Q&A Feb


If you have a question that might be unrelated to a post or just a question in general, this is the place for you.

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    • Thay couldn’t galvanise themselves to do it.
      Boom tish

      I thank you, I’m here all week…………………………..

    • I have been taking multi-vitamin and minerals since lockdown started and will continue after I get vaccine protection, ProfG vaccine status unknown and not sure I suspect the vitamins I bought him before lock down are gone. The hydroxylchloroquine has not been shown to work, but again trials are probably the problem

    • I have been taking multi vitamina and minerals since lock down started and will continue after I get vaccine protection it is one of my 5 a day…As for ProfG vaccine status unknown and he may have run out of the zinc tablets I bought him last March. The hydrochloroquine treatment has failed in trials…was it the tiral design

  • do you ever think fast efficient high efficacy treatment is likely to happen in the uk ? and what can a person with ms do to help push this forward?

    • I absolutely know that fast high efficacy treatment will happen in the UK and one is not going to get more fast that what ProfK is planning. What can people with MS do…Shun Neuros who don’t want to take part, as it shows their colours. OK this it sort of a little joke. It would be interesting to do Freedom of Information requests to find out what each NHS trust uses….I bet there are places that essentially they only use platform (CRAB) drugs and other places that use very few. Stay clear of the former. I will bet that the Sheffield will be the latter as they are willing to give people the option of high efficacy treatment, likewise I can bet that other places will be the former. I suspect that the MS Society have done this but are too nice to show this info, pharma will have done this. I wonder if this can be got by Bluetech? We have to give students projects to do

  • Do we have any evidence that there is a T cell immunity response / memory to a vaccine when no B cells are present? Curious how the mechanism works if so.

    For reference, I’m on Rituxan and have low IgG that requires me to get monthly IVIG. I had my first Pfizer vaccine 3 weeks ago with almost no side effects. I had my second dose 2 days ago and had a headache, body aches, the feeling of a fever / chills without an actual fever, and just general malaise. It’s already gone today. I wasn’t entirely expecting this (although hoped to!) due to not having B cells with the expectation that I wouldn’t really have an immune response to the vaccine.

    • It sounds like you had reactogenicity this is where you get reaction to vaccine and it is know that this is worse on the second injection of the Pzifer vaccine. However just because you may not have any B cells in the blood doesn’t mean you have no B cells. This has been shown with tonsil, lymph node biopsies, bone marrow studies where there are B cells. However it seems you have been brain washed to think that B cells are the only antigen presenting cells to induce immune responses but this is a major function of dendritic cells. You can make a T cell response when you have no B cells for example. Pedersen G, Halstensen A, Sjursen H, Naess A, Kristoffersen EK, Cox RJ. Pandemic influenza vaccination elicits influenza-specific CD4+ Th1-cell responses in hypogammaglobulinaemic patients: four case reports. Scand. J. Immunol. 74(2), 210–218 (2011). Hypogammaglobulinaemia is a genetic condition where you have not B cells and you have to have IVIG. They make T cells, I can find other examples. The question that is of interest is how long after the infusion did you wait before taking the vaccine. Give it about 14 days and get your bloods taken to see if you have made a covid response

  • Thanks MD – pic = nice reminder of Spring being on its way.

    Prof G – endorsement, if you were to need it, of your advice to all of us concerning maintaining our health – from one of todays BBC articles:

    One-in-three patients admitted to hospital as an emergency has five or more health conditions, such as diabetes, obesity or asthma, up from one-in-10 a decade ago.

    • The had popped up in the garden and they were in the supermarket last week, after the freeze they may all of had it

  • Why in your opinion is Ocrelizumab more effective than Cladribine if Cladribine depletes a larger variety of cells?

    I would like to go on Cladribine as I have failed Copaxone and Tecfidera, and Clad look attractive, but I am wondering whether going on Ocrelizumab would offer the potential for a more long-term remission.

    Looking forward to your reply.

