Ask Barts New Decade


If you have a question unrelated to other any other threads. This is the place for you

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  • Happy New Year!

    When the posts talk about treating early and effectively, I take the effectively part to mean one of the *mab’s or similar but what does early mean? Just as soon as possible after diagnosis or is there a generally accepted timeframe where it’s too late to be counted as early, say 1 year, 5 years, 10 years? Thanks!

  • First of all Happy New Year to all of you at the blog – and thank you so much for all the work you do.
    My question focuses on the past.
    It’s been a decade since this blog first went live – What improvements have you seen for people with MS during that time?
    I certainly think things have improved for pwMS since I was diagnosed (also ten years ago) – more DMT’s available, growing awareness, the creation and existence of this blog – but what is your opinion?
    Thanks in advance,

    • ProfG is glass half-full and is at the front line and will not doubt give an unbeat response. 2009 options were CRABS and Natalizumab. No Orals, No Choice of Big Guns, no concepts for remyelination and much more. But by 2009 and much earlier it was obvious to me that immunosuppressive DMT were not the only answer for progressive MS and here we are a decade later still contemplating monotherapies and this is frustrating to say the least. However we have seen success and some failure and compared to other Neurological Conditions there has been much progress.

  • Why does this blog always talk about so called progress in ppms..and ms is one disease when clearly ppms seems to stand apart in severity……”Diagnosed 6 years ago, zero change to MRIs, but symptoms worse everyday. Spine scans are a train wreck, brain scans unremarkable. EDSS-6.5-7.5. Wheelchair dependent. Now on ocrevious. Nothing helps. No good days.”

    • No sure I always talk of progress, we need to do much more for SPMS, PPMS but there has been progress and their are options across the spectrum. However, this is a double-edged sword.

    • Progress often starts small but accumulates with time. Ocrelizumab will give a PPMSer 4-5 years more time on their legs and may 9 years more time being independent, i.e. with upper limb function maintained. Is that progress? We now need to build on this.

      • Only if you meet the criteria-the rest of us still have nothing! I’d really like the chance of staying on my feet longer! Perhaps this is where the frustration comes from….

  • Gluten and dairy….I have excluded both, and sugar, for years. I aim to try the ketogenic diet this year, and am optimistic for an improvement. Is there any reason why I should continue to exclude gluten and dairy? I don’t have Celiac disease.

    • Re Peter 7:37
      Out of interest why have you been excluding gluten and dairy?
      A stroll down the special diet supermarket isle confirms very popular (and profitable!) things to avoid.
      All the best with keto diet 🙂

      • Because I have read that gluten is inflammatory and enhances the permeability of the gut lining. When the intestine has holes in it, incompletely digested gluten and casein particles can get into the blood stream, triggering an inappropriate immune response. Whether this is accurate or not, I don’t know… I have been avoiding gluten and dairy to be on the safe side. Now I would value some informed opinion.

        • Not sure of the evidence that shows gluten and dairy are bad for MS. You mustn’t believe everything that is out there.

  • Is Fingolimod considered a ‘high efficacy’ DMT or not? Your honest opinion would be appreciated. Thanks. – and a Happy New Year – and ongoing grateful thanks – to you all x

  • Why are my posts not been published?

    You know i will never go anonymous or another name,or another ip adress

    I dont need that, i could but i wont

      • I have had a quick look in spam….there were a lot from Hairstyles and when I cleared them it deleted the whole spam box of 90 comments, there were a a few from anono on the first page…maybe it has recognised them as a HSCT zealot and they go straight to bin. I cleared out 280 spams last week, sorry if you were in there but I the system is needs configuring as it is too arduous filtering 300 spmas for the odd one that is noI cant am not going to spend time

  • Use of DMTs Changing ‘Natural History’ of Relapsing MS, Study Says

    Results indicated that 25% of these patients took 10.7 years to reach EDSS 3.0 (moderate disability), and 25% took 16.3 years to reach an EDSS of 6.0.

    Among the group followed for 15 years after symptom onset, 19% reached an EDSS of 6.0

    In the study, patients were typically treated with DMTs within two years of diagnosis, with the majority (98%) receiving either interferons (brand names include Avonex and Betaseron) or glatiramer (sold as Copaxone, Glatopa and other generics), with only a small group (22%) given Tysabri (natalizumab), usually after reaching an EDSS of 4.0.

