Q&A March

Q

Today is Saint David’s day and I should be showing a picture of a bunch of daffodils (National Flower of Wales, in addition to the Leek), but instead you get a bunch of tulips for MsMouse

If you want to ask a question this is the place for you.

About the author

MouseDoctor

180 comments

          • Maybe they do. Since it’s still a relatively rare disease. The link isn’t as established. In one of Richard pryors Interview. Before MS was diagnosed. He mentioned his lifestyle of heavy smoking and long nights in comedy clubs eventually made him catch something.

        • Unfortunately with people discriminating those with disabilities, I chose to keep my MS to myself. I have been a musician but more or less gave it up after my MS diagnosis, due to it being a cut throat career. A lot of jealousy and being ripped off in the music industry.

      • Wouldn’t catching the virus be a good thing (if it doesn’t kill u) as the immune will be busy targeting another virus instead of self. Or can always bing infected be a plausible cure?

        • As far as I know, apart from making symptoms like fatigue temporarily worse, viral infections can trigger relapses and also activate inactive MS. I have slow, inactive PPMS and am very afraid of even common colds for this reason.

  • Which DMTs remain to propose to patients with smouldering MS and 60 years old? Just rehabilitation? Thank you for all your work

  • I hadn’t done any fine needlework for a few months and needed to return to it today but found the lack of sensation in my fingers a problem. Can anything be done to encourage feeling back into the extremities?

  • Hello MouseDocyor and thanks for the opportunity. What do we know about gluten sensitivity and Ms connection? Any chance to revers ms by putting end to gluten?

    • Mult Scler Relat Disord. 2019 Jan;27:156-163. doi: 10.1016/j.msard.2018.10.019. Epub 2018 Oct 23.
      The role of gluten in multiple sclerosis: A systematic review.
      Thomsen HL, Jessen EB, Passali M, Frederiksen JL.

      Abstract
      BACKGROUND:
      There is an increasing interest in diet as a modifying factor in multiple sclerosis (MS), and gluten has been suggested to affect MS.

      OBJECTIVE:
      The aim of this systematic review is to qualitatively evaluate the evidence on the role of gluten in MS.

      METHODS:
      A systematic literature search was conducted Studies on patients with MS, clinically isolated syndrome, or celiac disease presenting with MS-related markers were included, if they investigated effects of diets containing specified amounts of gluten or associations between gluten sensitivities and MS.

      RESULTS:
      Forty-nine publications presenting 50 studies/cases met the inclusion criteria. Study designs, methods, and outcomes varied broadly across studies. Two intervention studies found a positive effect of a gluten-free diet on disease-related markers in patients with MS. One prospective cohort study also found a positive effect of a gluten-free diet, while a survey found intake of cereal/bread to be protective against MS. Four observational studies did not find increased comorbidity of MS and celiac disease. Seventeen studies investigated the level of different gluten-sensitivity markers in patients with MS with inconsistent results. Finally, 12 cases and 13 posters/abstracts/master’s theses contributed to shed light on the topic.

      CONCLUSIONS:
      There is still not sufficient evidence to state whether gluten plays a role in MS, but limitations of current evidence have been identified and directions of future research have been suggested.

      • “CONCLUSIONS:
        There is still not sufficient evidence to state whether XYZ plays a role in MS, but limitations of current evidence have been identified and directions of future research have been suggested.”

        Why does all ms research end like this.

    • “Up to 150 patients (ages 18 to 55) are being randomly assigned to CNM-Au8 at low-dose (15 mg) or high-dose (30 mg), or to a placebo, every day for six months (24 weeks). Of note, concomitant immunomodulatory MS therapies are allowed.Trial goals will be measured after 24 weeks and through to possibly 48 weeks of treatment. Full study results are expected by mid-2021…At ACTRIMS, preliminary, blinded data from the first 34 participants (21 women and 13 men; mean age, 37.7) enrolled in the study, who have been treated with CNM-Au8 for up to 36 weeks was presented”.

      So why are the company talking about this study now it has a year and a bit to go and if it is blinded what can they say….They say “These preliminary results are encouraging as we progress to achieve the critical unmet therapeutic goals of remyelination and neuroprotection for patients with multiple sclerosis”

      Without seeing the data it is hard to make any sensible comments the mouse paper has just been published I’ll have a look.

  • Hello, I was diagnosed with RRMS in June 97 (23 years ago) and was on Betaseron for a year and a half then switched to Avonex for convenience as I was taking a lot of business trips. I was on Avonex for 17 years. Then switched to Aubajio in Feb 2015 as there was still some activity and was tired of injections. My blood pressure rose and my Gfr dropped gradually to 53 from 85, my neurologist did not think it is due to Abajio but we decided to stop due to Kidney failure concerns, It was stopped in June 2017. I have not had any flares for over 10 years now, from around January 2017 I started using Walker, they told me it is not safe to walk with Walking poles anymore. My neurologist believes that I have SPMS now, at the same time believes that there are some inflammation in the background and recommended Cladribine. I started Mavenclad (2 rounds one month apart) in March 2018 and repeated that for the 2nd year in March 2019.