  • Have you noticed any trends in heart rate reactions when infusing Ocrevus at faster rates? I just had my first dose of Ocrevus under the newly approved faster dosing rate in the US yesterday, and I found that my heart rate spiked to about 40% over my normal sitting heart rate about 3 hours after I got home, and stayed that way for about 4 hours. I’ve had elevated heart rate in prior treatments, but it typically happens before I leave the infusion center and doesn’t last as long.

    Silver lining: my Fitbit gave me credit for doing light cardio when I was really just sitting on the couch watching TV. 🙂

    • LC – I am no longer on Ocrevus; however, I experienced similar increased heart rate issues, even under the old drip speed. Went to the cardiologist and determined I now have a slight heart murmur. Nothing significant, just wanted you to know you are not alone. These drugs are very effective and also very destructive to other non MS functions.

    • How fast was your drip? Did they perhaps up the steroids, too? They put me to 200ml/h (IIRC but may well be wrong, the anti histamines don’t help memory) in summer without any odd effects other than very shallow breathing.

      No more odd than a combination of anti histamine and steroids would do, anyway.

    • Faster heart rates are a known side effect of ocrelizumab “These infusion reactions can happen for up to 24 hours after your infusion. It is important that you call your healthcare provider right away if you get any of the signs or symptoms listed above after each infusion”.

  • Has there ever been any studies into the use of recreational drugs being related to MS. For example, the ones you’d see at a rave, in the 90s. Asking for a friend.

  • I have a bunch of questions in no specific order. Answer the ones you’d like.
    1. How can we make up for lost time during 2020?
    2. You mentioned the huge literature on COVID-19, setting aside the “not spitting on others reduces chance of spreading COVID”, are there any advances that may help MS research i.e. virology?
    3. Will EBV vaccine work and if it does, would B-cell depletion+vaccine be an idea worth checking?
    4. prehabilitation and MS, any suggestions on regimens that are not strictly physical?
    5. Charcot MS, EBV, When? Not to disparage as I know the effort you’ve put into this. Maybe a pharma with no entry in the MS market would be interested?

    • 1. Time travel
      2. Vaccine development
      3. You have to test it. B + V up for discussion
      4. Charcot part II was put on hold with COVID

  • If CIS converts to MS….was it always MS in the first place? i.e if someone only stays at CIS does that make it a completely unrelated disease / phenomenon?

  • Prof G says MS is progressive from the start. The data for conversion to SPMS on anti cd20 meds is apparently poor, leaving patients to seek out alternatives. However, how do these two things tally up. If we’re progressive anyway then there is no conversion to take place?

    • There is no better alternative unless you are brave enough to go Ahsct. At least we know for sure CD20 meds do significantly slow down progressive progression. I would love to see evidences of Alemtuzumab being better than CD20’s, as nothing I’ve seen is convincing.

        • Where is the data (S. hauser is sat on it?) but the question is when was the rituximab started…I think the important result will be from diagnosis, but the question is how long can people realistically stay on CD20 depleters. IS is forever, or will complicates occur?

  • Is it possible to make a simple table showing how people on DMT’s like ocrevus should manage the intervals between infusion and vaccine to maxmise vaccine effectiveness , without undermining MS treatments? I keep forgettng. thank you Christine

  • I was wondering what your thoughts are on the Temelimab trial. I can hear ProfG say “Clinical trials are on and we will know soon” 🙂
    My question is more regarding the trial design and what the drug is trying to address.
    They are trialing it on people who have been on rituxan (maybe a potential maintenence treatment) as well it is trying to address underlying smoldering. This study seems to be employing some of the strategies ProfG has been advocating. Yay or Nay?

  • Evening
    Is there any evidence that breastfeeding reduces the risk of postpartum relapses? I am hoping Lemtrada has done it’s job.
    Also is there any evidence that children of mothers with ms should have higher than nhs recommended doses of vitamin d? I took high dose throughout pregnancy so again hoping this has helped.