  • Hello, happy new 20s and thanks as ever for the blog.

    I did ask this before, probably in a prolix fashion, and I didn’t understand the answer: but, bearing in mind the artificiality of the 3/4 distinctions in diagnosis, why is it that ocreluzimab is not prescribed or researched at all as far as I can see for ‘SPMS’ when it’s been proved efficacious in ‘PPMS’ and ‘RR’? Is this a matter of disease duration that make it a spent firework in the body of someone who’s got ‘smouldering’ and thought to be in smouldering SPMS decline? Or it what pulls the purse strings at NICE?

    I’m aware the NHS is burdened with hard money decisions, But if it’s a question that could be raised, I’d like to get it answered.

    Thanks for your attention

    • Because most SPMS is active SPMS and is covered by the US label. We were able to extract SPMS out of the RRMS population and showed it had an impact on PIRA (progression independent of relapses) or SPMS. We just need to convince the regulators that #MS_is_1_and_not_2_or_3_diseases 😉

  • Would DMT’s benefit every pwMs, regardless of stage , or activity on MRI’s? I realize that many medications are only for “active” MS, and that health insurance only approves medication for such. In a perfect world should everyone be on something?

    I know many have already said it, but thanks to the Barts team for all your dedication!

  • Happy new decade to all.

    Janus, the Roman god of beginnings, doorways, and transitions according to wikki. Looking into your crystal ball what do you see coming for the new decade?

  • Happy New Year!

    We’ve recently come across your Blog’s discussion of George Ebers and would very much like to relay this thoughts / concerns to the wider German MS community. Do you know of any way that we could contact him over there in Canada in order confirm that he’s o.k. with this? Does anyone have a current Mail address?

    Many thanks!

  • Happy New Year and thanks for al the great work on this blog.

    The use of senolytic treatment (like Dasatinib & Quercetin therapy) in MS hasn’t been discussed on this blog so far. Any thoughts about the chances of such a therapy in MS?

    • Dasatinib is protein tyrosine kinase inhibitor, not to be confused with a Bruton’s Tyrosine Kinase (BTK) inhibitor which has some effect on relapsing MS. I think there was a report before Christmas saying there was a trial failure but long term targeting of such targets is unlikelyl to be well tolerated in my numble opinion. Quercetin sounds like it is a neutriceutical flavinoid so unlikely to go anywhere fast.

  • What would you do?
    I have PPMS, diagnosed for 4.5 years….I walk badly, and not far with 2crutches, and not wanting to progress any faster( obviously!). Also have fatigue. I was working a fairly stressful full time job but now been medically retired 2years. I walked with a stick occasionally when I was diagnosed, so it feels like a speedy decline. I have not been eligible for off label cladribine due to LP not showing signs of current inflammation.
    Had MRI to see if any new lesions for Ocrevus (shortly after LP) but there was no evidence of activity so that was a no too! Declined gadolinium on most recent mri. It appears my mobility decline does not seem to be directly related to disease activity. As medicines are reliant on “proving” inflammation, I wonder if you have any suggestions on medications and how to access them.
    Any advice gratefully received, as I’d love to try and slow progression.

    • No easy solution in a situation like this. We would recommend that people with PPMS that is inactive volunteer for the ORATORIO-HAND study.

      • Thank you, it’s my only hope but a 50% chance of getting a placebo and the probability of having to have more gadolinium-I’m not sure I can commit. “ hope” is all I have-there is still nothing concrete for many PPMSers. The MS world is very skewed to advances for the majority, the minority are still left with nothing apart from hope, which doesn’t stop progression….just a little frustrating, apologies and happy new year.

  • Happy new year!!

    1) A question regarding remyelination; I guess it will depend on the type of agent, but in general, can you say anything about how old lesions these agents are likely to have an effect on? Say, will old damage be significantly more difficult to repair?
    2) A second question regarding remyelination; is there any forcast to when these drugs will hit the market?
    3) A third question regarding remyelination; are pwMS able to remyelinate naturally (to some degree) or is this ability defect? Is the only thing causing remission of disability the level of neural reserves?
    4) A fourth question regarding remyelination; some pwMS report disability improvement when starting new DMTs, especially those going from injectables to monoclonal antibodies and Cladribine. Is this because they dampen inflammation and allow remyelination to occur, or just the former?

