Q&A October


This month it is halloween so today we have the Devil Firefish

Sculpture from the East End of London

About the author



  • Hi guys

    Can you start to replace and pin the most recent months Q/A when you add it.

    Currently the August Q/A is still pinned and Septembers was just lost in the noise of the daily posts.

    Many thanks

  • I posed a question on an earlier blog entry about raised liver enzymes and the possibility that this could be caused by the Pfizer vaccination. If if doctors have said the elevation is fairly mild is it ok to have the booster? Assume it is as people with liver failure are having vaccinations

  • I heard a portion of pwMS who failed on antiCD-20’s mabs react to anti-IL-6 mab Tocilizumab, what’s the role of IL-6 in MS and what’s the efficacy of Tocilizumab like?

    • Mayb we have to get MSers misdiagnosed as NMOers, Where did you hear this news. I guess it can;t be universal benefit. Beauchemin P, Carruthers R. MS arising during Tocilizumab therapy for rheumatoid arthritis. Mult Scler. 2016 Feb;22(2):254-6.

      • India knocking out a generic version already. Hopefully opens the door for more studies with tocilizumab.

      • My apologies, it was a neurologist whos an NMOSD specialist rather than MS, I forgot the context so he might be talking about pwNMO instead of MS.

  • Could Dr G tell us what makes for the most efficient use of time in a review apt for both him and the patient, what type of things should a patient have thought about/ be prepared to answer? Etc

  • I have not quite a question but a request of some sort. Many times I have seen YouTube and here many of our MS Doctors explaining in detail what various MRI brain & spinal images look like for a person with MS & the types of damage, i.e. active lesions, smouldering lesions, brain volume loss, etc but if someone could do a post explaining other neurological tests that are done like EMG, NCV, etc. Also, perhaps another one on the various bands in a lumbar puncture test? I believe it would be helpful to some readers.

  • You have used the phrase “super responder” several times in past posts when talking about some patients that take Tecfidera. Please may I ask what your definition of this phrase is?

  • Will pwms on ocrevus be offered the third primary covid vaccine and then a booster. Many of us are getting nowhere with our medical teams who say they know nothing about the third primary and that it just means getting the booster after 6 months.

  • I usually try not to ask for medical advice online but I recently had my 1 year checkup and MRI. I’m currently taking Aubagio and my recent MRI shows no new lesions but a number of hyperintense foci. My neuro didn’t even look at my MRI and just read the report leaving me even more confused. I won’t bore you with the details but my question is

    What are hyperintense foci and how worried should I be?

    On a side note, bad 1st anniversary to me. 😀

    • No new lesions but hyperintense foci suggest these are the old lesions (with T2 they appear as white spots so hyperintense agains t the black background)

    • There is a paper by Dobson and Giovannoni European Journal of Neurology but it is history, supportive tests and knowledge

    • It is analysis of other trials a meta analysis is not a trial. the problem is this wont convince many people I suspect

    • Improving ones gut health helps anyone feel better. Why do you think so many so-called experts think they’re so smart writing up these diet plans for MS. Eating better, losing weight in a healthy way, clearing up sludgey gut, always makes someone feel better. If the body’s cells are working better because they aren’t weighed down, then of course everything works better. Taking probiotics is just a start. If a person continues to eat greasy, fatty bar pizza, Chinese takeout loaded with salt, Whoppers from Burger places, etc, then the probiotics are a mute point. I take a probiotic supplement every day. I eat healthy many a day. I also have a teenager her every so often peer pressures me into junk. I can tell within less than an hour how it’s affecting my MS in a negative manner. So long answer short, yes probiotics will help as long as you rid the sludge buildup & start eating healthy -vfor anyone regardless of what disease they have. But it’s never going to cure you. It boggles me that so many people feed into these so called diet related cures. If that was the case, all it would take is the juicer and all these Drs who specialize in MS would have to focus their attention to some other medical conditions and us MSrs can happily lead our disability free lives by just infusing our homemade juices into our arms instead of these potent drugs with multitudes of high risks associated with them. I wish all these studies on diet and probiotics would literally just stop. Focus time & energy and money on other studies. It’s fruitless! No pun intended.

        • I take a prebiotic fiber as well Steve! A different name brand though. Helps greatly & I don’t even know it’s there as it dissolves completely in my water, juice, tea, and such. Thanks for the tip though!

  • Thank you all again for your excellent work.
    I’ve been using your “clinicspeak” EDSS calculator and had a question. The EDSS score varies *very significantly* – two full EDSS points – depending on whether someone is able to walk for 8-10 km (!) without aid or rest or able to walk “clearly more than 500m” without aid or rest. No options in between. So how would you in abstract score the EDSS of people who, at least in terms of mobility (i.e ignoring other lingering symptoms), have plateaued at being able to walk, say, 5 km without rest?

    I also wonder if this is hairsplitting or relevant e.g. in terms of keeping an eye on progression.

