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MouseDoctor2

178 comments

  • With the expected release of license from the FDA to spinimod this year. Do you think it will be applied in MS RRMM along with an anti-inflammatory therapy to attack the two phases of the disease at the same time?

    • You need to wait for the label, i.e. will it be licensed for relapsing forms of MS or SPMS? The way the FDA licenses it will determine how it is promoted, used and reimbursed.

  • You mentioned previously that you are recruiting for the oratorio hand trial. Can you please provide more details on how I can apply to participate.

  • Would it be considered safe and feasible to move onto Natalizumab following failed treatment with Cladribine (further worsening and lesions on MRI)? Does the lymphocyte count have to reach a certain level ( .08 or higher?)to be considered safe enough to change?

    • There should be no problem someone moving from cladribine onto natalizumab even if there lymphocyte counts are not back to normal. Please note in JCV+ve patients that cladribine is classed as a previous immunosuppressive therapy, therefore, you couldn’t use the JCV index to assess PML risk.

  • Are uk allowed to run an EBV trial similar to the Australian one or do we just have to wait for the results from Australia? My chances of staying mobile are rapidly diminishing and I feel that I would greatly benefit from a trial involving EBV as this was unquestionably my MS trigger 50 years ago.

    • The CTL (cytotoxic T-cell) anti-EBV trial is being done in Australia and America by Atara Bio. We need to wait for the results. I assume if positive they may do a larger phase 3 trial and hopefully we will be included.

  • Hi, which DMD would you consider if you had RRMS (or active MS!?) and your lymphocyte count level is 0.06 at the moment?

    I am currently being tested to see if I qualify for Tysabri (JCV blood test- and strangely need to be flown to the Netherlands for their lab to confirm!) or would you consider Ocrevus which is relatively new but it has been noted that it has very little side effects and hugely more patient-friendly as you only need to worry about a few times a year!

    I would really appreciate any thoughts and I know you are unable to personally recommend but support, guidance, is all I ask!

      • Hi, I guess ‘time’ is such an issue with MS patients. Time to diagnosis, time to assess, time for tests & scans and then sadly the time it takes to see a Neurologist in the UK! We are desperately inpatient us patients and rightly so! The answers too to all our questions can be ‘time’ consuming and although we have a lot of faith in our MS community, the information they give you and the way they try to support you, again all is about ‘time!’ I would say, brushing you off as they deal with the barrage of workload set upon them (although I sympathise – I too work but would never speak to someone without respect & would always try to empathise). Anyhow, please see if there’s a way to communicate with MS patients to allow them to mutually decide what is the best that can be offered to-date in respect of DMDs and that it is correct with the latest findings, both positive and negative. God bless you all though, you are all amazing!

      • Hi Jane,

        I’ve heard other people mention blood is sometimes sent to a lab overseas for analysis, so may be it’s standard and routine.

  • Can we say Nataluzimab is now a viable option by using extended dosing intervals of 6-8 weeks for JC positive patients? It seems this great drug has lost favour to Ocrelizumab from many in the MS community but I feel O may be a bit oversold and until a different (better) dosing regimen is proven for better patient safety.

    • Yes, based on the Biogen data EID reduces your risk of PML by over 85%. I will do a post on why EID works; it is very interesting.

      Yes, I do think the MS community has adopted anti-CD20 therapy. I fear it is based on a NEDA-3 worldview and not an end-organ damage worldview of MS. I am worried that anti-CD20 therapies simply converts active MS into smouldering MS. The consequences of this hypothesis, if shown to be true has major implications for MS.

      To quote Professor Stephen Hauser from ECTRIMS 2017; anti-CD20 is not a panacea he mentioned that most of his patients on rituximab had developed SPMS after several years.

      I suspect we will need a B-cell therapy as a platform with add-on treatments on top to tackle the other pathologies driving worsening MS.

      • If Stephen Hauser has this data, then it should be published. Maybe time to stop paying lip service to pharma and time to put such information in the public domain so that people can make a better informed choice.

  • I was diagnosed in 2005, a few years after a relapse. Too late for the predisnone I then was given to have any impact. My leg remained effected and has slowly degenerated. I walk uncomfortably and with a limp. I was diagnosed as RR until I queried HSCT. I have also been having bladder issues for over a year and am waiting to see someone. I feel upset that there is nothing on offer on the NHS now I have been classified as SPMS. But with EDSS at 3-4ish (depends on who is assessing) I am keen to find out if there is anything that might help slow progression – even possibly on a private basis?

