smouldering affects of the disease it is you Prof G. Please don’t get discouraged or lose heart for the cause. I don’t have much hope and am eternally pessimistic but somehow I have faith in you. Even if you don’t personally find a “cure” I think you will push the right people in the right direction to do so. Thank you for what you and keep fighting for us. Providing REAL hope is as good a legacy to leave as any.
“If you have MS this post will be very depressing” No! It’s depressing when your MS care team tell you no new lesions means you are doing fine. This post makes me feel understood (even if it will take about 5 years for this understanding to reach my country)
Goodness I have so many responses to this article
Having had my first Ms episode in 1994 and the second in 1995 (which was suspected as being MS but only shared between a neurologist and my GP rather than with myself ) and because of how my disease has progressed I have always been suspicious of the drugs now given to someone promptly on diagnosis.
There is little long term proof that any of these drugs really work. I was clear for 10 years following my covert diagnosis so if I had received drugs and had had no further episodes for ten years, which was obviously going to happen anyway, I would have been classed as cured when actually it was always there and developing into a full-grown monster. You cannot even say that had I been diagnosed I would have had an MRI scan which would have have shown the disease because the scans are unreliable.
I I have always suspected that many of those lucky enough to be diagnosed straight away now and will be lucky enough to to receive one of the ever growing array of drugs will also have this growing monster regardless of any treatment which will then return at a later date either at full Force as mine did or, perhaps as you mentioned in this article, as what used to be called primary progressive. By this I assume you mean steady worsening without relapses
What are the stories of all of the people on the trials of tysabri and alemtuzumab?
Of those on the trial who had been recently diagnosed are they NEDA or did they just have the not uncommon disease lull and now have seen a return to active disease?
We never really here about the unsuccessful stories.
So if what you are saying is true and even the drugs which reset the immune system i.e. the ‘big guns’ to use your description like hsct and alemtuzumab may at best only delay the inevitable why are you bothering testing established drugs in Oratorio and chariot trials on those people already noticeably affected? I’m confused!!!
I thought your argument was that all drugs help MS regardless of where you are on the disease journey it is just Nice and budget restrictions which exclude anyone more severely affected with the disease. I cannot believe you have just changed your mind so am I misreading something?
On a lighter note….
Are any of the new drugs being trialled a favorite to stop smouldering?
In my stunning niavety after being diagnosed last November, I said something along the lines of “oh so you might have a relapse and then it usually goes away and gets better? There’s nothing really going on inbetween?”
No wonder they looked stunned!!
I had no idea that there are literally day to day “small” things going on all the time!
Which now kind of makes sense to me, why would there be overwhelming fatigue when there is no relapse going on…
This MS malarkey is CONSTANTLY day-by-day attacking our brain reserve/capacity I take it?
If these DMDs we all take are effectively doing nothing more than being a plaster on top of a scab and the scab’s source isn’t being treated then what real hope have we got?
When will EPSTEIN BARR be TREATED in us?
Surely there must be something NOW that can be taken at the same time as the DMDs??
PROF G WHAT IS THERE NOW FOR US pretty please????????
If inflammation is a result of a relapse, rather than the cause, do you think it is appropriate to refer to DMT’s as “anti-inflammatory” or would another term be more accurate?
Yes, maybe we should be calling anti-inflammatory as being treatment strategies targeting the peripheral adaptive immune response; we could also refer to them as being T or B cell-targeted therapies.
Please shout this at every dr you know because as a patient tired of being told I am fine because of HE DMD and “stable mri” despite how I feel and making me feel crazy for even suggesting progression independent of relapse.
While what you suggest is important the years of research won’t help a lick for any of us already diagnosed. What we desperately need, while we wait for more research, is access NOW to any and all options that have a chance at freezing the smouldering and that includes HSCT. This needs to be made available to ALL patients willing to try it, not just the ones who fail, as the best chance of success is if someone gets it early… still shocked that what we know may work is not given as an option when the alternative is guaranteed progression
But HSCT is just a potent anti-inflammatory.
Which is why HSCT seems to work better in early relapsing MS. You need to treat early before too much of the slow-burn pathology is set-up that drives smouldering disease.
Which despite our usual suspect naysayer curmudgeon of the abundant aliases, we definitively proved in our EAE model some time back. 😉
It must be so inconvenient when those with progressive MS halt their progression with HSCT too. (No alias here, by the way).
A lot of the focus of recent HSCT research has been on reversing disability – Dr Burt didn’t have an answer for me when I asked him why a stable EDSS of 6 five years after HSCT in an SPMS patient was not a success in his view.
For many, symptomatic reversal and improvements are a bonus – halting progression is the overriding goal.
The plural of anecdote is not data, Alison.