    Many thanks

  • https://pubmed.ncbi.nlm.nih.gov/34584250/

    Does the fact that there’s even a debate over why MS is becoming ‘milder’ on average. The question, is it DMTs or better diagnostics thats picking up people with milder MS.

    What does this mean for DMTs? If it’s not evident or clear that DMTs are making MS milder on average for people with MS. Surely is should be pretty clear if they work??!

    • Whenever I see something like this I find the answer usually has little to do with science and everything to do with Money. Study uses MS registry in Denmark for metadata. Danes with MS are costly to their universal care system. Article from several yrs ago says” [danish] MS-patients in DMT have 5.3 times higher secondary care costs due to medication in an outpatient setting,”https://www.valueinhealthjournal.com/article/S1098-3015(18)35305-1/fulltext#relatedArticles
      It is hard to quantify improved quality of life or the amt of increase of productive engagement in society because of a DMT. Much easier to say that the cost is too high for benefit gained from early intervention or prolonged use. Perhaps scientists who engage in such cost benefit analysis might enjoy carrying 50 lbs of rocks in a backpack blindfolded up Himmelbjerget with one shoe on a very hot day.

  • Can anyone well-versed in neurology help?
    If I want to see whether new lesions appeared or not, a comparison of last two MRI scans is needed, isn’t it? However, can two MRI scans be compared if they used different sequences for them? Also, in what instances of PPMS would you say it is an active disease and would consider Ocrevus as an effective therapy? (No enhancing lesions present in this case)
    Many thanks

      • There is a metric ton of misinformation online about alpha lipoic acid being a “mercury chelator” that will move mercury around from other parts of one’s body into one’s brain. It can all be traced back to a naturopath named Andy Cutler and his quackish “chelation protocol,” which he claimed could cure autism.

        To answer anonymous’s question above, there is no scientific evidence that alpha lipoic acid can cause mercury poisoning. High dose alpha lipoic acid has been studied in literally hundreds of human trials for all sorts of conditions and mercury poisoning has never been reported as an adverse effect. If it was able to move mercury into the brain it would probably be a controlled substance and not available on the shelves at the health food store.

  • Rituximab vs Ocrelizumab ?

    Basically the same

    P817 – Anti-CD20 monoclonal antibodies in primary progressive multiple sclerosis: a real-life comparative study of rituximab vs. ocrelizumab

    Conclusion: Our results show similar findings to trials using antiCD20 therapies in pwPPMS but in real-life conditions. Rituximab has similar effectiveness to ocrelizumab and therefore could be used in settings where ocrelizumab is restricted.


  • This is something I believe all of us can do.

    If you think more trials targeting ebv as a treatment for MS is something that is worth a go at then all of us can ask our multiple sclerosis societies 1 simple question.

    What are they doing to target ebv as a potential treatment for MS ?


  • Is Contrast MRI necessary? – my neuro has never ordered these for me – always have been non-contrast for diagnosis, baseline and follow-ups. I had a MRI scan for a different purpose and the radiologist was surprised that I had never had a contrast MRI before and they do contrast for all of their MS patients.

    • Neurologists and Radioligists have cut back on the use of contrast for MRI in MS patients over the last few years.
      Concerns about how long it may stay in the body for. Contrast still might be used to assist with MS diagnosis or as a baseline MRI scan.

    • What’s this about? Benign MS BS??? Is it possible to select treatment based on a MS phenotype? Is it wise to not start a DMT on women who want to get pregnant some day in future (and care for their baby too) 🥱

      • It will be great if we can spot the portion of MSers who will do well in the long run without treatment, be it 20%, 10% or 5%. For the rest of us, I guess it is irrelevant.

  • A week and a half ago at the EBMT Autoimmune Diseases Working Party meeting

    Dr Richard Burt said that one of the hypothesis for the efficacy of hsct in ms was that since the immunne system gets way way down (out of sight) that will give time for the BBB to heal and in is view that´s one of the strongest effect of the theraphy

    Now lets extrapolate that view for a dear drug off maven G

    What would you thing will happen?

    Blood-brain barrier permeability changes in multiple sclerosis during alemtuzumab treatment



      • I used to work on the BBB way back when. Immune cells aren’t just let in, they actively breach the barrier when lesions are formed leading to the barrier becoming leaky in these areas which can be picked up by MRI with gadolinium enhancement. Once the lesion resolves, the BBB reseals but it never quite has the same integrity that it did before in these areas. This might allow the entry of harmful compounds/chemicals from the blood into the brain which would normally be excluded, albeit at low levels. To my mind, this could be a mechanism for slow burning disease progression in MS.

      • Can’t imagine there would be any impact with local anaesthesia but would imagine a leaky BBB might have an impact on sedation, general anaesthesia etc.