    • At Barts-MS we think MS is one, not 2 or 3 diseases. If pwMS have active disease we offer them treatments.

      Using old terminology of progressive MS it doesn’t just come on. The pathology that drives worsening MS is there from the beginning. In other words, almost everyone with MS has progressive MS. It all depends on how you define it.

      • Ok thank you. I think you are saying it is because I don’t have active MS that I have not been offered a treatment. I am not at Barts incidentally. Apart from at diagnosis I have only had 2 MRIs – last year and the year before, to discount HSCT.

        I am wondering this: if you can have progression while RR, would you say there is no strict RR/non-RR classification then?

        I am perplexed as to why my bladder is suddenly causing me issues if the MS is inactive.

  • How to switch from Ocrelizumab to Cladribine?

    … measure the bcells and start Caldribine when they’re back at the LLN? But this can last 2,5 years!
    ….or looking only for the number of CD27+ memory B cells?
    …or simply starting 6-12 months after the last Ocrevus infusion?

    What’s the BartMS “Switching Algorithm” for this clinical situations?

    • smpc for oral cladribine states total lymphocyte count needs to be at LLN at the start. Anything else is currently not established in clinical practice.

      • Thank you for your answer, DrK.

        But I wonder if the smpc recommendation makes sense: total lymphocyte count at or above LLN is the regular finding in Ocrevus treated patients…only 20% develop lymphopenia because B cell depletion has only minor impact on total lymphocyte count.

    • If I may, we need to wait for the results of the higher doses of the antibody, as only the 18mg/kg dose of the previous trial showed benefit and still seemed too low to work. The higher doses might prove that temelimab is sufficient at all NEDA metrics (so not just complementary). The higher doses had no adverse effects.

  • #ACTRIMS

    RRMS Conversion to SPMS Is Preceded by Spinal Cord Atrophy

    The rate of spinal cord tissue loss is a strong indicator of conversion from relapsing-remitting multiple sclerosis (RRMS) to secondary progressive MS (SPMS), according to a finding presented at the fourth annual Americas Committee for Treatment and Research in Multiple Sclerosis (ACTRIMS) Forum 2019.

    Importantly, Bischof noted that this difference in rate of spinal cord atrophy could be detected up to four years before conversion to SPMS.

    Furthermore, according to Bischof, relapse rate, disease duration, the presence of new or enlarging lesions, and the use of disease-modifying therapies also did not discriminate RRMS patients who converted to SPMS from those who did not convert.

    Overall, according to the team, the annual rate of cervical cord tissue loss is “the strongest indicator among currently available imaging markers” of conversion from RRMS to SPMS.
    https://actrims.confex.com/actrims/2019/meetingapp.cgi/Paper/4177

    • Yes, but this is based on an EDSS (mobility) worldview. If you look at grey matter atrophy and cognition you would draw the same conclusions. Interestingly cognitive impairment usually develops first and is one of the reasons why MS causes early unemployment in MS.

  • ***Escalation Approaches to Multiple Sclerosis Fail to Prevent Unfavorable Long-Term Outcomes

    In a cohort study of 592 patients with MS, the findings were suggestive that real-world escalation approaches may be inadequate to prevent unfavorable long-term outcomes.

    Although after Harding and colleagues adjusted for the relevant covariates, there was no significant difference in the hazard of sustained accumulation of disability between groups, in total, 60% of those who escalated to a high-efficacy DMT were observed to develop sustained accumulation of disability prior to the switch, while they were still receiving their initial, moderate-efficacy treatment. Of the 488 patients who began on a moderate-efficacy treatment, 11.9% (n = 58) went on to receive a high-efficacy DMT.

    The switch to high-efficacy treatment was most often prompted by clinical disease activity (n = 52), while the almost all of the remaining cases were due to subclinical evidence of disease activity (n = 5) and a single case was prompted by clinician decision without evidence of clinically or radiologically measured disease activity during the year prior to escalation.