    From early 2017 I am getting weaker and weaker and can walk shorter distances, now with Walker or two poles, I can walk 200 meters very slowly and with pain in my legs. My MRI in Jan 2020 showed a lesion in my brain which wasn’t there last year.
    I was wondering if you consider my MS secondary (assuming that there is not only one MS) and if either way you recommend a more aggressive way of handling my MS and stopping any inflammation left by using Ocrolezumab instead of starting Seponimod which has a low success rate of 20%. Ocrelizumab / Ocrevus is approved in Canada (if my doctor can justify that I have RR or primary progressive MS). Also based on what I read in your blog if I read it correctly, it seems that therapies that target both T and B cells, i.e. alemtuzumab and HSCT are better than therapies that target mainly B-cells i.e. (rituximab, ocrelizumab, and cladribine). if my neurologist can justify that that I am still an RR patient she can prescribe Alemtuzumab as well which is approved here. Please kindly inform me of your recommendation and sorry for the long note.

    thank you,

    Frank
    Toronto, Canda

    • Dear Frank
      Thank you for your information but we cannot give personal recommendations, we are not you trating physician and we do not know all the relevant information.

      As to feeling therapies that target T and B vs B, until there is a head to head it is hard to make distinctions

  • I strongly believe in the flip the pyramid approach.One of the problems I suspect in getting more doctors to adopt “flip the pyramid” is what do they do in the event of new lesions or clinical new symptoms (even if just PIRA). Status quo is switch in that event but in the flip the pyramid approach there is no good alternative to switch to, status quo may have to become some tolerance of progression but how much? What do you tell doctors who ask what you do with a patient who went straight to first DMS of alemtuzab or natalizumab or ocrelizumab who shows up to their office with worsening symptoms or progression on MRI?

    • Strangely, I think it is a tulip pot in crackled white that I got in Amsterdam, but I agree it is a bit heart like. Seletti make a real heart shaped vase.

  • What are the longer term impacts on the function of a persons immune system following Lemtrada?
    (In other words, how will my immune system stand up to Covid 19!)
    Following the initial recovery is it back to full function?

    • I’m a PwMS who received Alemtuzumab. In the file notes I put together, I’ve a record of ProfG saying that after treatment our lymphocytes recover, but to a lower baseline, leaving us with low level lymphopenia. My levels two years post treatment are still low.
      However I’d not like you to take this as gospel, in case I misunderstood exactly what I read. Hopefully ProfG or one of the other neuros will answer this for you.

    • I am am not sure it is ever the same but no reason why the body should not make anti-viral response once the antibody has cleared

      • Thanks MD.
        I did pose this question again to ProfG on his post on COVID19 and DMTs on the 2nd March. Here’s what I asked and his reply:

        ProfG, do I understand correctly that lymphocytes replenish to a lower baseline following treatment with Alemtuzumab, resulting in low level lymphopenia? My levels are still low two years post infusions.
        Is it fair to assume this makes us more vulnerable to COVID19?

        Reply
        PROF G
        March 2, 2020 at 10:13 am
        No, not necessarily; lower than baseline still means you are competent. The normal range of lymphocyte counts is very wide; somebody with a count of 1.1 can be as immunocompetent as some with a count of 2.7. The absolute numbers are a poor proxy for immune competence; it is only below 0.8 that immune competency is likely to become a problem.

        I understand from an Aaron Boster vid concerning COVID19 and DMTs that the level can take 3/4 years to improve. Mine are currently 0.79 two years post infusions. I am therefore aware of the dilemma for myself and others who have received Alem that it maybe appropriate to self isolate at some point, or some of us may wish to make the decision to do this ourselves, but we still have to attend for monthly bloods. This involves a round trip from Kent to London for me, involving public transport. Despite the attempts of the London centre to have me screened locally they’ve been unable to provide this, so I’ve been taken back in house.
        I think the advice about Alem should take account of the duration of low level lymphocytes and not equate the issue solely with at the point of treatment.

        • There are some infections that occur when the lymphocytes drop below 0.8…I think this is tuberculosis is the first at belwo 0.5, you need to go lower for the viral problems like Herpes to show I think.

          If you look at the alem data you can see changes twenty years or more later (Cooles et al. Arthritis Research & Therapy (2016) 18:302)… However 2 years after the last infusion and the drug is long since gone and if an infection comes along and you can respond to it, there is nothing to stop that happening. Do you feel that you are fungus mungus in the past year with infection after infection..I suspect not. After the initial infusion you are at risk of viral infections.

          Maybe have another try to get you MS team to get you screened locally..aftet all if you catch something…you have maybe 2 weeks when you dont know it and you can donate that to the MS team, so its in their interest too. What are they looking for? cells…Are you tellling me a hospital can’t do that. OK I don’t know the answer to that really so check your team

  • So, a recent study about Vitamin D was released stating high dose vitamin D supplementation causes an increase in Calcium in the blood, which can worsen MS.
    If you take 1200 mg of calcium daily with moderate vitamin D supplementation (1,000 units) will this cause excessive calcium in the blood ? Trying to help prevent osteoporosis, but don’t want to encourage my MS to misbehave!
    Thanks.

    • I’m not a medical person but my understanding is that when you take vitamin d you shouldn’t supplement with calcium.

      Vitamin D helps one absorb calcium easier through our diet and therefore if supplementing as well can lead to excess and hence issues.

  • Anything special to report from ACTRIMS? Or has the reality dawned ECTRIMS/ACTRIMS is a synical exercise by pharma to stifle research for a cure and push their own agenda ensuring the gravy cow continues to deliver by pushing research in treatment focused end point?