        • Clearly, if my doctors at I need a medical procedure, I’m going to do it. The MS society says anesthesia is a safe. https://www.nationalmssociety.org/Living-Well-With-MS/Diet-Exercise-Healthy-Behaviors/Anesthesia-and-Surgery
          I’m sure this is generally true, but Based only on own my personal experience, however, I think a compromised CNS does impact how my body responds to anathesisia. For heavy sedation, I am told I am “sensitive” and don’t come around very quickly. After a 3 local shot lengthy dental procedure, my face remained drooped and not full functional for a week leading me down a research rabbit hole about dental locals and MS. There are A few reports, but not sure if so few mean really Yeti sightings. Ex https://www.sciencedirect.com/science/article/pii/S0187451916300683. And finally, I had appendix removal surgery with general and never went back to baseline MS ability level post surgery despite PT and all. I am interested to know if any other pwms out there had problems with anethesisa? Overlooked issue?

          • Yes SUEBEE! I have had over 21+ surgeries. As each one commenced, It became harder and harder. I figured it was age & amount of surgeries. Then 3yrs ago having major spine surgery, I woke with paralysis. Couldn’t walk for a long time. Right side barely came back and that was 3-6 months, then continued therapy with many broken toes to be able to come out of a chair. Still have partial paralysis upper leg. I rely on my lower leg spasticity to keep me mobile. I also made a rotator cuff tear worse during wheelchair transfers & falls so now I’ve been dealing with that. Told yesterday & for the past year and a half it needs surgery. There is option of Platelet Rich Plasma or Stem Cell injection but insurance won’t cover those. So I have been researching anesthesia as well. I was thinking back to my C-section prior to the spine surgery & after my daughter was born, my legs took a long time getting any feeling or movement back and medical team became worried. I also have numbness in my face & one side of face is no longer as symmetrical as the other as it droops a bit like I had a stroke (I am very vein so this really bothers me more than others). I came across an article in my research last night before I make a decision on shoulder. I was half asleep while reading so emailed it to myself to reread so your timing of your question was perfect. It is a very lengthy article but read it to the end. They have specific paragraphs related just to MS. The link to article is https://www.nysora.com/foundations-of-regional-anesthesia/patient-management/regional-anesthesia-patient-preexisting-neurologic-disease/

  • How would an antiCD19 treatment be different to an antiCD20+Ixazomib treatment? Are long-lived plasma cells depleted by these treatment strategies?

  • I have just recovered from the ‘SUPER COLD’ that everyone has been getting. I felt really ill but suddenly after a week my immune system seemed to get its butt into gear and I started to get better. I was quite proud of my immune system in the end! This was the first illness since starting Ocrevus.
    I remember reading about possible ‘cross immunity’ re: the common cold and covid19 at some point. Was there any facts that backed up if having had a recent cold might help against covid? And how would that work when cd20 depleted? It would be nice to know if there’s anything in that, considering the vaccines have seemingly done diddly squat..

    • It seems in recent times this idea of cross-reactive protection from past coronavirus infection is being increasingly challenged and it looks like the Crick data is the odd one out.

        • ☹️ bad enough to get a normal cold and think you’re gonna die until the pcr comes back. But No upside of cross -reactive protection either??? Pssstttt

          • I know right?!
            It’s a mix of relief when PCR comes back neg… but then also thinking at least if it was positive I’d recovered…. 🙁 Alas, the 1 night I went a bit wild in Soho I got a cold and not covid… prob still for the best!

  • I have a question about my disability and I honestly am not being sheepish or ignorant, I just don’t really understand a lot of what I’ve read in my own research.

    I am bed bound but can get into a wheelchair with assistance and stay there for at least four or five hours. I can’t stand at all, so obviously no walking or transferring on my own. I was diagnosed originally RRMS 19 years ago (2002), and it was revised as PRMS 5 years ago (2016), and a second opinion diagnosed me as in SPMS 15 years ago. Since between 17 – 15 years ago (2004-2006) I have steadily (somewhat) gotten worse in disability—one cane, two canes, 4-wheel walker, wheelchair, powerchair in 12 years. My question is twofold: first is there any way to test or know if it’s the myelin that is damaged or the actual nerve fibers? And secondly, and probably more importantly, can I be relatively certain that there is no regaining ability to stand at least at this point? The information I read—and it’s a lot—in researching is really confusing, and runs the gamut from terrifyingly and blatantly negative and clinical, to somewhat positive and clinical, to fairly positive and clinical or more accessible as well as ambivalent about what anything means. It’s exhausting and aggravating. Any help would be greatly appreciated. I just want to understand this insidious disease that has wreaked havoc in my life.

  • Please can a post be done on sexism in MS healthcare?
    How women’s health issues are sometimes assumed are women’s problems (menses, early menopause, menopause etc) and not recognised by GP’s as red flags needing more urgent attention by specialists at the hospital.

    • Gee anonymous, I don’t know what you are talking about. You must be overreacting, hysterical. Exaggerating. Needy, going through a tough breakup, depressed. Kids stressing you out? Do you have a therapist? Maybe you ask too many questions, feel urgency because you think about urination a lot, have trouble at school because you are not disciplined, you really are just hyperl sensitive to bodily sensations take a vacation. 😝😉

      • Wow, a lot of these comments are unnecessary?? Maybe it never happened to you or never happening where you are from but I wouldn’t assume it is not an issue everywhere.