    • Breast feeding yes

      PostG doses himself according to the vitamin D council, this is higher than the 40oIU

      Babies up to the age of 1 year need 8.5 to 10 micrograms of vitamin D a day.
      Children from the age of 1 year and adults need 10 micrograms of vitamin D a day. This includes pregnant and breastfeeding women, and people at risk of vitamin D deficiency.
      From about late March/early April to the end of September, the majority of people should be able to get all the vitamin D they need from sunlight on their skin.
      A microgram is 1,000 times smaller than a milligram (mg). The word microgram is sometimes written with the Greek symbol μ followed by the letter g (μg).
      Sometimes the amount of vitamin D is expressed as International Units (IU). 1 microgram of vitamin D is equal to 40 IU. So 10 micrograms of vitamin D is equal to 400 IU.

  • I know that being on gilenya, my covid vaccine response will be blunted but can you say by how much? Efficacy halved? Quartered?

      • Had my initial Pfizer jab an hour ago and it’s reassuring to know that as soon as you have any info on how blunted our immune response is – whatever the DMT involved – Alem in my case – we will be the first to know.

        When I initially found the Blog some 4yrs ago I hadn’t anticipated the sense of reassurance regards it’s provision of info extending to a pandemic, but the feelings still apply😄
        Thanks as always!

  • Cladribine has some limited T cells depleting capability… did anybody test T cells subtypes before and after drug?

  • I came across a company that is developing a drug for remyelination, it works on muscarinic receptor M1 the site says. The compound is PIPE-307. Do you have any idea/opinion on this?

  • I’ve started Aubagio as my first DMT. I am interested in getting the pfizer covid vaccine, the pneumonia one and also the BCG vaccine. Are these safe vaccines with my DMT as it advises against live vaccines (pneumonia and BCG)? Would really appreciate your input since this is my first relapse.

    • The EU label says “Two clinical studies have shown that vaccinations to inactivated neoantigen (first vaccination), or recall antigen (reexposure) were safe and effective during AUBAGIO treatment. The use of live attenuated vaccines may carry a risk of infections and should therefore be avoided.

      The BCG vaccine protects against tuberculosis and is a live vaccine. The pfizer vaccine is RNA against covid and the PPV The pneumococcal vaccine protects against serious and potentially fatal pneumococcal infections. It’s also known as the pneumonia vaccine. These are both non live

      nd non live

      • What’s the risk/reward ratio of the BCG vaccine as it says its good for recently diagnosed people. Would it be risky in my case and can the CBC test be used to determine the risk?

  • What types of infections have a positive correlation (triggers) with relapses/smouderings?

    Or what types of infections should we pwMS be extra careful to avoid? Other than covid-19 ofc…..

  • About 18hours after my first Pfizer vaccine I developed a patch of skin on my torso that was very sore/ sensitive to touch. This lasted only about 24hours. It does scares me in terms of neurological reactions and I feel slightly concerned re the second dose which for many is supposed to provoke an immune reaction. Can you provide any reassurance?

  • What is in your opinion safer?

    Natalizumab to Cladribine/Ocrelizumab or Cladribine/Ocrelizumab to Natalizumab in terms of PML risk?

  • are constant fasciculations (twitches) normal for ms ? i have had one in my hand for the last month and it is there all the time it never stops, could it be a side effect of gabapentin ?

  • pwms has to choose third DMD in the same amount of years?

    A) alemtuzumab
    B) cladribine
    C) ahsct
    D) nothing, let immune system stabilize in current environment

    (Previous DMDs, ocrelizumab 1st, teriflunomide 2nd, under 40 years old)

    Answer: B – small molecule thus bbb penetrating, lower reported adverse reactions, removes CNS bands, and less sledgehammery with similar effects. Hopefully after B comes D 😉

  • Prof G, in your November post on ‘Teriflunomide’s secrets’, you state that:
    “I have hypothesised in the past about teriflunomide’s broad-spectrum anti-viral effects and have proposed doing the iTeri study, i.e. using an anti-CD20 or other depleting DMT as true induction therapy and then using teriflunomide (or another DHODH inhibitor) as the maintenance therapy. The hypothesis is to allow peripheral B-cell reconstitution or recovery to occur in the presence of anti-EBV agents, which will prevent EBV-infected autoreactive (MS causing) B-cells returning.”
    Assuming a subject is responding well to teriflunomide (relapse-wise), could that imply that teriflunomide can fend off both MS (relapses, brain volume) and EBV(-reactivations)?