    • (1) Will old lesions be more difficult to repair….Yes I expect so. In all the pre-clinical study, there has never been any study to show that any of the agents can remyelinate chronically demyelinated lesions, essentially all studies examine the remyelination potential of agents on fresh lesions that would remyelinate anyway given abit more time.
      (2) The only company with ongoing trials I believe are biogen, the academic trails are unlikely to come to Market as they won’t be done well enough for licencing,,
      (3). I am sure people with MS are able to remymelinate naturally, there was a study looking at the grey amtter in 70-80 year olds and there was remyelination. However, MS lesions do become difficult to remylinate once they are scarred.
      (4) The later I suspect, just as ProfG says you may not need remyelination agents, you just need to switch off the damaging inflammation and then allow the repair to occur naturally.

  • Happy New Year.

    I wish to address a question related to my RR MS. It appears that I am affected from cognitive side with very little physical impairment. Things have become relatively more forgettable, less multi functioning than i used to. I am on Mabthera (rytuximab) right from the beginning of my diagnosis in 2018, (when i turned 40). Since then there were not any changes or new activities in MR , plus i am on gluten and diary free diet to avoid more inflammation caused by food. Here are my qiestions:

    Q#1. I wish to get your reflection on what are the prospects for my MS not being developed in further or reversing it back?

    Is there any hope for me to revers my MS and not developing to SPMS or getting dementia? Or what to expect? I mean therare so many success stories that ppl on new era medication are being successful.

    Q#2. If i will progress anyway, when it is to expect?

    Honest answer will be much appreciated. Thank you.

  • Imho DMDs like alemtuzumab & co. are the worst thing that happend to the MS research. Yes, fortunately, they provide relief for people with MS, but they brought causative MS research to a hard halt. MS won’t be solved by looking into the microcosmos of immune responses for another 20 years.

    Researchers should rather take a step back (again) to look at the bigger picture. Infections were suspected to be related to MS early on. There is a lot of evidence that different viruses, bacteria or fungi can be the causative factor in the disease. Nevertheless, there is hardly any research in this area and if there is, then it is usually only selective, looking at one possible cause/trigger instead of doing multifactorial research.

    Why aren’t people looking closer into EBV’s (and other viruses) potential involvement into MS?

    ‘EBV infected memory B cells recognizing a commensal microbe epitope eventually become EBV-free through memory B cell division. Once EBV free, these memory B cells can proliferate and recognize a cognate epitope in the CNS, causing inflammation and MS. The nature of the antigen in the CNS on which this cognate epitope is found remains unclear: it could either be a human antigen or an antigen belonging to a microbe present in the CNS (such as Toxoplasma gondii). Under EBV-free circumstances, B cells recognizing this “forbidden” epitope are generally not allowed to enter the memory compartment, greatly reducing the risk of MS in EBV negative individuals. When EBV infected, the LMP1 gene simulates CD4+ (follicular helper) T cell B cell conjugation in the germinal center, allowing a B cell recognizing a “forbidden” epitope to enter the memory compartment.’

    This hypothesis would answer a few open questions, especially those that see positive associations with EBV, other (bacterial*) infections, vitamin D status (**) and also the possible gut connection (***).

    *** ‘To clonally expand, the now EBV-free “forbidden” memory B cell that we have been following from the mouth must find a cognate antigen and an activated CD4+ T cell that recognizes a peptide from this antigen. Lymph nodes exposed to fungal antigens from the gastrointestinal tract and genitals provide the best environment for this chance event to occur—especially when these sites are colonized with Candida.’

    It would also explain, why Anti-EBV treatment seems to be effective.

    Or why other anti-virals seem to work:

    And last but not least, it would explain why various treatments against different infections always seem to help a subset of people while not doing anything for the rest. Because the responsible antigen might come from different sources. Also why antibiotics work for a limited period of time (****), since the underlying cause is not solved.

    IF the hypothesis is true, the best way to treat MS would be to clear potential bacterial or fungal infections and EBV (or another viral infection) at the same time. Just treating one of those things might only help in the short term or not at all.