        • I think very likely suebee is using wry humour to reflect the very sexism you’re talking about and in this way is validating the request you’ve made.

          For myself I remember being told that the extent I felt pain upon an examination was ‘unacceptable’ because this procedure doesn’t cause that level of discomfort. This was followed by being advised my problem was psychosomatic. I subsequently underwent surgery to resolve this ‘imaginary’ problem.

          As Suebee has so keenly illustrated these are the kind of responses women receive constantly.

          It would perhaps be helpful to have the post you’ve asked for, with advise on how women are best to react or navigate a situation when on the receiving end of sexism from healthcare providers, if they are currently unsure how to do this.

      • Gee Suebee, Who are you replying too? You don’t know anything about the person’s experience to state that crass response.
        I’m glad you don’t work in healthcare, and if you do I really don’t think you should. Perhaps you should take a course on empathy/ clinical empathy, there’s a free one online.
        Think about it.

        • You’ve misunderstood me. I meant it as a satirical response. I have been told or heard all these explanations about my own MS symptoms over the past 20 years. Sexism is prevelant in medicine. Apologies for offense.

          • Just to let you know I did read it that you were being sarcastic about how some Medics do treat women.
            Probably better to to put sarcasm in brackets

          • I immediately recognized the satire.
            In the decade it took me to finally get an MRI & MS. diagnosis, I saw several doctors, got to try an assortment of pharmaceuticals and was generally treated like a hysterical hypochondriac.
            Among these were at least 4 women. Not to say I couldn’t possibly have been treated worse!
            Oh, And, the Dr. that finally got it right was a woman too…

      • FWIW, as a male, aside of menstruation (well duh) and kids (which I don’t have), I have heard them all and a whole bunch more: you work too much, you hate your job, your erectile dysfunction is in your head (but here’s some viagra), you’re depressed, you need to do more sport (when I went to gym 4 times a week), go find a girlfriend (…)

  • What do you think of BTKi reducing the size of inflammation-associated brain lesions?

    Is this something that happens with other treatments, currently available? Or natural repair processes

    • Are they actually reducing the size or is it just pseudo-atrophy due to inflammation going down after the drug shuts off B-cells? Do you see the same early reduction in size with ocrevus or lemtrada? They need to rebaseline at 12 months before saying anything that BTKi are doing anything new.

      • The effect was of SEL slowly expanding lesions, it reduced the volume of the lesions, it looked to be having an effect on microglia and macrophages

        I’m assuming people where already on a DMT before starting in the BTKi trial so the effects must me in addition to there previous treatments. I’m not sure if any current treatments have an effect on SELs

  • I have just read the recent associated newsletter and I know a lot of the focus here is on vaccines/ocrevus but what I don’t understand is the gap between what is being shown by evidence to be true and what is actually being delivered. So, my neurology team has no knowledge about how I might access a vaccine (3rd vaccine, 9 months after my last ocrevus). My GP says it is nothing to do with them and 119 flat out say I’m not eligible for another vaccine and are not aware there is any difference between a booster and a third vaccine. I have spent hours on the phone trying to rectify this but to no avail. The gap between information expanded upon here and what is actually offered is ever widening, it’s hard (delayed by months and months) to even get more ocrevus never mind a covid or flu vaccine. Whilst this is an excellent way in which to disseminate information there seems to be little acknowledgement (because there must be a ton of people in my situation) of the NHS’s inability to implement much of this.

    • I believe the GPs are organising the vaccines. They need to follow GOvernement advice
      I assume your HCP can read….therefore direct then to the Green Book Chaper 14a (https://www.gov.uk/government/publications/covid-19-the-green-book-chapter-14a)


      Read page 20 It starts
      “Third primary dose for those aged 12 years or over”
      Some individuals who are immunosuppressed due to underlying health conditions or medical treatment may not mount a full immune response to primary COVID-19 vaccination.
      JCVI advises that a third vaccine dose be offered to individuals aged 12 years and over who had severe immunosuppression in proximity to their first or second COVID-19 doses in the
      primary schedule (Box). Most individuals whose immunosuppression commenced at least two weeks after the second dose of vaccination do not require an additional primary
      vaccination at this stage. The decision on the timing of the third dose should be undertaken by the specialist involved in the care of the patient. In general, vaccines administered during periods of minimum
      immunosuppression (where possible) are more likely to generate better immune responses. The third dose should be given ideally at least 8 weeks after the second dose, with special
      attention paid to current or planned immunosuppressive therapies. Where possible the third dose should be delayed until two weeks after the period of immunosuppression, in
      addition to the time period for clearance of the therapeutic agent. If not possible,consideration should be given to vaccination during a treatment ‘holiday’ or when the
      degree of immunosuppression is at a minimum. Advice for patients on chemotherapy is available at https://www.ukchemotherapyboard.org/publications