      • And assuming the 1st agent used to deplete b-cells is stronger than ocrelizumab.

        Teriflunomide does effectively “regulate” the immune system, so it seems to be a good maintenance drug to use after a STRONG depleting agent. However, teriflunomide has some pretty bad side effects, so maybe try and find another regulating agent with anti-viral aspects to use other than Teri.

        • would you care to elaborate on your comment:
          -I’m open to suggestions as to the “other regulating agent with (possibly EBV-specific) anti-viral aspects”…
          -And I’m not sure why teriflunomide would only seem acceptable after “a STRONG depleting agent”? What about pwms who have NEDA using nothing but teriflunomide? Would, for these patients, teriflunomide not prove to be sufficient in suppressing MS-activity – as well as possible EBV-reactivations?

          • I am not a neuro or scientist, I am just sharing my experience as a pwms.

            To answer MD, maybe ProfG DODO approach would be strong enough to get the b-cells hiding in the CNS. Or maybe using clad or alem first then maintenance with Teri.

            For your case, not sure how the theory would apply if you are not depleting before using Teri. If an anti-viral works without first using a depleting agent then maybe it’s not the b-cells. Do you get your lymphocytes tested? Be interesting to see where your b/t cells are with just Teri.

            I had a difficult time with Teri. Bone loss, hair loss, excessive bleeding, nausea, gastrointestinal issues, etc. however it did effectively keep my b-cells low (which were still depleted from ocrelizumab). I tend to be more prone to the drug side effects, so my experience is not the norm.

            The fact that I did not respond to either drug, on top of having serious adverse reactions to each drug, suggests my immune system response to these drugs is not normal.

            Hopefully clad will work for me. If clad does not work, then I am just going to do nothing and see what happens. Maybe my new “altered” immune system will be a bit less likely to cause MS relapses.

  • What does it mean if steroids initially resolve symptoms really well but the symptoms come back a few days after finishing a course ?

  • I was due to receive my first covid jab today but my surgery only have the one I am allergic to. They say to wait till more Pfizer arrives but haven’t said when that will be. Where is the best place to go for up to date info on vaccine supplies in the UK?

    • When you find it let me know, but ask you surgery if they ever are doing the pfizer jab (This has storage requirments), if they are not find a place where they are offering the pfizer jab.

      • OK thanks. They had Pfizer last week, my group came up a few days too late to catch the last of it. So close….
        I have made some enquiries locally but no luck.
        I raised the allergy issue with the surgery a few weeks ago but I don’t think they can choose who they vaccinate, rules is rules and I’ll just have to wait for the next batch.

  • My neurologist won’t prescribe me ocrevus because of covid and when I went to see my family doctor for a second opinion the other clinic denied my request for a second opinion because of covid what should I do for my next steps if I want to get started on ocrevus ?

    • I am sorry you are unable to fullfill your wishes. The Association of British Neurologists originally suggested avoidance of high effcacy DMT and still they indicate that risk benefit needs to be considered, this advice was updated in November 2020. I cannot give advice as it needs to come from neurologist

      • Thank you for taking the time to respond. I hope things get better I am just so scared that I would need to wait another 6-7 months before being able to access that medication. I just want a better futur. Thank you for the information you gave me it helps me a little. 🙂

  • I recently came across Osmosis’s Type IV hypersensitivity videos calling MS a T-cell mediated Type IV hypersensitivity disease (updated quite recently in 2019 still!!). Now that we learn MS is more of a B-cell mediated disease, would it be still classified as a hypersensitivity disease? I think I remember MD2 mentioned MS is more likely driven by immune complex just like RA and SLE. I would also like to ask would I do better in the long run if I try to minimize allergic reaction exposures? I have hay-fever and my husband is considering removing all bushes and grasses in our garden..