    After several years of reading MS research, I still find it surprising and extremely frustrating that even small successes in the treatment with various drugs are often attributed to complex immunological processes. Researchers almost never take a closer look at simple cause-effect relationships, only the most complex explanations seem to be interesting. Occam’s razor hardly seems to be known to anyone these days anymore.

    When can we expect causative MS research to pick up the pace again, with a closer look at EBV, HHV-6, CDV and other infection?

  • Food Coma
    Postprandial somnolence (PPS) or food coma is a normal state of drowsiness or lassitude following a meal.

    I solved my food coma by taking probiotics or home made kefir on an empty stomach.

    So it would seem that I simply do not have the bugs (microbiome) to digest my food.

    • My husband used to suffer with food coma terribly but since starting blood pressure medication it has stopped. Bread was the worse trigger and had to avoid it, it doesn’t affect him now though.

  • Happy New Year!
    What’s next when HSCT fails?
    ‘New’ treatment as Alem or Cladribine or follow up with Rituximab / Ocrelizumab or DMF?

  • My questions relate to cosmetic-related interventions and more specifically:
    Do you consider hyaluronic acid facial fillers and Botox dangerous for PWMS? And what is your opinion on breast implants?
    Can any of the above increase the risk for a relapse/disease progression?

    • They are dangerous for your pocket!

      Botox can be part of MS treatment, but not usually when it is put in your face. I wonder what the consequences of doing that (paralysing nerves) for years is going to be. You lose so much by having no facial expression and it is in my opinion not a good look. Check out Simon Cowell in his cyrrent advert…he can’t move much of his face.

      As for fillers ……once you start can you stop? Why put that rubbish in your lips? Having a ledge is not a good look and it will fall out of fashion. By which time you will have strectched out your lips, so you will be hooked. At least with a boob job you can reduce the skin but on your lips? You could look like a Mursi/Surma/women of Ethiopia. Also have a look what happens if you block an artery with the filler. It can happen…..I’m sure you look beautiful without the need for fillers and botox.

      Breast implants…I don’t need them, I have my own Moobs nearly an A cup:-)

      Breast implants and risk of neurologic disease. A population-based cohort study in Sweden
      O. Nyrén, J. K. McLaughlin, L. Yin, S. Josefsson, M. Engqvist, L. Hakelius, W. J. Blot, H-O Adami. Neurology 1998
      Conclusion: Our results provide no support for the conjecture that breast implants cause neurologic disease.

      • I appreciate your personal opinion on cosmetic interventions, but would it be possible to have a more direct answer on whether these interventions can have an effect on MS?
        If you don’t have knowledge on this (I know there is no active research done on it so I understand) then maybe dr Giovannoni does? Thank you

        • Direct response…breast implants insufficient evident it has any effect
          Botox is a treatment for a numbrer of MS related problems
          Hyluronic acid has influences on myelination but comsemtic use is not going to enter the CNS so to answer your question I have no idea 🙂

          • Don’t always agree with you Mousedoctor, but I’m going to speak from experience. I needed breast surgery and the subsequent reconstruction was thought to be too risky to my health. I chose not to compromise my wellbeing, that is, any chance of an MS relapse for cosmetic purposes. I may not look like everyone else, but am comfortable with my decision. Also, there is a chance the surgery has to be redone. My face is also numb and the thought of Botox is just asking for more trouble than I already have. Excellent plastic surgeons at my NHS hospital, so I wasn’t worried about a botched job.

          • Everyone is entitled to opinions.
            Botox is very well toerated based on most of the literature

  • Do you think MS society’s aim of raising 100 million to stop. MS in a decade is feasible? If not how many more ask barts new decade posta are there likely to be?

    • How many more ask Barts new decade posts?……maybe none, it perhaps depends on how much steam ProfG has left. Will NDG take the reigns….I will have been put out to grass by then if I have not popped my clogs, maybe I can guess post whilst growing mould.

      Can the MS Society raise the depends on the donors, but the they have created a bat to beat itself… We have been here (“Stop MS”) before, can this be done in a decade? You know how long the treatment development cascade is.

      • Thanks MD. I’m sure you’ve got plenty of decades left in you. Unless your looking to retire to the carrribean or get paid loads by pharma as a ms clinical trial adviser. If so why not! MS society I last checked has raised 45 million already. The synic in me says they really don’t want to stop MS but just slown it down. Theses societies become like mini cooperates and will never put themselvesnout of business. Let prey and hope they do.

