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    Study results for 55+ MS patients

    Has there been any movement on the study that some doctors have been participating in that is looking at how MS patients are doing by coming completely off of their MS meds when they are 55-60 years old? Apparently the theory is that by age 60 most of their patients have stablized (as much as can be expected, I guess) and taking meds wasn't worth it any longer. Was wondering if anyone had heard of an update on this topic?
    Wendy
    "There are signs everywhere...."
    "Life is wasted if it's not lived as an adventure."

    #2
    There are ongoing age studies, however, with limited data available at present.

    I would highlight the two most prominent positions regarding the cessation of DMTs around age 55.

    This first position is heard more and more these days and it is poorly reasoned, IMO.

    As stated by Dr. Anders Svenningsson it says that, and I quote, “around 55-60 (maybe younger!) the combination of a prolonged treatment effect and natural cessation of disease activity makes treatment of very low value, but you still retain the risks.

    So, I would say as a rule of thumb that if you are over 50 and have had a not so active disease anytime it might be worth trying discontinuing all therapies. Of course, keep yearly MRI controls.” End Quote


    Why is that position weak? Dr. Gavin Giovannoni explained it this way…

    “This advice (by Svenninggsson) is based on a leg/EDSS-view of MS and not an arm-, swallowing/speech- or cognitive-view of MS.

    Why should you write off someone’s cognition, etc. to MS because they are old if you can slow down the loss of function in systems with preserved reserve capacity? Your call.

    This is why we are doing the ORATORIO-HAND and CHARIOT-MS trials; to change opinion and to help pwMS who happen to be older and/or with more advanced disease.”

    Comment


      #3
      Originally posted by TheBeans View Post
      Has there been any movement on the study that some doctors have been participating in that is looking at how MS patients are doing by coming completely off of their MS meds when they are 55-60 years old? Apparently the theory is that by age 60 most of their patients have stablized (as much as can be expected, I guess) and taking meds wasn't worth it any longer. Was wondering if anyone had heard of an update on this topic?
      Hi Wendy

      From what I could find, trials on this are still ongoing.

      There was an observational study done at Cleveland Clinic, and the findings from the study were presented at the 2018 ECTRIMS (European Committee for Treatment and Research in Multiple Sclerosis) Congress.

      https://consultqd.clevelandclinic.or...-appears-safe/

      Take Care
      PPMS for 26 years (dx 1998)
      ~ Worrying will not take away tomorrow's troubles ~ But it will take away today's peace. ~

      Comment


        #4
        Dr. Corboy at the Rocky Mountain MS Center in Denver has an ongoing study looking at this right now. I believe results will be available sometime in 2020.

        Comment


          #5
          I do not have study information, but can tell you my personal experience.

          I was diagnosed in 2006 (age 52) after having symptoms of numb and heavy feet along with some "odd" neurological responses for a year or so. I received a diagnosis quickly and was on Rebif for 6 years with no symptom or MRI changes. In 2012 I chose to discontinue Rebif, hoping my MS had "burned out.". I was off Rebif for 6 years when, at the age of 63, I had a wicked relapse with an MRI that showed multiple new, active lesions and old lesions that had not been obvious before.

          Despite steroids and physical and occupational therapy, within 4 months I had to leave a full time job and go on short term disability, progressing to long term disability and finally Social Security disability. I went back on Rebif 2 months after the exacerbation. I now have hand controls for my car, a rollator, mobility scooter and stair chair lift.

          Whatever clinical studies might demonstrate, make the DMD decision you can live with. I am now left second-guessing my decision to stop Rebif in 2012. Good luck with whatever you decide!

          Comment


            #6
            Thanks Canary54 for sharing your experience. It is that fear that keeps me on my DMD.

            If you don't mind me asking, did you have symptoms for a while prior to diagnosis? I am wondering if the burnout period may be a function of years from onset of symptoms versus a function of age.
            Kathy
            DX 01/06, currently on Tysabri

            Comment


              #7
              Originally posted by pennstater View Post
              Thanks Canary54 for sharing your experience. It is that fear that keeps me on my DMD.