  • In the event that the covid epidemic never happened and that you had positive results of your famciclovir trial in MS where would we be today ? Would we be currently recruiting for a larger phase 2 clinical trial in ms ? Who would of been interested in continuing to fund this trial in the event the pandemic never happened and that the results were positive for a larger phase 2 trial ?

  • Very late to be asking a question this month but I’m going to try anyway!

    Over the last few months I’ve noticed that I’ve become somewhat careless when typing anything from text messages, to emails to reports. I seem to be making far more spelling mistakes than I used to or missing words out of sentences. Now I’m aware of it, I’m trying to type more slowly and I check things a million times before I send them, but
    it’s really annoying as a) I’m an English Language teacher and b) I used to be able to spot spelling mistakes a mile off. I also realised today that I sent my students a document with spelling mistakes in it a few days ago which is a tad embarrassing.

    Could this be related to my MS or am I just making excuses for myself? I haven’t noticed anything with my spoken language but with the writing it’s becoming increasingly obvious.

        • As we all know cognitive issues are a critical part of MS and I therefore respect ProfG very much for Brian Health: Time Matters in MS. I’m 57 and if I’m tired then my typing on my phone or iPad deteriorates + I can’t automatically spell the odd word – I can’t ‘see’ it in my mind when trying to sound it out. I can find it helps to give myself a few mins break and come back to it. Verbal ability is generally listed as one of those areas a deterioration is not seen.

          Hope this very recent study is a bit of a boost, as it was for me:

          Know you may well be doing this already, but if not then might I recommend taking 1200mg of Lipoic Acid. There was a study showing it has a positive impact on whole brain atrophy.

          • Thanks, Fi. I probably just need to slow down and check more when I’m typing.

            I have some Lipoic Acid capsules but haven’t been very good about taking them. It says 2 hours before food on an empty stomach on the bottle which kind of rules out any time except before bed for me and then I end up falling asleep on the sofa without taking them! Also I’ve seen some articles saying you shouldn’t take it if you’re on L-Thyroxine for thyroid issues, which I am. MDs or Prof G, do you know if that’s really the case?

            I didn’t know that the dose used in the clinical trials was so high! That would be 8 of the capsules I have per day.
            Thanks for the link to the article on the cognition studies. I’m taking part in a clinical study where I get a battery of cognition tests every year so we shall see. Last year’s were a bit of a disaster….

  • If one has PPMS that has been inactive and stable for years, is there any reason — theoretically — why an mRNA vaccine like Moderna’s would contribute to worsening symptoms a week or so after getting the first shot? Like increase the size of a cervical spine lesions to worsen dysesthetic extremity pain severely? I’m just interested in what might be any theoretical connection. I did feel tired after the first one, but I have had MMR boosters and the pneumonia vaccine in the past 19 months with no affect on MS symptoms. So the sudden worsening is surprising but obviously is likely a coincidence. Even if that is the easy explanation, is there any theoretical connection that is even possible to link the two? Pro-science, pro-vaccine, get your shot!

    • This happened in Israel with the pfizer vaccine, a relapse occurred shortly after vaccination years after stable disease. This vccines can cause fatigue muscle aches pain etc

  • Hyperhidrosis and MS – between the age of 15 – 25, I had a problem of hyperhidrosis on the palms of my hands, dripping sweat constantly. Then the problem subsided, and my palms were totally dry for 15 years. Now, I’m 41, quit my DMT a few months ago, and suddenly my hands start sweating again. Not dripping yet, but you can clearly see they are wet all the time. Could this be related to MS-activity?

  • latest in our series of webinars discussing COVID vaccines.

    COVID Vaccines and the immune system
    Wednesday 3rd March
    4pm GMT / 11am ET

    I’ll be joined by Prof. Ellie Barnes, Professor of Hepatology and Immunology at University of Oxford and Dr Anna Goodman, Infectious Diseases Consultant at Guy’s and St Thomas’ Hospital London.