      • L. O. L. We all need a flag pole to pin our flags too! Even Sci fi is jumping on the band wagon. One recent movie plot involves pharma engineering a virus which cause zombie like symptoms. In order to cash in on the cure already developed. Sounds familiar?

          • Ha ha. I guess the answer to my original question is emphatic No. Hmmm strange to receive stinging response. Unless my question has stung? Waiting for AAN2020 and ECTRIMS2020 with trepodation and excitment. Back to drinking my pint of Stella…. In a council estate pub. Full of MS plebs

  • MD2 of course your messing with me. I’m sure like MD and Prof G you have string publications that have changed the face of MS research, inspite of being funded by pharma. Just playing devil’s advocate.

      • As for ACTRIMS, I had’t looked through the programme. Pharma save their major reports for AAN but the posters should be interesting.

        I predicted single cell T cell sequencing to get the antigen in MS, and the answer is anti-viral responses that cross-react with MBP…I’m wrong this is all perfect just as the dogma machine suggests.

        P245 – The Power Of Single Cell Technologies; From T Cell Receptor To Antigen(s) In Multiple Sclerosis
        N. Saligrama et al.

        Background:The role of T cells in Multiple sclerosis (MS) and experimental autoimmune encephalomyelitis (EAE) is well established. However, long-standing quest in MS is to determine key T cell antigen(s), which drive the initial response.Objectives:Objective here is to comprehensively understand of the T cell receptor (TCR) repertoire in MS with a focus on identifying and targeting dominant T cell clones.Methods:Major bottleneck in understanding T cell responses in health and disease is the diversity of TCRs and the vast variety of antigens that they can encounter. To circumvent these, we have taken a sequence-based approach to T cell responses and developed a robust single T cell paired TCR sequencing and phenotyping method and a bioinformatic analysis pipeline, which can group TCR sequences into clusters sharing specificity. Further, we have developed unbiased highthrouhput technologies (yeast peptide-HLA library and mammalian functional selection methods) to determine antigen specificity of TCRs in an unprecedented level.Results:By using single cell paired TCR sequencing and mass spectrometry-based cytometry (CyToF), we have analyzed both MS patients and healthy controls (HC) with respect to their overall immune system and the specific T cell types. At a single cell level, we have analyzed TCR repertoire and phenotype (using 10X genomics) of brain homing, activated CD4, CD8, and gd T cells from the blood and CSF of 28 recent onset untreated MS patients and found significant T cell clonal expansion which is not seen in HCs. We find shared TCRs between blood and the CSF in MS patients and in CSF, CD8 TCRs are highly clonal. Moreover, we find convergence of TCRs between MS patients suggesting of TCRs with shared specificity. Using yeast displayed peptide-HLA library which contains a billion peptide antigens, we have screened expanded CD4 TCRs from HLA-DR*1501 homozygous MS patients and found ligands. Surprisingly, some of the peptides identified resemble viral peptides and these can activate primary CD4 T cell clones from MS patients and they are cross-reactive to myelin basic protein.Conclusions:Our study highlights the value of studying T cell specificity and activity from ‘the bottom up’; that is, identifying the T cells that are most active in MS or any disease by single-cell paired TCR sequencing, using activation markers and clonal expansion as key indicators, and ligand identification either with a yeast library or candidate antigens and reporter cell lines transfected with the relevant TCR pairs. This is very much in contrast to traditional methods that typically involve knowing what the relevant antigens are

      • If fact very little…the alemtuzumab work was and that has perhaps backfired as we are now working on anti-alemtuzumab antibodies as a consequence

  • Many pwMS including myself have pinned their hopes on re-mylinization using clemastine fumarate, an over the counter anti-histamine following research outlined in the blog some time ago. in the UK this is sold under the trade name Tavegil, but in recent weeks everywhere has been increasingly showing as out of stock. Turns out that the producers have stopped making it – but Wiki[edia is not a very reliable source. Does anyone know whats going on here? This feels like a kick in the teeth for MS-ers. Thanks Pharma.

      • Can you provide a link please? Sorry – can’t follow your cryptic meaning. On its own was never an option – DMT and this seems blindingly obvious, but not now its been withdrawn.

        • Metformin Restores CNS Remyelination Capacity by Rejuvenating Aged Stem Cells.
          Neumann B, Baror R, Zhao C, Segel M, Dietmann S, Rawji KS, Foerster S, McClain CR, Chalut K, van Wijngaarden P, Franklin RJM.
          Cell Stem Cell. 2019 Oct 3;25(4):473-485.e8

          • Thanks MD – it will take me weeks to understand all of it, but noting else to do as I’m currently pre-self-isolating in practice for the real thing!

          • 🙂
            OK be Safe…..however as you can see the implication is that remyelinaion agent without rejuvinization is not the best

        • “Can you provide a link please? Sorry – can’t follow your cryptic meaning. ”

          Dr. Robin Franklin…says you need metformin mixed with your clemastine drink..

  • How do I wipe my bum with no toilet paper? Sock or tea towel? Local supermarkets have been stripped bare of tissues and bog roll 😡

      • Apparently bidet sales in Australia are also up – in this mornings news!
        Have I missed something? Can you eat toilet paper if you are self isolating?
        At least now it is possible to recognise who voted for the current Australian prime minister… they’re the ones in the supermarket with a trolley full of toilet paper and no food.