  • There was an article about having 2 illnesses not just M/S I cant find it. Can you guide me in the right direction please. xx

  • What would you do next? Lymphocytes low after Cladribrine and now even lower on Tecfidera. No DMT is not an option as MS is very highly active and condition deteriorating. Back to Tysabri with extended interval dosing?

    • We can’t give personal advice. One wonders if you have been on Cladribine and presumably failing the logic of a lower efficacy treatment. Obviously one needs context but the blog is not the place for this discussion

  • I am currently being assessed for ocrevus for ppms. My last mri was on a 3.5 machine with contrast. This time they have sent an appointment at a hospital which uses 1.5 without contrast will this be sufficient to show any new disease activity.

  • Hello, I would be very thankful to receive an answer to my question listed earlier. Question is
    what are the prospects for RRMS patients being affected from the cognitive side NOT much physical? Are we talking about dementia? What are the prospects? I am taking Rytuximab right from the beginning of my diagnosis 2018. Since then no changes OR new activities is detected on MR. i am 40 years old. Following gluten and diary free diet. Any chances of my MS not developing any further to SPMS or reversing it back?

    • In some people MS is a cogntive rather than movement issue.
      If you start with high efficacy agent and it keeps active disease at bay, ths is a good sign

  • I recently read the book ‘It’s All In Your Head’ by neurologist Suzanne O’Sullivan about psychosomatic & functional illness’ ( as I have always been fascinated how the mind can impact the body with symptoms (shout out to IBS whenever stressed out!).
    As someone who actually has MS – what is the incidence that even WITH a neurological disease some of your symptoms become psychosomatic, is that quite common – especially just after diagnosis when you’re being hyper vigilant? Is there anywhere I can read about this? Thanks, Hannah

    • As someone who also has MS. I’ve had a habit of telling myself repeatedly that I’m making it up or ‘buying into’ my symptoms especially after having read a similar sounding book. As a result a couple of my relapses have gone on for much longer than they should have. Try not to be paranoid but also trust yourself. If in doubt talk to your care team. I’ve been working hard to stop doubting myself and hope you can do better at that than I do.

    • “slick marketing surrounding stem cell treatments…”

      No Chemo…no cure is the mantra on the hsct forums.

  • Something of a mundane question perhaps in the world of science and neurology but is there any chance of a post on what to avoid consuming for the many of us immunosuppressed.
    I’m interested in Chuckling Goat Kefir – packed with live cultures apparently, but is this safe following Alem?

    Ditto with regards to travel etc – my husband has just had yellow fever vaccine and I see from the notes he came home with that this is not permitted for those immunosuppressed.

    Appreciate this is something that could be addressed by MS nurses, but as ProfG said in an interview last year – they’re all burnt out. Certainly my MS nurse is overwhelmingly busy. Also, of course, they can only answer one person at a time, whereas Bart’s lifestyle posts can reach the many.

  • How safe is it for a patient with advanced MS to have a general anaesthetic for a minor operation? Should it be avoided if at all possible?

  • Do you know if it is fairly common for patients with Multiple Sclerosis to struggle with paranoia and for these paranoid thoughts to become more of a problem as the MS reaches the advanced stages? What can be done to help someone who is really struggling with these troublesome thoughts?

  • Treatment mechanism of Cladribine

    Could you please provide a somewhat more in-depth explaination of how Cladribine is supposed to work?

    Case in point: on the one hand we’re told to keep track of lymphocytes before and between courses: “don’t take couse 1 if you’re over 1000, don’t take course 2 if you’re under 800,..” implying that the main effect of Cladribine would probably be to reduce (B-cell, T-cell,..) lymphocytes.

    On the other hand, Cladribine is classified here as an IRT (Immunesystem Reconstruction Therapy) in line with HSCT, Lemtrada,.. This would likely imply that permanent changes are happening as result of “elimiation” of “wrong” lymphocytes. In that case, decreased lymphocyte levels would probably in fact be an undesired “side-effect” of treatment. If lymphocytes didn’t recover even 18 mths after the initial course, then no further treatment would be recommended.

    So what is the actual goal? Depress lymphocytes for a certain amount of time or reconstruct them (albeit cautiously) ?