    We’ll explore the latest ZOE data from over 500,000 logged vaccines to understand how they are working in the real world. We’ll cut the data to look at efficacy and after-effects in the different vaccines and different groups. We’ll unpack what this means for people with compromised immune systems, including those on immunosuppressive drugs.

    Professor Tim Spector

    On behalf of the ZOE COVID Symptom Study team

    I’m flagging this up for anyone who registered with the Zoe Study and wants to join the webinar.
    4pm isn’t a good time of day for me, otherwise I would have joined. Hope anyone who does can feedback to us – MD? MD2? ProfG?

        • Atacicept was designed to get rid of plasma cells. It depletes mature B cells, plasma cells and immunoglobulin levels, notably it was tried in IgA nephropathology and depletes IgA. So maybe a BS opinion. Plasma cells make IL-10 therefore they are immunoregulatory = Standard opinion:-)

          I am aware of the regulatory plasma cell idea and the IgA concept…people are so intent on linking this to microbiome and guy

          I have now had a look at the poster which does not appear to independent of Roche. They use Th17 adoptive transfer in SJL mice and the effect of anti-CD20 looks quite good, they show depletion of B cells in brain, is that because animals didnt get disease and if animals didnt get disease you wouldnt expect to see any cells. So why is anti CD20 so good here when it is rather pants in other models.

          The elevated IgA in blood is skewed by high results in 3/6 mice. Do Ig levels go up with anti CD20 treatment in humans… The answer is no. IgM levels drop by 25% in first year and by 50%, IgA and IgG levels drop with time. Is this more data that is not going to see the like of day except in an abstract published 2-3 years ago (Derfuss et al. The presentation is on the ECTRIMS website. However we have reported this in Baker et al. 2020

          Does BAFF increase with anti CD20 therapy the answer is yes, it also increases with alemtuzumab too so nothing special here. It has been suggested that because there are no B cells there is nothing to use the BAFF up

          They plan to block the effect of anti CD20 with atacicept

          • Ok

            So the idea of deplete all the cns resident plasma cell with bortezomib or another

            Proteasome inhibitor maybe not so good

          • I guess we will out soon as trial is ongoing….there was a EAE suggesting proteosome is is beneficical fingers crossed.

          • Thanks
            Complexity never ends

            Our recent data revealed a role for IL-10 in hematopoiesis, by promoting myelopoiesis, and in accelerating aging-related features. We have evidence that IL-10 is accelerating cellular
            senescence and are pursuing these findings further


            From Porto

          • Atacicept is a quite large protein, I think it does not go into the brain that much. So I also think it did not deplete PCs from CNS. Also, due to the increased of relapse activity if this happened and that was a benefit this was masked and then the trial was halted very early so no chance to say anything. Another point: if we can’t have it both ways (I really like this view), then how can PCs be anti-inflammatory and at the same time make antibodies to activate immune response?

          • Good point.

            In EAE the barrier opens and because they are so small the antibody can travel abit so you can get antibodies in abit and based on the data presented some animals got disease and they got antibody whilst they had disease…you cherry pick the animal (with or without disease) and the section (with or without the cells) you want, give it to the boss and they make it fit the story. (I guess if I do the experiment myself I will then believe it).

            They should have got the cells out of the tissue and the meninges and qualitated the whole lot….This is what we do to monitor nerve loss and guess what the referees dont want that they want a stained section. Even in a diseased animal you can find places where there are no lesions you can get what you want. This is the funny bit as people pick histology that doesn’t match their clinical data, then you know they are cherry-picking thier data…..I guess some people learn to do experiments by number e.g. do 3 experiments of 5 in a group, in a prescriptive way. It is tragic:-(

            The other point is in reality the apprarent worseing is because very few of the group had disease activity, more than normal, but not every body

          • P.S. Remember also that there was a BAFF trial, which we reported and this would do the same as actacicept (Anti BAFF/APRIL) in the context of their hypothesis, yet there was no the evidence that disease, worsened. It did however increase memeory B cells so maybe if they are right then anti-BAFF wont increase IgA and anti-APRIL/BAFF will as this information is a flaw in our argument,

            However hang on this does fit with the human data.
            “Atacicept showed a consistent, dose-dependent reduction in serum immunoglobulins IgA (-13% for atacicept 25 mg, -52% for atacicept 75 mg, and 7% for placebo), IgG (-10%, -31%, 7%, respectively), and IgM (-38%, -69%, and 7%, respectively) through week 24. Notably, there was a dose-dependent reduction in o-galactosylated polymeric IgA1 (-25%, -60%, and 0%, respectively) through week 24.”