    • Try that global online store. I’ve been buying my loo roll that way for a couple of years and had no problems buying it yesterday.

    • Yep I saw the news in Oz and no grass (due to bushfires) as an alternative double bummer…The new campaign doing it Doggy Style

    • People of Asian origin, Find amazing Western societies wipe and not wash. I guess its due to diet. When your diet is bland and not spicy you can get away with wiping. Even then eeee….

  • Do you think this German study that correlates higher Vit. D (25(OH)D) levels to fewer inflammations and less disability increase is sufficiently powered to make a dent in this ongoing discussion?

    https://www.frontiersin.org/articles/10.3389/fneur.2020.00129/full?utm_source=F-AAE&utm_medium=EMLF&utm_campaign=MRK_1262035_54_Neurol_20200305_arts_A

    Objective: To investigate the associations between hypovitaminosis D and disease activity in a cohort of relapsing remitting multiple sclerosis (RRMS) and clinically isolated syndrome (CIS) patients.

    Methods: In 51 RRMS and 2 CIS patients on stable interferon-β-1b (IFN-β-1b) treatment recruited to the EVIDIMS study (Efficacy of Vitamin D Supplementation in Multiple Sclerosis (NCT01440062) baseline serum vitamin D levels were evaluated. Patients were dichotomized based on the definition of vitamin D deficiency which is reflected by a < 30 vs. ≥ 30 ng/ml level of 25-hydroxyvitamin D (25(OH)D). Possible associations between vitamin D deficiency and both clinical and MRI features of the disease were analyzed.

    Results: Median (25, 75% quartiles, Q) 25(OH)D level was 18 ng/ml (12, 24). Forty eight out of 53 (91%) patients had 25(OH)D levels < 30 ng/ml (p < 0.001). Patients with 25(OH)D ≥ 30 ng/ml had lower median (25, 75% Q) T2-weighted lesion counts [25 (24, 33)] compared to patients with 25(OH)D < 30 ng/ml [60 (36, 84), p = 0.03; adjusted for age, gender and disease duration: p < 0.001]. Expanded disability status scale (EDSS) score was negatively associated with serum 25(OH)D levels in a multiple linear regression, including age, sex, and disease duration (adjusted: p < 0.001).

    Interpretation: Most patients recruited in the EVIDIMS study were vitamin D deficient. Higher 25(OH)D levels were associated with reduced T2 weighted lesion count and lower EDSS scores.

  • With covid19 all of a sudden people start to take seriously the risk of infection whilst on DMTs. I have had 2 severe EBV-infections whilst on DMF (with lymphocytes 05-0.8 in the last five years). Last one took me totally out for 10 months, but when I raise the issue with neuros, it was always said it was simply bad luck. (And they check for JC-virus again, because well PML is serious). Now, everyone seems to agree that on DMF with LC below 0.8, you are at greater risk. I know EBV is usually not a serious infection, but why does it seem so difficult for neuros to actually adapt the DMT to the patient at hand?

  • Want Brain health?

    +Ketones

    – Carbs

    Study shows low carb diet may prevent, reverse age-related effects within the brain

    What we found with these experiments involves both bad and good news

    The bad news is that we see the first signs of brain aging much earlier than was previously thought. However, the good news is that we may be able to prevent or reverse these effects with diet, mitigating the impact of encroaching hypometabolism by exchanging glucose for ketones as fuel for neurons.”

    “We think that, as people get older, their brains start to lose the ability to metabolize glucose efficiently, causing neurons to slowly starve, and brain networks to destabilize,” said Mujica-Parodi. “Thus, we tested whether giving the brain a more efficient fuel source, in the form of ketones, either by following a low-carb diet or drinking ketone supplements, could provide the brain with greater energy. Even in younger individuals, this added energy further stabilized brain networks

    Additional findings from the study included the following: Effects of brain aging emerged at age 47, with most rapid degeneration occurring at age 60. Even in younger adults, under age 50, dietary ketosis (whether achieved after one week of dietary change or 30 minutes after drinking ketones) increased overall brain activity and stabilized functional networks. This is thought to be due to the fact that ketones provide greater energy to cells than glucose, even when the fuels are calorically matched. This benefit has previously been shown for the heart, but the current set of experiments provides the first evidence for equivalent effects in the brain.

    https://medicalxpress.com/news/2020-03-carb-diet-reverse-age-related-effects.html

  • The paradox…..What does a pwms do when they “flipped the pyramid” and the high efficacy drug failed? Switching to another high efficacy immunosuppressive drug carries too high of a risk profile and moving down the pyramid is pointless. The data suggests going with the big guns first seems to provide the best long term benefits, but what happens when it doesn’t work?

    • HSCT perhaps. If you know why it failed it may help what to do next, some people cannot respond to certain treatments due to their biology

        • yes indeed he can, we have a paper doing the rounds looking at alemtuzumab, once this is out of the way we will set our sights on other agents, we have ethics in place to look at mavenclad and we may then design a test. We could even monitor covid19 responders…but we are behind the curve and spread too thin. We need some staff as DrA can’t make new agents and also do the testing for alemtuzumab.

          However there may be genetic rasons why people may not response we need to find out why

      • ‘some people cannot respond to certain treatments due to their biology’

        Is there screening available for that before embarking on a new treatment?

        • It is not in company interests to acknowledge this and lose sales so they dont investigate this

          We have identified mavenclad non- depleters and we have a basis for a test developed, we have to put his together and see if it is relevent .