HSCT certainly is a good option but it is not a one size fits all therapy.
You’ve used that line before, Mousedoctor – time for some new material? You need new writers.
I’ve never claimed HSCT is suitable for everyone with MS, but it’s undeniable that it has been effective for more than solely RRMS.
Talk to King’s – they have data relating to patients with SPMS and PPMS who have been successfully treated with HSCT.
I’ll keep using it until the message is understood, Alison. 🙂
Bless your heart.
I do enjoy our banter. x
Incidentally, the SPMS patient with the unchanged EDSS was from Dr Burt’s own data and was an example he used in his presentation…
I’m not sure I’m following. The real disease is smouldering, possibly caused by a virus. The relapses, the inflammation – which current DMTs tackle – is the body’s reaction to the initial damage. I was getting the impression that the smouldering will happen whether there’s unhelpful relapse reaction or not. 🤔 You are 100% certain that this relapse inflammation is part of the initial insult, is required to perpetuate MS?
Re: “You are 100% certain that this relapse inflammation is part of the initial insult, is required to perpetuate MS?”
Not 100%, but pretty sure. Initial relapse rate (first two years only), disease activity on MRI (baseline lesion load and first 5-years of activity) imprint on the MS brain and determine outcome 20+ years later. This is why we talk about early and effectively. However, even if we get in early and effectively a strategically located slowly expanding lesion or SEL will be enough to cause smouldering MS and progressive disability.
A depressive read indeed, but thinking outside the box is what the MS community need to one day reach a kind of cure. What i dont understand prof G is that there has been post on this site with people and pasients of yours on tysabri for 10+ years still being stable. Wouldnt that mean that there is not PIRA with these pasients and that DMT early on will stop PIRA from happening?
A fan from Norway
Are you sure that all patients have SMOULDERING MS?
Can you say that?
Re: “Are you sure that all patients have SMOULDERING MS?”
Check-out the post-mortem studies; the most recent one from Oxford shows 100% have ongoing active pathology at post-mortem. The problem with the material is that they were collected in the patients who missed out on early effective DMTs.
Its seems to me that ms is a very heterozenous disease this all inclued the very benign couse (5 ;10%)
Are they Smouldering too?
What about the alemtuzumab .hsct patients?
You are trying to “one size fit all” kind of scenario (pharma friendly)
There are user on this blog that are neda at 10+ after alemtuzumab
And aparently their edss did´nt change are they Smouldering MS?
Is this just your opinion in a sea of opinions?
Bitsch A1, Brück W. Differentiation of multiple sclerosis subtypes: implications for treatment. CNS Drugs. 2002;16(6):405-18.
There has been tremendous progress in the immunomodulatory treatment of multiple sclerosis (MS) during recent years. With the introduction of interferon-beta, glatiramer acetate and mitoxantrone (recently registered for MS in the US), there are at least three therapeutic strategies that have proven effective in large phase III studies. However, not all patients with MS respond well to treatment with these drugs. This may largely be a consequence of disease heterogeneity. From a clinical perspective, patients with different disease courses show different treatment responses. Patients with relapsing-remitting MS are more likely to respond to immunomodulatory therapy than those with a progressive disease course. Studies of patients with secondary progressive MS have yielded inconsistent results and, so far, there has been no positive phase III study of immunomodulatory therapy in patients with primary progressive MS. Pathological evidence indicates that subtyping based on clinical findings alone does not reflect actual disease heterogeneity. In a large series of biopsy and autopsy specimens, at least four subtypes could be identified with respect to oligodendrocyte/myelin pathology and immunopathology. As long as the only method of identifying subtypes of disease is histopathology, differential therapy will remain a future goal. Thus, there is an urgent need for in vivo markers of immunopathogenesis in an individual patient that would allow treatment to be specifically directed towards a given pathological focus. However, at least from a theoretical point of view, some therapeutic approaches appear very attractive. Plasmapheresis and/or intravenous immunoglobulins could most plausibly be the best approach for the immunopathological subtype of MS, which is characterised by antibody and complement deposition next to demyelinated axons, in order to remove antibodies. The subtype of MS that is associated with heavy macrophage activation, T cell infiltration and expression of inflammatory mediator molecules, including tumour necrosis factor-alpha, may be most likely to respond to immunomodulation with interferon-beta or glatiramer acetate. There are other subtypes of MS in which viral infection or oligodendrocyte degeneration, rather than autoimmunity, appear to play a role. It is possible that these could benefit from antiviral therapy, oligodendrocyte protection or oligodendrocyte transplantation, although therapies based on these latter approaches have yet to be developed.