            Also https://n.neurology.org/content/90/15_Supplement/P1.394
            Cerebrospinal Fluid IgA Levels Correlate with Disease Activity in Patients with Multiple Sclerosis; A Novel Finding (P1.394) Alexandra Tse, Antara Finney-Stable, Jerry Lin, Saud Sadiq……Surely if IgA was a marker of protective plasma cells then it should be another way.

            However, if you are trying to support some idea like IgA secreting protective plasma cells generaterate in the gut somehow controls disease in the brain, you just ignore the reality that does fit. We are all too polite to ask the question “Does this sound like a crock..?” Their response will be stop being a A-hiole you can have you cake and eat it. I look forward to seeing the paper in “Cell” 🙂

          • First paper is ok but it about serum IgA.
            The second was also on IgA but in CNS. I think I have come across several papers saying that IgM IgG correlate with disease activity so I would be quite sure to say that if you have a plasma cell that makes antibody then it is not for regulatory reasons. To me plasma cells must be removed from the CNS and possibly also their precursor cells.

          • I agree a plasma cell in the brain is not a plasma cell you want….It goes back to the Th1 vs Th2 story, so we will have PC1 and PC2 soon, I guess thhtey are PCreg just like we have had M1 and M2 and A1 and A2 and already these have been discredited. It is too simplistic the Th1 and Th2 story never quite worked in humans and I always thought Th1 and Th2 = bad you dont want either and couldn’t be bother with it. We could never show the TH2 effect cell we got out of animals were mainly Th1. Once I got a paper from one of the Th2 labs to review, I followed the reference trail. i.e. reference to method was to a paper that didnt have the methods, but had a reference to a paper, with a reference to a paper and was shocked when I saw what was done. You got the cells out of the animal, put them in culture stimulated with antigen to make them grow for 2 weeks. Then restimulated them again for another 2 weeks and then assayed them for Th2 activity 28 days later. So you expand something with a culture condition. No wonder I am a cynical.

    • I’m sorry I don’t know I havent been let out for a year:-)…..science conferences were cancelled…they could not afford the cost of putting them online.

      • MARCH Q&A
        How common is core weakness in MS? What about having a weaker core than limbs? I have trunk weakness. I am mobile, however, my weak core severely limits the amount of time I can comfortably stand or sit. My physiologist said it is less common. My PT seemed surprised at my dramatic rubbery wobbly walk after a quick stationary bike ride or my stiff awkwardly bent posture after a few reps of a core exercise. My hip flexors and back pain kick in after being upright for short time, followed by feeling like I am carrying 50 lbs of rocks. What is best way to strengthen my core? I’m desperate to strengthen my core because it has severely restricted my mobility. What methods have helped pwMS?

  • Diagnosis and Treatment of Multiple Sclerosis

    Like this bit 🙂

    Lifestyle Modifications

    Lifestyle modifications may reduce comorbidities and improve outcomes. Based on observational data and a small pilot study, physical activity is associated with improved symptoms and anti-inflammatory effects and may be associated with larger brain volume.65,93 In 1 randomized clinical pilot exercise intervention study (N = 42), significant improvements in fitness as measured by peak oxygen consumption and 6-minute walk distance, as well as improvements in depression symptoms, fatigue, and tested verbal learning and memory, were observed.93 While the evidence for physical activity improving outcomes in MS is currently based on small trials and observational data, there is little risk to the patient and physical activity can add a nonpharmacologic approach to a patient’s treatment regimen


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