              If you don't mind me asking, did you have symptoms for a while prior to diagnosis? I am wondering if the burnout period may be a function of years from onset of symptoms versus a function of age.
              "The infamous "burnout" of MS may be less than hoped for, in fact, whether it exists at all is debatable. Just because there are no new lesions, or enhancing old lesions that appear on standard 1.5T (tesla) or 3T MRIs does not mean there are no lesions or no MS activity.

              Gray matter lesions not appearing on 3T MRIs may be occurring, they are just not seen except on 7T or higher tesla MRIs. Because no new lesions are seen standard MRIs and progression is not evident for a number of years does not mean MS has "burned out". It may only be doing a "slow burn". MS, as a chronic, progressive disease may frequently slow, however, rarely totally cease activity. MS is sometimes compared to an iceberg which is 90% under the surface.

              The trade-off may wonder about is... if the med I take is primarily targeting inflammation, and new inflammation has not appeared (at least not seen on 3T MRI) for years, can I safely stop my DMT, should I stop my DMT?

              The answer can only be made individually.

              Here are some relative thoughts posted a few years ago by a brilliant doctor...

              https://multiple-sclerosis-research....ing-curing-ms/


              "The current thinking is that MS is an autoimmune disease of the central nervous system that is driven by focal inflammatory lesions. We think the MS lesion, or focal inflammation, is responsible for both acute (now) and delayed (in the future) neuronal loss.

              Permanent loss of neurological function (impairment or disability) is due to neuronal loss, which can be measured clinically (neurological and neuropsychological examinations), electrically (evoked potentials), on MRI (brain atrophy or loss of brain volume) and/or biochemically (spinal fluid neurofilament levels).

              Acute Neuronal Loss (the Shredder or Scissors): Inflammation transects neuronal processes, or axons, acutely that results in loss of function. If the lesion is an eloquent site it causes a relapse.

              Loss of function is then restored by the surviving axons taking over the function of the lost axons, or other areas of the brain taking on new functions, we call this axonal and cortical plasticity, respectively. Recovery can only occur if there is sufficient reserve capacity.

              The accumulation of damage and ageing reduces reserve capacity, which explains why recovery from relapses tends to fail with more advanced disease and with age. This is why it is important to treat MS early so as to protect reserve capacity.

              Delayed Neuronal Loss (Slow Burn): Neuronal processes (axons) that survive being transected are compromised and never recover fully.

              They may remain demyelinated, or if they are remyelinated the myelin sheath never gets back to what it was in health. In addition, the so called microenvironment within the chronic MS lesion is stressful to the axon. All this programmes the previously damaged axons to die off over time.

              This is why anti-inflammatory therapies that switch off the development of new focal inflammatory lesions may not prevent the delayed neuronal loss that characterises progressive MS.

              Even if we were able to cure MS as an autoimmune disease we may not be able to stop, or prevent, progressive disease from occurring in the future as it may already be programmed to occur from previous damage that has accumulated in the past. In other words progressive MS is like a ticking ‘time bomb’.

              Premature ageing: We seem to forget that as we get older we lose brain this is what we call age-related cognitive, or neuronal, decline.

              From the age of 35 our brains start to shrink and our neuronal systems start to fail. The manifestations of this are not that subtle; how often do you battle to find the right word, or remember an important fact, only to find that your memory has failed you.

              Similarly, your balance is just not as good as it once was; you realise that you can’t put on your trousers standing-up unsupported and you have to resort to sitting down, or holding onto to a piece of furniture, for balance. If we all lived long enough we would all dement from natural ageing.

              Evolution never designed our brains to live as long as we are living today. What protects us from the ageing process is brain reserve; the more brain reserve we have the later we will present with our dementia.

              As MS reduces brain reserve we hypothesise that people with MS (pwMS) will notice age-related cognitive decline earlier than the general population. So even if we cure you of your MS you may still get a drop off in neuronal function earlier than expected that is simply due to ageing. However, this drop-off in neuronal function will interpreted as MS-, and not age-, related decline.

              The insights above highlight some of the reasons why we started the ‘Brain Health: Time is Brain’ campaign and why it is going to be so hard to prove that we have cured MS. However, if we don’t define what a cure looks like we won’t find it. I am very aware that a lot of people in the field disagree with me on this.