      Box: Criteria for a third primary dose of COVID-19 vaccine
      Individuals with primary or acquired immunodeficiency states at the time of
      vaccination due to conditions including:
      Individuals on immunosuppressive or immunomodulating therapy at the time of
      vaccination including:
      those who were receiving or had received in the previous 3 months targeted therapy for
      autoimmune disease, such as JAK inhibitors or biologic immune modulators including
      B-cell targeted therapies (including rituximab but in this case the recipient would be
      considered immunosuppressed for a 6 month period),

      Reinforcing immunisation
      JCVI have advised that adults who received a primary course in Phase 1 of the COVID-19
      vaccination programme (priority groups 1-9) should be offered a COVID-19 booster vaccine.
      This includes:
      ● those living in residential care homes for older adults
      ● all adults aged 50 years or over
      ● frontline health and social care workers
      ● all those aged 16 to 49 years with underlying health conditions that put them at higher
      risk of severe COVID-19 (table 3)
      ● adult carers and those experiencing homelessness
      ● adult household contacts of immunosuppressed individuals

  • Question mouse doctor I see that tolebrutinib should be completed in 2023 for relapsing ms and they are measuring brain volume loss so we could have an idea of the effects of brain volume loss in progressive ms with that trial just like what happened with ibudilast ?

  • I don’t know what anyone’s personal thoughts are on this, but does anyone know what the requirements are for PAS in Britain, Europe or America in regards to MS?

  • https://pubmed.ncbi.nlm.nih.gov/34633951/

    >A significant association was observed between higher baseline levels of Glu and an increase in EDSS during follow up (b = 1.06, 95%CI 0.47-1.66, p = 0.003) as well as PBVC (b = -0.71 95%CI -0.56-1.38, p = 0.002) and CT (b = -0.15, 95%CI -0.06-0.33, p = 0.01).

    I thought this was interesting in light of the fact that several anti-convulsant medications have had positive phase 2 trials in MS by now. Too bad none of the pharma companies with patents on newer drugs are interested in testing their drugs in MS.

  • Apparently Mononucleosis is running rampant throughout my daughter’s high school! She became extremely ill. I brought her to her Dr for Covid testing. Covid, Strep, Flu all negative. They then said they were going to test her for mono. Bingo. Positive. I then find out after calling school that many kids are being sent home not feeling well to get Covid tested. Then parents calling back in stating they were Covid negative but they have mono. And most, if not all of these kids have been vaccinated for Covid & masks are still required within her school. QUESTION! I know that most of everything that I have read says that you cannot get Mononucleosis twice but there have been rare occasions when it has reactivated… If a person who has MS & had mono (37yrs ago though) is currently in same household with & taking care of that said someone else who has an active EBV/Mono infection, can their chance of an MS relapse be greater or a reactivation of Mono be greater? And Question 2… Do you think that perhaps the Covid vaccine might be playing a part in reactivating it?

      • I would be interested to know what drugs are prescribed for EBV-reactivation. I have been told there are no EBV-specific anti-virals, and doctors (in Belgium at least) are very reluctant to prescribe other herpes anti-virals off label.
        Any information on useful anti-virals to treat reactivating EBV is very welcome! I have had 2 reactivations in the past 5 years.

  • I have progressive relapsing multiple sclerosis, and I have been bed bound for a couple years. Am I bed bound for the rest of my life? With each relapse I have Felt less movement in my legs each time until now when I don’t really feel anything when I try to move my legs… if that helps in characterizing my disease status. Thank you for your time and consideration.

    • Just a patient here – you need to get treated, and only the neurologist who exams you will be able to give you the answers. If the drug is suitable for you I have read Alemtuzumab/AHSCT has shown the best possibility for function recovery. Followed by other high efficacy DMTs like Ocrelizumab or Cladribine.

      • Thanks for the reply.
        Actually I have been treated…many times. I was diagnosed 19 years ago and have been on ms meds the whole time. Been steadily getting worse since the beginning until I became bedridden. My neuro always says the same thing… that I’m “stable” and my prognosis is “guarded,” which doesn’t mean a whole lot to me when I went from being able to stand to NOT being able to walk or stand for the past 4 years, and my ability with my limbs gets less and less over those 4 years, albeit slowly. I’m on Ocrevus right now, but waiting for my next dose because of Covid vaccinations.. I don’t know if that helps….

  • Quiet provoking paper

    CNS inflammation after natalizumab therapy for multiple sclerosis A retrospective histopathological and CSF cohort study

    Our findings suggest that natalizumab does
    not completely prevent immune cells from entering the CNS and is associated
    with an accumulation of plasma cells, the pathogenic and clinical significance
    of which is not known. As B cells are considered to serve as a reservoir of the JC
    virus, the observed plasma cell accumulation and reduction in dendritic cells
    in the CNS of natalizumab-treated
    patients may potentially play a role in PML

    Moreover, T cell numbers were also not lower when the interval between the last natalizumab infusion and the biopsy or autopsy was short, indicatingthat T cells may enter the CNS despite natalizumab

    plasma cell numbers were significantly increased
    in active demyelinating lesions of natalizumab-treated
    MS patients

    Although high
    B cell and plasmablast percentages in the CSF after
    natalizumab treatment are associated with ongoing
    disease activity (43), we could not find an association
    between increased plasma cell numbers and a natalizumab
    treatment failure.