          We have alemtuzumab non-depleter, but to find out why we need more samples and more people.

          We know of FC receptor variants that can influence treatment of effects of IgG1 antobies. Not sure if they effect MS alemtuzumab and ocrelizumab (more unlikely due to high dose used) doses

          • You (and/or Angry) are barking at the wrong tree in that case.
            Does he hold full ownership regarding rughts and latent or are they shared with UCL?

          • I am not sure you know which tree we are barking at and as for right I am not sure why we share any rights with UCL…we dont work there

      • Thanks MD! Unfortunately, HSCT is not yet an option in the U.S. and the clinical trials fill up before one can even apply.

        I agree 100% about needing to know why the drug failed, so I can make a more informed decision about what to do next. I pushed the neurologist (at one of best MS clinics in the U.S.) for increased testing, MBR, IRC, Anti-drug antibody testing, anything!!!! but was dismissed before I could even finish my thoughts. “Stop drug X and pick a new drug”. It is just frustrating, these doctors hand you brochures about all the DMTs and say “pick one, but educate yourself first.” Then you educate yourself and the doctor says “stop Googling, you are misinterpreting the data (mostly the data coming from your group). You think these neurologist would want to know why drug X failed, so they could use that data in future decisions with other pwms that display similar biological make ups.

        Sadly, without more information or additional tests, I am now left with only one course of action, do nothing and hope the effects of the failed drug last on the longer end of the bell curve. With the coronavirus going around, I guess my new approach has some benefits.

        • We (our group) are misinterpreting the data….I guess that are opinions from some of our peers. Last week I heard a senior person talking and I realised my my mind is on a different planet…., in reality I think your choices should boil down to one or two.

        • “Thanks MD! Unfortunately, HSCT is not yet an option in the U.S. and the clinical trials fill up before one can even apply. “………The u.s. trials are also full myelo..and remember half get placebo treatment…It is t cell repertoire renewal which determines hsct success not strength/amount of chemo. About 2,000 have been treated in Russia/Mexico…at cost of $50,000…small beans compared to DMT prices.

  • “If you are infected, the use of surgical face masks may reduce the risk of your infecting other people, but there is no evidence that face masks will effectively prevent you from being infected with the virus. In fact, it is possible that the use of face masks may even increase the risk of infection due to a false sense of security and increased contact between hands, mouth and eyes.”

    https://www.ecdc.europa.eu/en/novel-coronavirus-china/questions-answers

  • I would love to see a full post on b-cell therapy and COVID laying out the issues with immature vs. mature b-cell function, immunoglobulin depletion, vaccine efficacy, etc for a lay reader. I feel like maybe I get it from reading through the comments but could use your help. Many of us are facing the decision of whether to delay or change treatment and where to be vigilant in the meantime.

    • I agree but I guess there are many unknowns, do we know if ocrelizumab inhibits childhood vaccine responses and if it does how quickly does that happen, can we make responses to upper rispiratorytract infections. It will take time to do the reading if the information can be found…it won’t be in MS I suspect

  • What is your view on the Brigham and Young’s study on the possibly beneficial effect on MS of probiotics? Given that it is only a pilot study, is there any reason for me not to take a probiotic on the basis that at worst it is unlikely to do any harm? (I am SPMS.)

    Ann Neurol. Author manuscript; available in PMC 2018 Oct 11.

    Published in final edited form as:
    Ann Neurol. 2018 Jun; 83(6): 1147–1161.

    Published online 2018 Jun 8. doi: 10.1002/ana.25244
    PMCID: PMC6181139
    NIHMSID: NIHMS975663
    PMID: 29679417
    A probiotic modulates the microbiome and immunity in multiple sclerosis
    Stephanie K. Tankou, MD-PhD,1,2 Keren Regev, MD,1 Brian C. Healy, PhD,1 Emily Tjon, MS,1,2 Luca Laghi, PhD,3 Laura M. Cox, PhD,1,2 Pia Kivisäkk, MD-PhD,1,2 Isabelle V. Pierre, BS,1,2 Lokhande Hrishikesh, MS,1 Roopali Gandhi, PhD,1,2 Sandra Cook, RN,1 Bonnie Glanz, PhD,1 James Stankiewicz, MD,1 and Howard L. Weiner, MD1,2

    • My views on the microbiome studies are well known, if you want to take a probiotic the chances of a problem are low as it is essentially sold as food….but they can contain live bacteria and if you have no immune system I can’t comment on effect. I will keep an open mind once the study has recruited I can give you a guess of wha I think could happen.

  • Ocrevus & covid-19 question – Am I right in thinking that, if an Ocrevus patient gets this & survives, they will/may not develop resistance so could be vulnerable to getting it again?

    (apologies if this has been covered in one of your other posts on covid-19)

    • It depends what s stops the reinfection and probably antibody will be important, but if you survive once the chances are you will survive again, but answer is I don’t know, as the immune system CD8 will be much more active

  • Bats and virus

    Bats can carry viruses that are deadly to other mammals without themselves ever becoming ill. In fact, bats are natural reservoirs for viruses that have some of the highest fatality rates of any viruses that people acquire from wild animals – including rabies, Ebola and the SARS coronavirus.