              Defining a cure in MS: Based on what I have said above you may be cured of our MS, but still have progressive disease.

              The difference between progressive disease that is due to previous damage and that which is due to premature ageing is that the former should burn-out, i.e. after a period of time your worsening disability should stop.

              In comparison, premature ageing is unlikely to stop. In comparison defining a cure in people who are young, with reserve capacity, who have been treated earlier would be easier.

              Importantly, a cure can only really occur in relation to induction treatments, i.e. treatments given as short courses that address the underlying ‘cause’ of MS. Maintenance treatments that need to be given continuously can’t cure MS, because when you stop the treatment MS disease activity returns."

              Comment


                #8
                I stopped my DMD, because there were no changes on MRI. A repeat MRI after still showed no changes.

                I have read about another kind of scan, though. Maybe I should request one of those?

                Comment


                  #9
                  MyOak - thanks for the article.

                  Originally posted by MMMMS View Post
                  I stopped my DMD, because there were no changes on MRI. A repeat MRI after still showed no changes.

                  I have read about another kind of scan, though. Maybe I should request one of those?
                  Just curious, as I struggle with this same scenario. No changes in MRI for years, but that is what the DMD is supposed to do - stop relapses. I had one lesion stable for 6 years on earlier drugs, started Tysabri, and it shrunk. My question is what made you take the risk? What were decision point factors? Wondering if things that I may not have considered that I should. What did your neuro say?

                  I have been going back and forth on this for a few years, I've had mild progression, but all related to symptoms that were part of earlier relapses, no new symptoms. Is that the med working or SPMS? My last neuro was of the opinion, why risk it? Preferred I stay the course, but recommended that rather than stopping all together, go on Ocrevus. See my new neuro in 6 weeks and this is one of my top discussion points. His PA was of the opinion any progression, even if mild, I should consider different med. Can't wait to hear his opinion.

                  As far as scans, I know some of the research facilities/hospitals use more powerful MRIs(7T) and can look at both white matter and grey matter (as MyOak pointed out). They used to think MS was just a white matter disease, but now say grey matter involved. Traditional MRIs (1.5T nad 3T) can't see grey matter. They may also use functional MRIs, but don't know anyone that has had one.
                  Kathy
                  DX 01/06, currently on Tysabri

                  Comment


                    #10
                    It was no changes on the MRI. No disability. And the Copaxone shots were creating divest in my skin. I stopped taking the med a few years ago now, and there are still no changes.

                    I hope I'm one of the lucky ones and not just one of the thick-headed ones. 😆


                    Originally posted by pennstater View Post
                    MyOak - thanks for the article.



                    Just curious, as I struggle with this same scenario. No changes in MRI for years, but that is what the DMD is supposed to do - stop relapses. I had one lesion stable for 6 years on earlier drugs, started Tysabri, and it shrunk. My question is what made you take the risk? What were decision point factors? Wondering if things that I may not have considered that I should. What did your neuro say?

                    I have been going back and forth on this for a few years, I've had mild progression, but all related to symptoms that were part of earlier relapses, no new symptoms. Is that the med working or SPMS? My last neuro was of the opinion, why risk it? Preferred I stay the course, but recommended that rather than stopping all together, go on Ocrevus. See my new neuro in 6 weeks and this is one of my top discussion points. His PA was of the opinion any progression, even if mild, I should consider different med. Can't wait to hear his opinion.

                    As far as scans, I know some of the research facilities/hospitals use more powerful MRIs(7T) and can look at both white matter and grey matter (as MyOak pointed out). They used to think MS was just a white matter disease, but now say grey matter involved. Traditional MRIs (1.5T nad 3T) can't see grey matter. They may also use functional MRIs, but don't know anyone that has had one.

                    Comment


                      #11
                      If you are on a DMT and MRIs are stable and no exacerbations the assumption is the DMT is working. However, it is also possible for the same thing to happen even if you don't use a DMT.