    Treatment concepts in MS and
    NMOSD with atacicept (TACI-Ig),
    which reduces circulating
    B cells and plasma cells by the neutralization of
    BAFF and APRIL, were stopped due to disease exacerbations
    (44, 45), raising the question as to which role
    plasma cells play in disease activity. Growing evidence
    indicates regulatory properties for plasma cells during

    Warning sign for your trial aof plasma cell depletion in the cns?


    • Arnt Barts on the case of plasma cells in the CNS with the Sizmous trail?

      Plus BTKi which are obviously in world wide trials, good chance they will inhibit plasma cells

      Are OCBs antibodies from plasma cells?

      • I have an idea for MS research but would like to conduct this research myself and do the write up. It’s medical but not with a drug intervention.
        I’m planning on returning to uni to study a master’s degree to become a HCP and possibly see if this idea can be researched for the dissertation part of the course.
        Is there any other way I could do this research? I’ve considered an MPhil or PhD but I already have a research master’s degree and feel I just want to get on with the research. Many thanks.

        • Since you would need a thouroughly worked out proposal anyway, why can’t you start on that? If you don’t have the right ‘credentials’ yet, you will need it to be quite footnote-laden anyway, in order to be acceptable, quite regardless of its content.
          I have a Phd in one field, and started doing research in another, and I found I needed to prove myself again and again, often to people who know much less about the topic involved.
          This is not meant as a discouragement (quite the contrary), but as a warning not to expect good or even great ideas to ‘speak for themselves’.

          • Thanks. Looking online, there is the option of being an Independent Researcher, but it more common in the humanities than the sciences, but still possible. To get an article in a well known journal it needs to be affiliated with a university.
            Some independent researchers have been known to use the university they obtained their degree from, though this seems it might be a bit of a stretch. Some will use their place of employment as the affiliation.

          • As a non scientist, I’ve wondered about this type of quandry before and speculated a possible option may be to draft a well researched footnoted proposal, get a neuro or phiso to make a comment, and submit to grant awarding agency with request to fund hiring a team including specialist considered “academically qualified” to run experiment, analyze meta data, survey patients, or what have you. In essence, you’re idea person and you find a scientist who is game and also find their grant funding. Two ideas I dream of implementing are: 1) providing local gym access to pwms to use unique but currently commercially available (expensive and scarce) stationary HITT machine which allows for quick resting of different muscle groups while other limbs are active and then quantifying increase in quality of life, endurance, and strength to users; 2) large survey of pwms denied or terminated long term disability and documenting MS disability level(s), employment, and income outcomes over following years. (I dont want to read one more study studying a fatigue perception scale after slow and steady workout or ways to survey depression in pwms in the next two weeks… ) Pwms need out of the box creative thinking to help live best life, and I think crowd sourcing ideas from pwms and collaborating with “academic specialists” is a great way to achieve this. Good luck Anonymous Future HCP! Don’t give up idea!!! We need your perspective in health care!

  • I had recent surgery. I was going to have a relaxant, then oxygen mask, which I could hold if I wanted and then the anesthetic. I was wheeled into the anesthetic room, given the relaxant and I was off asleep straight away. I woke up and surgery was over!
    Either I was given too much relaxant for my body size or I’m very sensitive to it. I wasn’t awake for the oxygen mask and anesthetic injection.

  • Hello MD- Thanks again to you and everyone there for your service to, I guess, the world. So I just inquired to Google what a CRAB drug is, as it gets mentioned here often, and up comes a link to Barts where you invent the acronym. Pretty cool! You may or may not recall me, I am an X-CRAB man, I guess, 20+ years on interferon beta 1b (Betaseron, here in the US). Back in the day, 1995, when it first came out and I went on it, there was nothing else. Notta. In a “Men’s Group for MS”, we were all on it and I don’t recall too many objecting to the every other day subcutaneous injections and occasional fever, etc. It was all we had (besides steroid infusions and Bee Stings) and we were very happy that something had finally come out FDA approved. Fast forward to your “CRAB” posting (about 2015, I think it was?). You reviewed a German study concerned with adherence to CRAB drugs, where only 30% or so took their CRAB drug as prescribed in the short term, or forever after two years in the long term. (I was unaware it may have been this low!)