    Bats have a suite of antiviral defenses that keep the amount of virus in check. For example, some bats have an antiviral immune response called the interferon pathway perpetually switched on. In most other mammals, having such a hyper-vigilant immune response would cause harmful inflammation. Bats, however, have adapted anti-inflammatory traits that protect them from such harm, include the loss of certain genes that normally promote inflammation. However, no one has previously explored how these unique antiviral defenses of bats impact the viruses themselves.

    https://elifesciences.org/articles/48401?utm_source=content_alert&utm_medium=email&utm_content=fulltext&utm_campaign=11-March-20-elife-alert

  • Wondering if there is anything I can do to boost my lymphocyte count which has been persistently low for several months following treatment with Cladribine last year? Do you recommend any particular vitamin/mineral supplements or is there any medication that could be given by GP to boost numbers?

    • There are growth factors that can boost cell numbers….with cladribine ther is very slow recover of some subsets, this is one reson why it is active in MS.

  • Hi, I completed round 2 of Lemtrada on the 18th February. My first bloods and review should have been yesterday the 11th March, however, this was cancelled due to concerns Re: Covid 19.

    After round 1 last year my lymph count was still at zero at my first monthly review. How concerned should I be? I have seen lots of advice telling pwMS to delay treatment of Lemtrada, Mavenclad and Ocreveus be several months or switch to another DMT but no advice for those of us that have just received treatment whilst the covid 19 virus was in its infancy.

    • Maybe profG will comment but you must have been advised to be vigulant for the the first few weeks/months by your HCP, maintain that advice as you did round one, whilst your immune system boosts. I trust you did not have too many viral infections last time and then trust it will be the same this time. Your new B cells start to repopulate after the first month up by 3 back way above normal by 6 months, maybe this could be an advantage, I don’t know.

      • Hi Mouse Doctor, thanks for your reply, nasty bout of shingles 3 months post round 1 and a cold at 9 months but well other than that. Will follow the general advice and hope I am lucky and avoid Covid 19 and any other viral infections!

        • Cold for months it seems about normal round here I’ve been snuffling since Crimbo. Have they given you anti-virals?

  • I was on Plegridy for 4 years without any issues. I came off of it one year ago because of Gastrointestinal issues (Flatulence, pain, weirdly colored feces). I switched to Aubagio but Aubagio didn’t work out on me (I had a relapse and progressed). Later it turned out I had H. Pyroli in my stomach (I was given antibiotics for that).

    I decided to go back on Plegridy hoping that the GI issue is resolved. Unfortunately, it seems that it is not resolved as I am having the same issues. I am determined to find a way to manage this time.
    Do you have any suggestions? Is there any medicine or life style change that may help?

    I appreciate your help and great blog.

  • Hi,
    I’m in the US but it’s getting crazy. I am scheduled for my Ocrevus on 4/6. I have been trying to reach my MS specialist but they haven’t returned my calls. It’s been 2 weeks. I am not sure how active my MS is and I was hoping to get an MRI to check for new activity to see if it was really necessary to get my Ocrevus in a few weeks. Or maybe check my B cell count to see if I am actually at high risk. I’ve been on a Ocrevus since last May so this would be my 2nd full dose.

    I have been told so many different things. I am definitely in the crap gap. My fatigue is terrible and my memory and cognitive stuff is a terrible mess. That’s how mine started, cognitive issues. I know I “need” the Ocrevus by the way I feel but not sure if I need it enough to risk this virus. Any opinion? I’m in Louisiana where the cases went from 1-19 cases within a week or less.

    I just don’t know what to do if I can’t get my neuros advice.

  • A question on the ABN guidance on DMT and covid19: how come it is recommended to continue betaferon, DMF, teriflunomide…, but it is advised to stop ALL DMTs once an active covid19 infection has been diagnosed?

  • This is a mouse question (and nothing to do with COVID-19 🙂):

    With all the interest in repurposing drugs for remyelination and neuroprotection (clemastine, metformin etc) wondered how these might compare to siponimod acting on S1P1 and S1P5 in CNS? In the EXPAND paper:

    Siponimod readily crosses the blood–brain barrier(12) and findings from preclinical studies suggest that it might prevent synaptic neurodegeneration(13) and promote remyelination in the CNS(14)

    https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(18)30475-6/fulltext#back-bib14

    Familiar names on ref 14 😉

  • If a patient with MS has a low lymphocyte count (below 0.8) and develops a fever, should they just self-isolate and see if symptoms stay manageable or should they try to contact their local hospital/neurologist for advice?

  • MD help me out here – if there are 10,000 infected in the UK already (most asymptotic, granted) – then 19 MSers are happy Coviders as well (based on prevalence figures of 190 per 100,000 in England).

    How come we have not heard of a single case yet? Is there a real-time reporting system of some sort Neuros subscribe to beside the post-marketing monitoring registers?

    Tony

    • You are making an assumption that those 10,000 are the average population. However not alot of people with MS I know have family memebers or themselves jetting off to China for a couple of days, whizzing through Korea and Signapore and importantly having skiing holidays in Italy.
      The wealthy plan get the kids infected before the country collapses when the plebs get it:-)

      However, it will come, if the government is testing only 2,000 a day…there are thousands of people untested. ProfG had a neighbor with symptoms and stuck at home, with 111 taking days for a response…eventually told to go to testing centre outside of London…but they have no car.