    Bonus question: What would the purpose of a third treatment cycle be if, say four years after therapy start, renewed disease activity is registered? Would the 3rd cycle serve to once again reduce lymphocyte count or to “reconstruct” even more lymphocytes?


  • With Harry and Megan leaving the Royal Family. There was a flood of hateful/evil comments from her sister Samantha Markel who has MS. My question is can MS make person evil or more evil? Or change their persona? From loving elder sister to jealous greedy bully?

    • MS can change your personality and behaviours and is perhaps one contributing factor to why many people with MS become divorced.

      Whether this an issue with Ms Marvel I cannot say and have no interest in discussing.

      The Royals can do what they like, I don’t want too pay for the protection of Tony Blair or particularly David Cameron, but the Nation does. Why is this interesting…Oops there goes my OBE

      • Yes okay. I get brain damage effects personality. But to become more calculating does not imply damage. Or are we saying evil is merely symptom of compromised brains and not a mind set? Or is there something more sinister happening in terms of biological processes?

      • Please can I suggest a separate post on the subject of Multiple Sclerosis and personality/behaviour changes? It would be interesting to hear what neurologists have observed in their patients over the years and insightful to also hear from people with MS how much they and their closest family members have been affected by personality/ behaviour changes since their diagnosis of MS.

    • This is based on a study done in mice and is an antibody toxin molecule, however antibodies probably dont penetrate the marrow very well and is the toxin safe in humans.
      This currently is science fiction and we do not endorse this company or product.

    • Yes the Zeus trial I think ProfG called it.

      We do not have the bandwidth to do every trial that our neuros come up with. Likewise we do not have the best expertise to lead the trial. However, Richard Nicholas is an excellent choice to lead the UK effort. Importantly it doesn’t kill our neuros to learn that other places have heard our ideas and have actually done something about it.

      I see ProfG as a juggler who is throwing balls (ideas) into the air as he walks forward. We allow some to fall to the floor if they we think they are dodos or we the idea is too early for us to understand what he is on about, Some we try to catch, but there are simply too many balls us to deal with, so we are happy that others catch them. We can always refer people in our care into those studies. It is one of the beauties of being in London. The neuros work together.

      If we had a nice benefactor who dropped us a few million we could increased our bandwidth and we would have done a lot more than we can do now. However if you get too big you end up chunring-out crud.

      We can live with the idea that we thought of, perhaps first….even if this doesn’t get acknowledged. OK I’m blowing our trumpet and we can have parallel evolution and other people can have the same ideas. When I had the moment of thinking about memory B cells, but when I did my reading I found out that someone had already had the idea. The difference between me and some of my peers is that I admitted that other people have ideas. I have recently seen a paper where the work was probably one ideas but we were not credited with it although our paper was cited for something else indicating they know about our ideas

  • Why do some people with few lesions have a high level of disability and some people with many lesions on the spine have no disability. Is it assumed it is just a matter of time before they become disabled?

    I have read that being diagnosed after 40 and having lesions on the spine are a poor prognosis, but what is your experience with that demographic if they start on a highly effective DMT and show no signs of disability?

  • Question :

    One plasma cell secretes 10.000 antibodies per cell per second

    In the bone marrow of an healthy adult(40 -49 years ) exists +- 500 plasma cells

    That make 10000*60*60*24*500 =432 000 000 000 of antibodies every day

    Are they all pathogenis in pwms

    Pathogenic memory plasma cells in autoimmunity

    Automated enumeration of lymphoid and plasma cells in bone marrow to establish normal reference ranges


  • How much concern should those of us taking DMTs have of the recent outbreak of Coranavirus in China.

    With seasonal flu season already occurring, and the likely increased spread of the virus due to the Chinese New Year taking place, could this be a particular unique cocktail for disaster ?

    if you have a low immune system surely this kind of virus is going to be super risky ?

  • I am on Tysabri. I am in my late 40s and do not have the JC virus. I read somewhere the virus lays dormant in the tonsils before entering the bloodstream. Could it be possible I am negative/will stay negative since my tonsils were taken out?