    So here’s the question: Relative to many who apparently run into the stubbornness of MS today with DMTs, is it possible that CRAB drugs and especially beta 1b, being considered low efficacy, has anything to do with only a few subjects (in studies) actually taking it as prescribed and for a longer period than two years? I ask this because I have done quite well over my 30 year MS history and have nothing else to point to other than luck, a few Solu-Medrol courses, and Betaseron. Sure, I am concerned about progression and smoldering and some deficits from my RRMS days have increased a bit, but overall nothing (“yet”?) has come close to the dreadful symptoms that were possible. God bless everyone not in my boat. What do you think? Poorer results with studies including Beta 1b, in part because few adhered to the regimen?

    • CRAB = coxpaxone, rebif avonex, beta(s/f)eron so a first line platform agent…It is used isn’t pharmaland..I didnt invent the word…they are efficacious in about 30% of people and many people switch from them within a couyple of years is it poor compliance an issue, probably in some if you dont take it it wont work

  • For professor Gavin giovannoni,

    One way to grow the amount of evidence for EBV being in the casual pathway to ms. You can apply much of the same idea you had for the prevention study follow up family members of people with ms ( those who are at higher risk of getting ms ) and follow neurofilament levels as their ebv status changes from negative to positive in a larger and higher risk group of individuals.

    • They will have to develop a long lasting formulation get a patent and do a trial but the cost of prozac isnt going to increase. Inflammasome tauted to be problem in MS pozac did do a thing

  • Question to MD, with all this covid related immunology research, what’s the trickle down benefits for PwMS, MS treatment and research. Excluding covid-19 vaccine efficiency and AB count.

    • Trickle down benefit…maybe an EBV vaccine…as for research it has had a dreadful effect personally speaking

      We have taken the anti-drug testing we developed and have moved it onto remote blood spot tests based on our covid research

      • “We have taken the anti-drug testing we developed and have moved it onto remote blood spot tests based on our covid research”……..MD1 say it is not so!! I hope the move is only temporary. I know COVID research is important, but so is your anti-drug antibody (ADA) work. Look at what you and your team were able to achieve with respect to ALEM.


        Most of the data for OCR indicates the risk of developing ADA is <1%, but speaking as one who became “allergic” to OCR, the ADA test would have been very informative and might have prevented me from having future infusions, which caused some nasty short/long-term side effects.

        Guess the drug companies do not want to know the real risk of developing ADA, so there is limited funding or interest…..other than maybe from the thousands of pwms currently taking ORC or any other depleting agent for that matter.

        Stupid COVID! I hope once this passes (in couple of years at this pace) you can transition back to researching ADA testing.

        • Misunderstanding the ADA was based on drawing blood now we can do it using the post. We are expanding our ADA testing to all MS antibodies. The ocrelizumab has been made and we have some spots from failers. We have just got some samples of rituximab failers from Sweden too.

    • Now why didn’t I think of that… It’s a no-brainer to me actually. I figured everyone already knew this. 🤷‍♀️ No wonder I’m so messed up. The saying where I live, “if you don’t like the weather & temp, just wait an hour. It will change.” I get a couple good weeks in fall & a couple good weeks in spring. The cold actually exaggerates the leg & arm paralysis. Numbing my legs to point they won’t hold me up or move. The heat exaggerates other MS symptoms. My T1d, extreme heat I think plays a factor in how effectively my insulin works – I always seem to have days in summer that I get an unexpected higher than normal glucose. Btw, there are studies that say you can freeze fat & it melts away… it’s a double bonus. Bring on the cold. 😂
      Good article Luis. I’m just being facetious trying to make myself laugh. Laughter is the best medicine.

  • Binge in B cells

    Naive human B cells engage the receptor binding domain of
    SARS-CoV-2, variants of concern, and related


    A subset of
    recombinant antibodies produced by naive B cell precursors bound to SARS-CoV-2 RBD and engaged
    circulating variants including B.1.1.7, B.1.351, and B.1.617.2, as well as pre-emergent bat-derived
    coronaviruses RaTG13, SHC104, and WIV1

    No infection no vacines …Still protection


    More food for the antivaxx?

    • You can find all sorts of antibodies and immunoreactive cells in people, including to loads of autoantigens yet these people do not have autoimmune disease. People don’t appreciate the immune system and antibody responses etc operates at random and amplification only occurs when the antigen is seen for real. The B cells identified here are naive precursors and it is highly likely the person would be overwhelmed by COVID before a mature immune response could be made against it, so this isn’t really protection in any functional way. However, these B cells can be triggered to mature by vaccination to mount a very good response.
      So once again, proof that the anti-vaxxwers are gullible morons.

    • If the story of Nrf2 was so strong why is DMF not a better protecter against progression?. I used to push the buttons to argue that it didnt get into the CNS very well but I think MMF (breakdown product of DMF) does

  • Mouse doctor since you have experience in immunology have you thought about applying for a grant to develop a small molecule to inhibit EBV at the preclinical stage or perhaps in vitro ?

  • Hi,
    I have been on Ocrevus for over a year (two infusions) and would like to switch to cladribine – as I am getting tired of the anxiety re efficacy of the Covid-19 vaccine. My last infusion was in March and under my neuro’s guidance I have delayed the next one.
    Question: if I switch to cladribine should I get another Covid-19 vaccine? I have had three already – last one a few weeks ago. I doubt this is even a possibility – or should I just wait for my B-cells to regenerate?