    “In a real-life setting, long-term outcomes were more favorable following early intensive therapy [versus] first-line moderate-efficacy DMT,” Harding et al. detailed. “Contemporary surveillance strategies and escalation protocols may be insufficiently responsive. This finding is particularly relevant as patients in real-world practice are typically selected for an EIT (early intensive therapy) approach to therapy on the basis of clinical and radiological features predictive of a poor outcome.”

    For adverse events (AEs), of those receiving alemtuzumab (n = 100), 87% developed infusion-related AEs and 47% developed autoimmunity (35 thyroid, 3 immune thrombocytopenic purpura, and 13 other), but no serious infections or treatment-related deaths occurred.

    “We found that although patients were selected to receive EIT on the basis of poor prognostic factors including more active disease, it was this patient group that had better long-term outcomes,” they concluded. (!!)

    https://www.neurologylive.com/clinical-focus/escalation-approaches-multiple-sclerosis-fail-prevent-unfavorable-longterm-outcomes

  • Dear Barts Team,
    I am currently looking into High Doses Biotin. We have spotted in the latest study research results the following remark (see: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5098693/)

    ” … More new or enlarging MRI lesions occurred in the MD1003 arm than in the placebo arm during the double-blind phase. Future trials should include careful assessment of MRI activity to rule out an unwanted pro-inflammatory effect of biotin. There are no published data on animal models concerning a potential pro-inflammatory effect of high-dose biotin. …”

    This is quite puzzling and also a scary remark. Is this a serious risk? Or do we just see the normal inflammatory activity of MS. It is probably the case that statistical data is insufficient. But maybe you could comment on this issue.

    Would taking Ocrevus in addition to High Doses Biotin ease this problem?

    Kind regards,
    Alexander Mass

    • We have discussed this before on the blog. It could be a chance finding (type 1 error) and needs to be looked into in the next trial. Science is about confirming observations. I can’t think of a biological reason to explain why biotin may trigger activity.

  • referring to the UK, please can you make a guess about the proportion of female to male neurologists, those with a specialist interest in MS?

    Thank you.

  • 1) Are bilateral priventricular white matter lesions that are not similar to Dawson’s fingers related to MS?

    2) Is a 4-min blurry vision a symptom of MS?

    Thank you very much in advance.

  • Hi Prof. G,

    1) Are bilateral priventricular white matter lesions that are not similar to Dawson’s fingers related to MS?

    2) Is a 4-min blurry vision a symptom of MS?

    Thank you very much in advance.

    • The diagnosis of MS is not an MRI diagnosis, but clinical. The MRI has to be interpreted with caution. Visual symptoms in MS tend to be longer in duration than just 4 minutes.

  • Is it standard practice in the UK to be told by an MS nurse look at the MS Decisions webpage and decide which DMD you want?
    How would a person reeling from being told they have MS be in any position what so ever to make an informed choice?
    Would people with other illnesses be given a choice of 10 medications or however many there are for MS for something else medically wrong with them… the onus should be on the doctor what would be the right thing to prescribe surely?

    • Really interesting take. I am inclined to agree and have been doing some digging around and casting my net a bit to try and understand the rationale behind this approach.

      I am putting a post together regarding this in between job hunting and managing fatigue.

      Watch this space.

    • Ali that’s worse than my first ever meeting with an MS nurse who, despite my telling her the neuro had mentioned Tecfidera, spent the whole hour showing me the various injectable DMTs and demonstrated on herself how I should expect to inject correctly.
      As you say when reeling from the diagnosis, you require sometime given to engaging with you as a person and a gentle introduction to this new world you’ve suddenly found yourself in!
      I found that checking out the NHS and British Neurologist Assoc guidelines and eligibility on treatment is a good place to start as this will inform you of the DMTs available dependent on your diagnosis. As you’ll find from this brilliant site, there maybe the need to seek to avoid the application of the escalation model.
      Though primarily aimed at the US viewer, some of Aaron Boster vids on YouTube are really helpful for providing accessible info on various DMTs.
      Best wishes obtaining the treatment best suited to your needs.