  • DMT s

    Objectives: To evaluate how the traditional prognostic predictors vary in three subgroups of relapsing MS patients defined by age at onset: Pediatric Onset Multiple Sclerosis (POMS ≤ 18 years), Adult Onset Multiple Sclerosis (AOMS 18 – 49 years) and Late Onset Multiple Sclerosis (LOMS ≥ 50 years).

    Conclusions: Real-world data from the Italian MS Registry suggests that prognostic predictors can vary according to the patient age at onset. However, continuous DMTs exposure reduces the risk of CDP regardless of the patient age at the first DE.

    Exposure to disease modifying drugs reduces disability progression in pediatric-, adult- and late-onset relapsing multiple sclerosis: real world data from the Early Multiple Sclerosis Italian Cohort (E-MUSIC)

  • 5 weeks since latest MRI
    Not reported on yet, nobody has even looked at it
    2 more weeks?
    then neuro looks at it
    then gets typed up
    then sent out
    10 weeks ish?
    this normal?

  • Unexpected immune response in brain, spinal cord could offer clues to treating neurological diseases

    “We expected the macrophages would be present in the area of injury, but what surprised us was that microglia actually encapsulated those macrophages and surrounded them—almost like police at a riot. It seemed like the microglia were preventing them from dispersing into areas they shouldn’t be,” said Plemel.

    “We found that both the immune cells that protect the central nervous system, microglia, and the immune cells of the peripheral immune system, macrophages, are present early after demyelination, and microglia continue to accumulate at the expense of macrophages.

    “When we removed the microglia to understand what their role was, the macrophages entered into uninjured tissue,” explained Plemel, who is also a member of the Neuroscience and Mental Health Institute.

    “This suggests that when there is injury, the microglia interfere with the macrophages in our central nervous system and act as a barrier preventing their movement.”

  • For PWS who are about to start an IRT, does the coronavirus outbreak put these patients at higher risk?

    While it is only just been reported that the first 2 people in England have been infected, given the transmission rate of the virus and potential for this to turn into a global pandemic, should neurologists be considering a delay with starting treatment?

    Professor Giovannoni – you posted a lot about this ( (the virus) on your twitter account – will you put any consideration into this when making your decisions?

    • You are at risk from any infection and one you have no immunity to is a risk. If it is virulent then you are at extra risk.

      If you have any immunosuppressive you are at risk.

      So tomorrow’s papers have a more.interesting story than Brexit.

      It will be interesting to see when this outbreak is finished what the demographic will be…..

  • It’s difficult—if not impossible—to get any replies/information to my queries anywhere about progressive phase of MS. Don’t need answers per se, just some basic info as a reference. In the progressive phase, as opposed to the inflammatory phase, it’s just degradation of nervous tissue at that point, correct? So none of the DMTs are effective at this point, correct? I’m just trying to understand since I don’t have a neurological science degree, and no one has replied to emails sent to professors and doctors. I am bed bound with barely functional triplegia. It seems to me that all the disease modifying therapies are created to slow down or somewhat impede the attacks on the myelin. But in the progressive phase the attacks have already pretty much ceased, and the axons are just in a process of disintegration which the DMT aren’t designed for, correct? Just trying to get a good understanding of the disease and where I may be in the process

    • Don’t need answers per se, just some basic info as a reference. In the progressive phase, as opposed to the inflammatory phase, it’s just degradation of nervous tissue at that point, correct?…Unlikely when you look at people with progressive phase there are inflammatory lesions and in inflammatory phase there are progressive lesions. However the progressive bits need a different type of treatment. These are generally not available

      None of the DMT effective…Incorrect. There is no question people with active (inflammatory lesions 15% of PPMS respond. If we look at hand function there is responsiveness, but we need extra treatment.

      You may be eligiable for chariot MS but it may depend on eligiability criteria.

  • One more question. I have only seen information tangentially on this, but could MS actually be considered a metabolic disorder with immune system mediated aspects instead of an autoimmune condition only?