  • What do you think of evobrutinib reducing the volume of slowly expanding lesions?
    It seems like it would be good news for progressive ms too, right?

  • Professor Gavin already looked at the rate of MS individuals in the HIV population well do we know the rate of MS individuals in those talking famciclovir ? Is their a protective effect ?

  • Here is a very interesting paper: https://diagnprognres.biomedcentral.com/articles/10.1186/s41512-021-00106-6

    > We selected eight baseline prognostic factors: age, sex, prior MS treatment, months since last relapse, disease duration, number of prior relapses, expanded disability status scale (EDSS) score, and number of gadolinium-enhanced lesions.
    > The optimism corrected AUC of our model is 0.65, indicating a relatively small discrimination ability of the model.

    What I take away from this is that most of the factors that neurologists typically use to classify their patients as having “mild” or “aggressive” MS actually have very little predictive power in terms of future acute inflammatory disease activity. This just further reinforces the irresponsibility of the escalation therapy approach—neurologists are making decisions about relative risk-benefit ratios without having any information that would allow them to correctly evaluate the risks!

  • When it comes to the covid vaccines, is there any concept yet as to how much protection a t-cell response but no antibody response might offer?

    • Not yet but this data will surely surface the Brits are doing their best to infect on another and by chance those on anti-CD20 will get infected, I know that prof G has said we have had hopsitalisation

  • Given that vaccines have been out for 6+ months now and we’ve had the delta wave (so presumably lots of data points!), are there any studies being published for vaccine efficacy (either infection or hospitalization) on anti-CD20/rituximab/ocrelizumab? Any rumors of unpublished data? Obviously, lots of articles on antibody levels, and we can guess at what that means for immunity, but I haven’t seen any data on actual immunity. Are these studies being done? Is it just a function of them getting written up and published?

    • studies are being done in UK it is called OCTAVE but problem is there are few people with MS. I am sure the MS register is monitoring this too

      We posted a paper by Konig and clearly infection happens but that is not surprising. Infection is controlled by antibody levels and they wane with time and unfortunately if you had the AZ vaccine you start with a low and often almost non-existant levels of antibody. Add anti CD20 to that and you have two hopes 1. Bod Hope and 2 No Hope. This is why it has been binned for the boosters. In immunosupresed people there is about a third more hospialisations however the vaccine is protective. As for people with anti CD20 I suspect you are at risk of infection but those T cells will help protect against severe covid…..Data to follow no doubt.

  • Not sure how to get this to the blog’s admins but when you google Barts MS you get google ads for what I understand is a laser bandaid that fixes your MS gait issues. Not sure if you guys can report that.

    • I just searched Barts MS and didnt get an advert…do other people get this?.

      Has ProfG started to monitorise the blog?

      The other thing that happens is that you can some times get targetted ads for example if I go to you tube I always get Grammarly because google realise I cant spell…Have you been searching gait issues. Maybe you have been talking and your phone or “alexa” has been listening…Have you ever noticed that you talk about something and the next thing it pops up on facebook or should I call it Meta….Doesnt Mark Zuckerberg look like an Alien in that video?. They made 8 billion a quarter after tax thats 8 billion and five quid before Tax:-)

      • I searched Barts MS on google and I got the expected results. I think MD1s second explanation is more likely the case 🙂

        And yes, I do not even use any voice activated devices in my home, yet if the wife and I are talking about say “carbon fiber canes” and I open my phone to google it, before I can even finish typing “carbo……” the first suggested result is carbon fiber canes, despite the million other products it could possibly suggest. So for sure something seems to always be listening or watching these days.

        Agreed about Mark Z. He is the picture found under the definition of a humanoid. The promo for the meta universe did not help.

  • T time

    Vaccination is one of the best ways to prevent severe COVID-19. Two doses of mRNA vaccine protect against serious illness caused by the coronavirus SARS-CoV-2. They do this, in part, by encouraging the immune system to make specialised proteins known as antibodies that recognise the virus. Most of the vaccine research so far has focussed on these antibodies, but they are only one part of the immune response. Vaccines also activate immune cells called T cells. These cells have two main roles, coordinating the immune response and killing cells infected with viruses. It is likely that they play a key role in preventing severe COVID-19

    In people who had never had COVID-19 before, the second dose of vaccine improved the quality and quantity of the T cells. The same was not true for people who had already recovered from COVID-19. However, although their T cells did not improve further after a second vaccine dose, they did show signs that they might offer more protection overall. The proteins on the cells suggest that they might last longer, and that they might specifically protect the nose, throat and lungs.


    mRNA vaccine-induced T cells respond identically to SARS-CoV-2 variants of concern but differ in longevity and homing properties depending on prior infection status


By MouseDoctor



Recent Posts

Recent Comments