  • Hello Prof G
    I was diagnosed with MS 2 years ago at the age of 52.
    I have been reading and researching ever since and feel that in the MS world, there is (quite rightly) a focus on those who are diagnosed in their 20s and 30s and that us older PwMS are largely forgotten about.
    I feel my own neuro has already written me off and doesn’t want to engage in any discussion around long term planning on how best to deal with my MS.
    I feel I have a lot of living still to do and I don’t want to just sit back and let MS take over my life. I’d like to switch neuro but I’m not sure how to go about finding the right one.
    Anyway, what’s your view on how people diagnosed with MS in their 50s should approach their disease? What advice do you give your patients?

    • Interesting video from Aaron Boster about switching neurologist. A tricky topic that he approaches very well – IMHO.

      PS: Am 50, had it 26y, and I feel that there is as much, if not more, responsibility with me the patient to ensure that I am getting the correct blend of what I want and what the neuro thinks I need. I rely on them to stop me from harming myself in my push to get the best available treatment.

    • The evidence is not there to support it, but the trials of hyperbaric oxygen therapy were done in an era when we didn’t know how to power and do definitive trials. More recent animal work would suggest we need to rekindle oxygen therapy.

  • Prof G: “I can’t think of a biological reason to explain why biotin may trigger activity.”

    What gives me pause here is that, when biotin was first being looked into, it wasn’t apparent why biotin would do anything at all for MS.

    I believe biotin, at much lower doses, taken by those hoping for stronger hair and nails, can cause acne and rashes. So entirely innocuous it is not.

  • If a young (20’s) patient with very early PPMS (EDSS 1) with no inthratecal IgM synthesis at baseline starts on a high efficacy therapy such as Ocrelizumab; and having achieved NEPAD on the first year; would ie be realistic to expect no further disease progression in the near future?

    Can you further explain the slide from the Ocrevus launch in Egypt, in which a 76% reduction in reaching EDSS 7 is proposed for patients with PPMS and EDSS <6?

  • Alemtuzumab is a very potent PIRT, but her long term effect might be lasted when the proinflammatory cells comes back, so the disease return and patients need retreatment. (Cambridge trial 10 years follow up.)
    Could Alemtuzumab be a “cure” (in relation the disease caused inflammation) or not?
    How can we measure the sign of disease related inflammation the best? (When the disease returns half a year means 0.25-0.65 bvl loss)
    The neurofilent level of the blood coupd be good?

  • So really, what you are saying is when to achieve the best outcome for a patient requires 3rd gen, high dose IV atibiotics it is fine to sanction and prescribe oral 250mg amoxicillin because the patient prefers it and they are clinically proven to better than nothing?

  • I keep thinking about Gadolinium Deposition Disease even though I have normal kidney function. I was on CombiRx Study starting at diagnosis in 2007. About 9 or so MRI with Gad in about 7 years.
    Since they’ve discovered Gad in Mollusks in an estuary in France downstream from a Hospital, it is certainly possible I have retained Gad in my body. My neurologists have been appropriately skeptical. I however, suffer every day with severe pain and skin issues I suspect might be GDD. I don’t expect you to agree but please consider the possibility. Especially when multiple scans are done in a short period of time. I believe the Gadolinium is accumulating at Scarred places like old healed skin lacerations. Food for thought.

  • I have an “SEL” on my spine, which has made my right leg over the years, practically useless. I was diagnosed with MS in 1999, am a patient of the Prof, and have been on Tysabri since 2010. Are you aware of any restorative drug trials which maybe in the pipeline, which would restore function ?

  • PML risk on Natalizumab:
    Can you give a summary of percent risk for PML on Natalizumab, given JC status (positive vs negative), and dosing schedule (monthly vs extended interval).

  • Any recent studies done on fampridine long term use? Does it speed up progession and is it as effective for long term as it is after the initial trial period.

  • Is it known if there are demographic similarities in patients that develop PML on Natalizumab such as gender, age, weight (BMI), etc? I haven’t been able to locate any of this information so I’m assuming it is kept deep in the vault at Biogen but it would seem like a further means of reducing the risk further than EID.

  • If a person has PPMS and was managing to work until 12 months ago but has since deteriorated so that now they can only move around the house by holding onto furniture and need a wheelchair for outside. and their MRI shows no signs of disease activity. What would you propose they do to stop themselves from getting worse? If they could find the money should they pay for HSCT or pay Ocrelizumab? Or do you have any other ideas?