                      You can have stable MRIs and still progress with or without DMTs.
                      Diagnosed 1984
                      “Lightworkers aren’t here to avoid the darkness…they are here to transform the darkness through the illuminating power of love.” Muses from a mystic

                      Comment


                        #12
                        Pennstater:

                        I've had an unusual course of MS. I had what, by my description, my neurologist believes was my first MS exacerbation in 1977 at age 23. MRI not available in 1977. Our small town GP was preparing to test me for a brain tumor when I gradually began to improve in about 3 weeks. I experienced complete recovery and my GP said it was just a "what the heck was that" virus.

                        I experienced ABSOUTELY ZERO symptoms for the next 29 years. I never had another exacerbation after 1977 until the one in 2017 that led to my disability. However, my disability has progressed since going off Rebif in 2012. So, I have had 2 exacerbations in 42 years. However, I am definitely Secondary Progressive at this time. I also am now afraid to go off Rebif, because how much worse could I get with another exacerbation!

                        Comment


                          #13
                          My MRI's were also unchanged before I started on Copaxone. In my case, I think there is no way if telling if it helped or not.

                          Originally posted by SNOOPY View Post
                          If you are on a DMT and MRIs are stable and no exacerbations the assumption is the DMT is working. However, it is also possible for the same thing to happen even if you don't use a DMT.

                          You can have stable MRIs and still progress with or without DMTs.

                          Comment


                            #14
                            Pennstater...

                            I empathize with you, Kathy as you consider a change in DMT or going off the one you are on.

                            My spouse made the transition from Tysabri to Ocrevus a couple years ago so if you don’t mind I will share some of the thinking that went into that decision and what has been learned since.

                            First, IF you do choose a similar transition, it would be wise, IMO, to schedule the first infusion of Ocrevus as close to the last Tysabri infusion as your neuro will do. Of course, the reason for doing so is to present the smallest window of opportunity for MS rebound due to a lack of DMT coverage.

                            Fortunately, Tysabri does provide MS coverage in some for around 8 weeks. We know that because of extended dosing with Tysabri. Certainly, there appears adequate coverage for most at 6 weeks with Tysabri.

                            JMHO, but it seems extraordinarily foolish to go much beyond 6 weeks for a washout period. Why wash out protection against MS if there is minimal conflict between Tysabri and Ocrevus, which appears to be the case? My spouse’s first infusion of Ocrevus was a day or two short of 6 weeks, I believe, from the last infusion of Tysabri. I see the least risk in the shortest washout period.

                            I feel uncomfortable identifying the anti-malarial she used prior and during the transition period because using it was the result of personal study, not doctor's advice. An anti-malarial was used for the possibility of diminishing JCV, hopefully decreasing the chance of PML. Also, it appears to have some good effect against EBV. I do not suggest anyone else do the same. I suggest treatments based on your doctor's advice.

                            However, one might choose such a course personally, individually, after thorough study if convinced something is largely harmless and might have benefit. I’m reluctant to identify what was used because people run out, buy something, and use it w/o adequate knowledge. Perhaps, by mentioning it a researcher somewhere may think it makes sense, as it did with me, to investigate this hypothesis. In any case, this particular transition from Tysabri to Ocrevus went flawlessly… no MS flare-up, no IRIS (immune reconstitution inflammatory syndrome), no problem whatsoever. Yes, it was a trial of one but please recognize that a trial of one is close to meaningless, scientifically.

                            Separately, I would add that a JCV vaccine is currently being developed. I don’t follow that research closely since PML is not a concern on Ocrevus. However, if the JCV problem were solved, Tysabri would be an extremely attractive DMT. It is quite attractive even with the PML concern. It can be a great DMT for those who respond to it. It does appear you are one of those excellent responders to Tysabri, Kathy.

                            Tysabri can be so good that it may lure one into thinking they have a mild case of MS when their MS may be mild only because of Tysabri.

                            Adequate response to a new DMT is not guaranteed; a small percentage develop neutralizing antibodies to each of the DMTs, including Ocrevus. Individual response is unknowable ahead of time.

                            Next thought… be prepared for a good deal more fatigue on Ocrevus than with Tysabri. That is true in this household and doctors have reported other Ocrevus patients saying the same. Only by taking Adderall can the same level of function be achieved in this household with Ocrevus.