  • strange things are happening to my mris and I frustrated. Recently I went to facility to do control scans and now the answer came back saying that 1/3 of all T2 and FLAIR lesions disappeared and some (the largest) downscaled in size. I do control mri rather every ear or two For 6 years now and those lesions stood they ground on every image, except this last one.
    When I got DCMs recently and played with them I noticed they they does not disappeared completely but rather…faded to the point you can’t notice them until you put contrast to the maximum and then shape of some of them could be revealed .. but the color difference with surrounding tissue is so minuscule.
    So my question what does this mean. Am I “cured”? Was initial diagnosis wrong? Is mri machine malfunct (I do all the scans on same apparatus, but it is a pretty old one Philips make with very old Sun Solaris workstation, straight from 90s attached to it)?
    So I’m very frustrated

  • He does not think it would be good to have a section in which news will be sent in quarantine so as not to give false hope to patients. I mean news of this kind. I’m not saying what they are a lie, just alerting people that they can be sensationalists or just try to raise funds.
    News laike those.

  • masitinib phase 3 trial has shown significant positive effect in secondary and primary progressive MS. Is this the beginning of the end of MS?

    • Let’s see the effect and the side effect but sounds like we are moving in the right way. Masitinib inhibits the receptor tyrosine kinase c-Kit. It also inhibits the platelet derived growth factor receptor (PDGFR)…is this a good thing or is the rodent oligodendrocyte, lymphocyte-specific protein tyrosine kinase (Lck), focal adhesion kinase (FAK) and fibroblast growth factor receptor 3 (FGFR3)

      • Thanks MD for your reply. I’m sure they will release more at ACTRIMS. Given this a major breakthrough in neuro degenerative diseases. Can barts do a blog on this drug and the breakthrough it represents.

        • I have had a look at the press release. My enthusiasm is feeling broken I am sorry to say. The maufacturer says it works at 4.5mg/kg, but doesn’t work at 6.0mg/kg. I have to say my alarms bells are ringing.

          How are you going to sort out the dosing does 3mg/kg work better or les s, with such a bell shaped does reesponse curve it will be problematic and makes you wonder if the 4.5mg/kg dose was a fluke.Some people with MS will weigh 50kg overs 150kg so getting the right dose is going to be critical if this is correct. Why would more be less?

          • Yes. That stumped me. But given the press release is written by non scientific people. I think they meant to say at higher doses no significant improvement as observed althen lower dose. Which could make sense if the lower dose is enough to have full effect. Remember this has shown a postive effect in ALS and Asthma. Unless they’ve got the biogen spin data wagon to meet any endpoint. If so we are all doomed. Get ready for revolution in non effective treatments sold at exubrent prices.

          • OK I have had a read and done a post…..I must admit I don’t understand the logic/rational of what they are attempting to target, but probably it is an immune thing and their first trial was 3mg/kg and 6mg/kg. This trial centred on 4.5mg/kg with a dose escalation arm. What they are targeting in Asthma and ALS may well be different and that the agent is been spread widely in such disparate conditidions, suggest they have no real idea of how it works or why it works.

            That there is a signal in ALS is a promosing sign.

            I suspect the press release was written by someone saying to big pharma “come and buy me!”. A small company is not going to do the necessary studies unless they partner with a current MS player. Who has the lolly and the vision is key.

            Why did mastinib start life as a dog medicine, there has to be a story there.

  • Are there any inside news on bexarotene and the Cambridge group?

    The first results should had been released in late 2019 but I haven’t found anything.

    I guess that is not very good news…

    • It’s a bit of a theme re Cambridge. We’re still eagerly awaiting the publication of the results of the CAM-Thy trial 😉

      • Waiting so long when it arrived you must have missed it…It says the original idea was problematical because keratinocyte growth factor does not work in humans as occurs in monkey.

        Keratinocyte growth factor impairs human thymic recovery from lymphopenia.
        Coles AJ, Azzopardi L, Kousin-Ezewu O, Mullay HK, Thompson SA, Jarvis L, Davies J, Howlett S, Rainbow D, Babar J, Sadler TJ, Brown JWL, Needham E, May K, Georgieva ZG, Handel AE, Maio S, Deadman M, Rota I, Holländer G, Dawson S, Jayne D, Seggewiss-Bernhardt R, Douek DC, Isaacs JD, Jones JL.JCI Insight. 2019;5. pii: 125377

    • Silence is not a good thing when it comes to trials. It says it has not been plain sailing…if they (Cambridge) are right a you need to anti-age the macrophages then it says this study fails. We have to wait and see.

  • I had round 2 of lemtrada last month and not yet had my first bloods, as I work in a hospital I am not sure when it would’ve safe to return?

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