    • I am sure when it happens the grape vine will say.. Italy will be the first port of call I suspect, but we are more.likely.to here bad news than good news…it simply travels faster

      • There’s someone who commented on the MS Society UK Facebook page tonight who’s on Ocrevus on who said she’s got corona. Said she’s doing ok to anyone else who’s worried.

  • If possible a reaction/some advice on this please report coming out of France

    Health minister Olivier Véran, who is a qualified doctor and neurologist, tweeted: “The taking of anti-inflammatories [ibuprofen, cortisone … ] could be a factor in aggravating the infection.

    “In case of fever, take paracetamol.

    “If you are already taking anti-inflammatory drugs, ask your doctor’s advice.”

    Thanks.

    • Ask your doctors advice…these anti-inflammatories like Ibrurofen and not in the same league as some DMT. It is a csase of a little knowledge is dangerous. If you have an infection don’t take immunomodulatiory/suppressive drugs…my mumcould have told you that and she let school at a early age. Paracetamol reduce fever…read the packet. I don’t think anything earth shattering

    • Re Ibuprofen
      Ibuprofen 400mg three times a day (over the counter dose) will bring a temperature down but is not an anti inflammatory dose. Can be taken alongside paracetamol if necessary. Ask your pharmacist!

  • Here’s a question that’s eluded everyone about the corona virus. At what levels of lymphocyte levels does the corona virus becomes severe? Just looking for number not a rhetorical answer. If you don’t know give a guess. Surely experts in immune related disease you have a good idea?

  • For over 40 years I was told by doctors and nurses that because I had MS my immune system was compromised. Suddenly all the Coronavirus information is focused on pwMS on DMTs. Not only there seems little interest in SPMS or PPMS people that have no access to the treatments we are once again ignored.
    So my question is, are we more susceptible to the virus than the rest of the population? I know that if we get the virus it will be more serious, but that isn’t my query. Please help it’s not on any website.

  • Pharma conferences are very good,

    To get covid -19 infection Biogen (natalizumab marker)

    Biogen has been hit hard by an outbreak of the coronavirus following a management meeting in Boston two weeks ago. Shortly after the meeting, the company disclosed that three employees who attended had tested positive virus and directed those who had been at the meeting to work from home. However, it soon upgraded that directive to a full quarantine for all attendees when the number of infected jumped. As of Wednesday, there were 70 infections linked to the conference, out of the 92 total in Massachusetts, local media reported. The World Health Organization declared a pandemic on Wednesday

    https://medcitynews.com/2020/03/biogen-facing-covid-19-outbreak-teams-up-with-vir-biotechnologies-on-coronavirus-antibodies/

  • Is there any data on PML risk in pwms switching from Ocrevus to Tysabri?

    There is data that suggests the risk increases when you switch from Tysabri to Ocrevus, but what about the other way?

    • We are British it is always Tea Time…Lukily you can’t eat it as that would be striped from the shelves….However IL-2 was what led me to think about memory B cells as interleukin 2 is a memory B cell growth factor

  • Something is worrying me a lot.

    This emphasis on cough and temperature to distinguish COVID-19.

    I know someone (in their 20s, no health condition) who has just been diagnosed with COVID-19 who has only had tiredness, blocked sinuses. No temperature or cough.

    No wonder it is spreading so fast. It is not being picked up. This advice about temperature and cough is wrong. Dangerously wrong.

    • It has been clear for some time that many young people are essentially asymptomatic and yes they can spread it, but at least they are not coughing so the spread is somewhat minimised, especially if they wash their hands well and regularly and keep their hands away from their face (important for everyone to get in to the habit of this).
      What worries me more is that a test has been used for someone who is essentially healthy, and probably should have been told to go home and stay there at least until they felt better. Imagine if everyone who went to the Dr with those symptoms was tested. Tests which are already in short supply would be non-existent.
      Unless there was any other relevant risk factors such as known contact with someone who has tested positive then they should never have been tested.

      • Rubbish. I, as a vulnerable person with MS, am very glad to know that my relative has COVID-19 and not the common cold. So are their parents/grandparents. And countries most successful at tackling this virus are doing a lot more testing than the UK. This is recommended by WHO.

        Again, emphasis on cough/temperature is misleading.

        • I think the Government has made a grave mistake by not testing people if each person infects 3 people knowing you have the virus hopefully ensures you stay your distance and isolate. Every one is having snuffles and snuffles and you hear a cough and you SH1 your self,is it a cold or COVID? South Korea has tested 270,000 people we test when you are in hospital
          https://www.sciencemag.org/news/2020/03/coronavirus-cases-have-dropped-sharply-south-korea-whats-secret-its-success.

          The next set will be to test people who have antibodies to the virus, they are vaccinated and can become productive parts of society.Perhaps we should have made a test but we are in Lockdown

          • I think I heard a lady from WHO – who was disagreeing with the UK’s previous tactic of herd immunity – saying that it’s not known yet whether COVID-19 virus infection leads to long term immunity. Hopefully it does…

      • Korea sorted an infrastruture and was running as a testing machine in days….we have enough expertise to test for virusees but we were not prepared enough and have not mobilised our resources for such a scenario

  • An important question concerning vacation after HSTC:
    I am member of a Norwegian Facebook group for people having received HSTC. The official guidelines are that pwMS should complete a vaccination program after HSTC following an established protocol. However in the Facebook group there is a general consensus that vacation may trigger MS. One person says that she got her first attack the day after she received a tetanus vaccine; another person says he had his first clinical debut a day after a vaccination for hepatitis. Thus they recommended not to receive vaccines after HSTC. My questions are: 1) may you develop a clinically manifest MS attack in the course of 24 hours? 2) Do you in England discourage vaccination after HSTC. Norwegian health services follow recommendations sett by The European Society for Blood and Marrow Transplantation (EBMT).