  • Alemtuzumab ACTRIMS CARE-MS II Data

    DALLAS — Alemtuzumab (Lemtrada) continued to show benefits in clinical outcomes, lesion load, and brain volume loss in relapsing-remitting multiple sclerosis (MS) for 8 years, an extension study of patients from the CARE-MS II trial found.

    At year 8, 70% had improved or stable disability scores compared with baseline. Over years 2 through 8, 66% to 76% of patients were free of MRI disease activity each year. The median cumulative brain volume loss over 8 years was -1.06%, with brain volume loss -0.19% or less annually in years 3-8.

    “We’re seeing very low rates of brain volume loss,” Singer told MedPage Today. “Patients are preserving brain tissue.”

    Of 435 alemtuzumab-treated patients in CARE-MS II, 300 (69%) completed 8-year total follow-up. In total, 44% of CARE-MS II patients received neither additional courses of alemtuzumab nor another disease-modifying treatment through year 8. About half (51%) of CARE-MS II patients who entered the extension received one or more courses of alemtuzumab over 8 years, with 29% receiving just one additional course.

    “When people require a repeat dose, the data supports that they fare very well,” Boster told MedPage Today.
    “the safety profile was consistent through year 8 and there were no new signals,” Singer said.

    The incidence of adverse events was reduced in years 3-8 compared with the core CARE-MS study (years 1 and 2). No immune thrombocytopenia events occurred after the 48-month monitoring period from the last alemtuzumab dose. The incidence of infections declined from years 4 through 8, and the incidence of serious infections was 3.3% per year or less through 8 years.

    https://www.medpagetoday.com/meetingcoverage/actrims/78328?utm_source=dlvr.it&utm_medium=facebook

    • Sounds like good news, I would be much happier if they did not do the fundge of saying 65-75% did not have lesions each year they should tell us the proportion of people lesion free 25% with lesions each year means that every one could have had lesions. It suggests they are hiding something and we have caught them doing this in the past

  • (MD will get nuts :P)

    Evobrutinib, Merck KGaA’s oral candidate for relapsing multiple sclerosis (MS), is safe and can significantly reduce active brain lesions over 24 weeks of treatment, results of ongoing Phase 2 study show.

    Results showed that the mean number of active brain lesions (referred to as T1 lesions on MRI) measured from week 12 to 24 in patients taking evobrutinib dropped as the dose increased – 4.06 (low dose), 1.69 (mid dose), and 1.15 (high dose) — compared to those on placebo (mean number, 3.85). (The mean number seen in the Tecfidera group was of 4.78, but a treatment comparison is not the trial’s objective.)

    Researchers also saw a significant trend for a reduced annualized relapse rate (mean relapse rate per year) with evobrutinib at 75 mg taken once or twice a day, with a better response at the higher dose — 0.13 in the 75 mg once daily group, 0.08 with 75 mg twice a day, and 0.37 in the placebo group. (The Tecfidera group had an annualized relapse rate of 0.20).

    Treatment-related adverse events were similar between the low- and mid-dose evobrutinib groups and placebo, but higher for evobrutinib 75 mg given twice a day.
    The most common was an increase in the levels of liver enzymes, indicating possible injury to the liver. All adverse events were reversible and asymptomatic, the team reported.
    Evobrutinib was seen to be well-tolerated, without any cases of serious infections.

    https://multiplesclerosisnewstoday.com/2019/03/04/actrims2019-evobrutinib-significantly-reduces-brain-lesions-in-relapsing-ms-phase-2-trial-shows/?utm_content=bufferf0f2b&utm_medium=organic+social&utm_source=facebook.com&utm_campaign=buffer&fbclid=IwAR06gzXG39elCoOq3gpsIMXPPJy8rHU-zAmoLrgaZaG0h6QRGDbQXE6enXE

    https://actrims.confex.com/actrims/2019/meetingapp.cgi/Paper/3602

    • Thanks this was reported at ECTRIIMS 2018 and further supports the importance of B cells in relapsing MS as this is not a T cell kinase.