No scientist or medic but the paper on ‘subtypes’ written way back in 2002 makes it sound to a layperson as if MS is not ‘one disease’ as I’ve read in this blog many times but actually an umbrella term for a number of different illnesses with some similar symptoms. (Am I right in thinking from your synopsis of the paper that some ‘subtypes’ are caused or driven by a virus, others by autoimmunity etc?) If this is the case why aren’t we having a wider range of tests when diagnosed? Wouldn’t that information be necessary to develop treatments for all the ‘subtypes’ or illnesses called ‘MS’? Confused.com
I respect you ProfG for always being someone who tells it how it is, but with a focus on ways to progress things in the treatment of MS and also in facilitating living with it as best as we can.
It can sometimes be an emotional challenge to read some post material, but you never simply leave it dangling there, like some rotten fruit. Instead, you highlight routes research should take, or those areas you and others have successfully initiated. Or you make known lifestyle options such as mindfulness, D-Mannose, or intermittent fasting.
I also respect you, and others such as MD, for being so driven and energetic in the pursuit of improving things in the world of MS. Today I met with a friend of mine who is an OT. I said that I wouldn’t be in the place I am with my MS if it’s wasn’t for the Bart’s Blog! Told her everything from pushing for Alemtuzumab to the supplements I’ve chosen to take are as a result of accessing this site on a daily basis. I’m NEDA thanks to alemtuzumab, but I’m also 56 in Dec – ‘the new Black Death is ageing’ So I know that I am focussing now on smouldering MS and my age due to the info you provide and making life style choices accordingly. When you and others of the team do retire there’s gonna be one f***ing great big hole and I’ve found I’m already worrying about that…😆
I’d echo Patrick in saying that I hope there’s some good results in the trials of neuroprotection and remyelination agents.
Totally second Pharmer B reply.
Until trials get underway for neuroprotection, remyelination and, one day, antivirals – there are still so many people without any basic dmt at the bottom of the pyramid.
SPMS has to be the largest unmet need. According to the MS Trust that is about 38,000 in the UK alone. Gavin, what do you think about siponimod? Inside the CNS is it potentially acting as more than an anti inflammatory? Will pwSPMS have to tick the active box to qualify for treatment? So many people with relapses bubbling away under the surface but impossible to spot against the background of existing weakness, neuropathy, fatigue and pain. Plus not many pwSPMS get regular monitoring let alone MRIs.
Then there is the (smaller population) of pwPPMS unable to tick the active box for ocrelizumab.
Not to mention everyone EDSS 7+.
Roll on Chariot and O-hand!
What are the risks with anti-viral therapy following immune reconstitution (alemtuzumab)?
They are not with side effects and the cost a lot of money. We need class 1 evidence to show they work. Professor Julian Gold and I have been trying for about 6 years to get a HAART trial funded in MS. We will keep trying.
Are there any biomarkers for “smouldering MS” that would be sensitive enough to support trial results on a shorter time frame than 10+ years?
So are you saying in effect is that despite DMTs being given to reduce inflammatory episodes …ms will inevitably progress to SPMS ? And that now a relatively longer period of time has elapsed since these DMTs have been available this can now be properly assessed .If that is so it is what I have always suspected might be the outcome.
I like the name”Smoldering MS” makes me 🤭 laugh. Thank You. Oh man you have 2 have something that does with this disease. Thank You for the work you do 2 help others. It would be nice not 2 hurt & function normally again. Can’t wait for an end 2 MS. I’m the 5th in. Blood Line in my family 2 get MS & hope no one else gets this disease……again Thank You for Your Work 2 find Help, Cure
Care-MS II had an impressive results (bvl, arr, EDSS stability and improvement) as well. In spite of the fact the patient had ms for 5 yrs an average, and had more advanced ms (3.0 EDSS an avg. /0-5/).
So when is too late to prevent smouldering ms?
Does smouldering ms connect with the age related decline? (SPMS, PPMS starts later an average,)
Unfortunately, I completely agree with the progression of MS, though I am highly aware of symptoms. I have not found a suitable treatment for my MS, having failed most meds I tried. I entered a clinical trial of high dose Cytoxan that made me feel normal, but it only lasted 1.5 years, followed by various infections from a re-booted immune system. My neurologists that listened to my claims about progression of disease are either not local, retired, or changed specialties.
I recently changed from Ocrevus to Kesimpta, which I am waiting to start due to my current Solumedrol infusion. I told my neurologist I didn’t like Ocrevus and the delay of washout period from Tysabri caused severe symptoms and my doc didn’t think the new right leg weakness mattered, so he did nothing. My last MRI during Ocrevus showed advanced disease, not on previous MRI reports.
Only prayer and wishful thingking will improve my condition that I am tired of trying to prove is worsening. After diagnosing myself in medical school abroad, The medical community needs to spend time listening and less time presuming everything is normal.