    Thanks!

  • Does the information proceed that in the past Chloroquine has already been used to treat MS? I know that Hydroxychloroquine is still used against Rheumatoid arthritis and SLE. Would Favipiravir have any effect against EBV?

    https://academic.oup.com/jid/advance-article-abstract/doi/10.1093/infdis/jiz656/5673088?redirectedFrom=fulltext

    https://www.nature.com/articles/s41421-020-0156-0

    https://multiplesclerosisnewstoday.com/forums/forums/topic/japanese-flu-drug-clearly-effective-in-treating-coronavirus-says-china/

  • For MS Selfie page: I was treated with 3 days of Lemtrada Jan 21-23. I live in the US and began voluntary self quarantine March 9. My previous Lemtrada dose was January 2017 and I have received Rituxan several times between Lemtrada doses. Last Rituxan September 2019.

    I am 46, female, Non-smoker, well controlled HTN, of normal BMI and in otherwise good health with a very healthy diet.

    How long should I maintain quarantine? In either months or blood counts?

    Thank you.

    • I will let prof G answer this but you should have been given some advice on infection control by your HCP. You are at risk whilst your immune system recovers.

  • Is vitamin C good or bad for MS? I want to start taking 1000mg of liposomal Vit C per day. I am on glat. Acetate.

    Looking forward to your reply.

    • I am not a doctor
      But vitamin C is good for health. You can’t store it so don’t take to much. Watch out if you have the fizzy ones that you take in water. A few years ago a certain supermarket brand obviously changed some E number and since then I have had bright orange wee as I am not breaking down the colouring.

      I believe it makes the immune system healthy now you could argue that it is not a good thing for MS, but I’m not going there…you need a healthy immune system to fight infections.

      Many moons ago I used to work with guinea pigs. My boss could not repeat some work they had done in the States and it seems that vitamin C was part of the answer to get a good immune response. Therefore, every thursday the piggies would get a cabbage, which is packed with vitamin C, to eat…They loved it. We would get them delivered on wednesday and they could smell it or they knew what was coming as their squeaks would turning into a chatter between wednesday night and thursday morning.

  • Hi MD (or anyone else).

    I’ve noticed over the last 10 years that some time (more than a month) after a brainstem lesion causes a relapse, that I start feeling off balance and have to sometimes focus when walking. It then goes away. This is too recurring of a pattern for me to ignore and wanted to ask whether you have any suspicions why this is occuring – could it be a B/T/anyother cell repairing the damage in the brain and spine which is causing me to feel like this?

    When it first started happening I thought it was just another relapse, but it seems to always happen after some time following the first occurrence of a new relapse.

    I’m about to go on immunosuppressive therapy and was wondering whether the timing of administration of therapy matters after a relapse (i.e. if the B cells that Ocrevus kills might be responsible for the healing or teamwork of cells responsible in healing). Hope that made sense. Thanks 🙂

    • I;lll let profG do the neurology.
      The immune response always has a balance of good and potentially bad guys, on balance ocrevus gets rid of the bad guys

  • Everyone needs to listen to this NHS doctor and get everyone they know to listen too!
    Can’t get the link, so if you’re interested you will need to go on to YouTube and search: LBC – Dr Jack.
    He was interviewed on the Tom Swarbrick show a couple of days ago.

  • Is COVID19 neurotropic?

    Answer COVID19 invades:

    Nose
    Pharynx
    Heart
    lung
    Spinal cord
    Gut
    Skeletal muscle
    Bladder

    All over the place

    (In rhesus monkeys)

    As shown in Figure 2f
    (left panel)
    , v
    iral replication
    was found
    in n
    ose
    (
    10
    7
    to 10
    8
    copies/mL)
    ,
    pharynx (10
    5
    to 10opies/mL), lung (10
    4
    to 10
    7
    copies/mL)
    ,
    gut (10
    4
    to 10
    6
    copies/mL)
    ,
    spinal cord
    (
    approximately
    10
    4
    copies/mL), heart
    (
    approximately
    10
    4
    copies/mL
    )
    , skeletal muscle
    (
    approximately
    10
    4
    copies/mL
    ) and bladder
    (
    approximately
    10
    4
    copies/mL
    )

    Reinfection could not occur in SARS-CoV-2 infected rhesus macaques

    https://www.biorxiv.org/content/10.1101/2020.03.13.990226v1

    Sharing is caring

  • Please could you confirm the safe upper limit per day or per week for vitamin D3 supplementation? I currently take 4000 IU per day but read conflicting advice about possible risks/benefits of high doses for people with MS. Should I reduce the 4000 IU amount to every other day or even less?

  • Hey there,

    I was wondering as to whether or not it really is essential that an MS patient needs to try and fail a DMT before exploring HSCT. I was meant to start Ocrevus, but it got postponed until further notice because of COVID-19. My RRMS symptoms have continued to flare up in the meantime. After quite some research, HSCT does appear to be the clear way forward, but I am worried I am not eligible because I have not tried and failed a DMT. I would really appreciate your thoughts on this.

    Thank you for your time.

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