                            Kathy, as you know, Tysabri keeps certain B-cells from crossing the BBB. The obvious problem is that if the Tysabri washout is too lengthy those problematic B-cells can get into the CNS and cause a murderous flare-up of MS as sometimes has happened coming off Tysabri.

                            Ocrevus kills the problematic B-cells Tysabri keeps out of the CNS. It does not kill all B-cells but it does kill several different types. Some doctors believe, as do I, that over-depletion of B-cells may inevitably lead to increased risk of serious infections and cancers. IMPORTANT NOTE… ONLY TIME AND DATA WILL TELL.

                            It will probably take years of data gathering and analysis for proof Ocrevus does or does not increase those risks. I personally believe it will increase risk of both. Is there a way to manage that perceived risk? Yes, I think so, as follows…

                            My Treatment Concerns with Ocrevus

                            Ocrevus is dosed every 6 months, however, there exists strong scientific evidence of effectiveness for 18 months following cessation presented in “Long-term safety and efficacy of ocrelizumab in patients with relapsing-remitting multiple sclerosis Week 144 results of a Phase 2, randomized, multicenter trial”.

                            Given there are B-cell controlled infections and given that Ocrevus potently diminishes B-cells are we not likely to see serious infectious complications arising from overdosing Ocrevus? Recovery of the cell type targeted by Ocrevus varies individually; it seems risky and foolhardy to keep adding more ocrelizumab to an amount already achieving maximum effectiveness.

                            Since we have the capability to track measurable endpoints via B-cell counts in blood work why should Ocrevus be dosed at fixed 6-month intervals and not on measurable endpoints? Others have made this point, “Anti-CD20 Cell Therapies in Multiple Sclerosis-A Fixed Dosing Schedule for Ocrelizumab is Overkill.” https://www.ncbi.nlm.nih.gov/pubmed/29123374

                            Dosing Ocrevus every 6 months does not appear warranted by science or reason; it does appear dangerous by taking needless risk.

                            Treatment is always a balance of competing values, but understanding that, we would not want to add risk needlessly via fixed interval dosing. The result for some people may be catastrophic and we want to avoid that possibility as much as possible, especially if reducing risk is as simple as personalizing a dosing schedule.

                            Deviating from the scheduled 6-month dosing is being done on a limited basis in the US. However, it takes an exceptional neurologist working with a patient to do so.

                            Every six months may be great for controlling MS but doing so may leave one exposed to higher risk of serious infections and cancer. Getting the next infusion of Ocrevus only when the B-cells Ocrevus kills has reconstituted makes sense; it makes little sense to keep killing something already dead when we need our immune systems as functional as possible to fight infections and cancer.

                            Blood can be tested for the types of B-cells Ocrevus kills. Only if/when those reconstitute do they need to be killed again by the next dose of Ocrevus. Not every neuro agrees with this protocol but fortunately, my spouse’s neuro did agree to proceed with the next dose based on what her blood work shows.

                            I am so grateful for this amazing doctor! At 6 months if the B-cells Ocrevus kills remain low or non-existent why hammer the rest of your immune system down with another dose of unneeded Ocrevus? Is that medically prudent? Is it financially prudent?

                            Kathy, it may be worth waiting for additional Ocrevus data to understand if there is increased cancer and/or serious infections on 6 month dosing. Personally, I believe there will be more risk but no one can say for sure w/o data.

                            Mavenclad is worth a look, IMO. It may not be quite as effective as Tysabri or Ocrevus but it does leave your immune system much more intact. As we age and MS activity diminishes somewhat, perhaps Mavenclad could be an excellent fit for some in that group… effective enough to control MS while leaving the immune system intact enough to fight off infections and cancer.

                            I understand people wanting to stop DMTs late in life and for some it will work out. For some, stopping may not be best. The situation is always individual.

                            There is wisdom in what Linda in Colorado says… if it ain’t broke, don’t fix it.

                            Comment


                              #15
                              Thanks MyOak. Lots to think about. I am still JCV negative and infusing every 6 weeks, virus status checked every 3 months. So I am fortunate.

                              As for Ocrevus, various cancers run in the family. So I am hesitant for that reason. I didn't know about the increased fatigue. More to think about.
                              Kathy
                              DX 01/06, currently on Tysabri

                              Comment

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