      http://biogps.org/#goto=genereport&id=695

      This agent works in EAE when anti-CD20 did not. This again shows us that CD20 B cells have a minor…i.e. no important role to play in EAE, which is T cell mediated. Further indicating that some EAEers are looking too hard for positive data…..Yep there are some prominent labs, where I now no longer pay any attention to what they do, as they can’t interpret their way out of a paper bag let alone understand their own data and the chance of them reporting something real is unlikely. However the kinase is found in macrophages and monocytes and thus target something new and maybe this accounts for the action in EAE. However Even though Brutons tyrosine kinase is expressed in the myeloid cell lineage, mutations in the BTK gene lead to prominent B cell—specific defects in mice and humans, hence it has been considered as a target for the selective inhibition of B cells

      We tried to get our hands on one of the first generation bruton tyrosine kinase inhibitors quite a few years ago, but unfortunately one of the companies involved was not interested in MS.

      Whilst this shows up one of the less effective MS drugs…on first glance I am not dancing for joy quite yet and the effect may have been better the MRI lesions drop from 3.85 to 1.15 so about a 70% depletion which is beta interferon terretory not 90% as found with anti CD20. It is said not to be a cell depleter so you have got it for ever. Maybe we can do better

  • A question for all you neurologists who contribute to this blog. If you personally had MS, which DMT would you choose at the outset of your therapy, in light of current research/science/experience treating your own patients?

        • Interesting to know why you’d choose it over Ocrelizumab.

          I was steered onto Ocrelizumab over Alemtuzumab, and the reason cited by the London neurologist was that they felt the risk to my kidney function was too great.

          Thank you.

        • A related question – is there an age at which you’d change your decision (due to possible reduced efficacy with ageing) – e.g. if making a decision in your forties?

        • Any answer to a question beginning “If you had MS what would you…” is going to be pure, largely useless conjecture. Decisions on treatments must depend on so many things. Medical conditions, age, physical constitution, attitude to risk to name but a few.

          And actually having MS is always going to be different to imagining having it, although I understand you are as well informed as anyone could possibly be.

      • Uauuuu

        “A large number of the HSCT zealots seem to ignore the fact that HSCT does not result in a cure in many pwMS treated with HSCT and that there is an issue of HSCT-related mortality. The latter is often conveniently ignored”

        https://multiple-sclerosis-research.org/2018/01/is-hsct-for-everyone-or-not/

        Aparently for YOU it is

        “So would I refer pwMS for HSCT? No, not as part of routine clinical practice

        “you need to ask yourself the question what if I am the unlucky one? Am I am ready to leave my family and loved ones prematurely?

        Aparently YOU are

        https://multiple-sclerosis-research.org/2016/02/clinicspeak-reflections-on-hsct-after-the-fallout-of-the-bbc-panorama-programme/

        “At the end of the day adoption of any treatment is a slow process and is data driven. The data has to be good quality. The reality at the moment is the quality of HSCT data as a broad treatment for MS is simply not good enough, in particular its relative efficacy and risk-benefit profile relative to other DMTs,”

        Gavin GiovannoniWednesday, September 06, 2017 8:38:00 am

    • Hi, I’m extremely interested in replies in respect of ‘what would do’ if you were me! We all know every drug carries risks and can not be suitable too. But if you were in our MS shoes ‘what would you do?’

      Also, a fellow MS friend after 20 years of being on DMD has been informed by their Neuro that they now have secondary progressive MS and as this person is in their 50s there has been very little support and monitoring (I convinced them to organise an MRI with Neuro as they hadn’t had one for years) – They feel devastated and let down that it might have been avoided, had they been looked after more. Is this normal practice and surely if this person had been monitored, spoken to and regularly checked that they could have changed drug and avoided the disease progressing? They also felt that their age seemed to be a problem and they didn’t receive more support, because of it!

  • I was recently prescribed a course of oseltamivir (tamiflu) after a positive test for H1N1 flu
    For some days after taking the tamiflu, I felt much more energised . It was easier and faster to get out in the morning and go for a walk/run. And this despite the fact that I was recovering from a long flu. Usually it takes me really long just to get started in the morning

    Could there be a link? Has Tamiflu ever been studied in the MS context?

  • 2 questions

    Has anyone got an update on Ocrelizumab being approved for progressive ms?

    For people with worsening MS after 2 courses of alemtuzumab are you preferring a third course or a change to a ocrelizumab?

    • Once you are treated with alemtuzumab you can’t be treated with ocrelizumab under the NHS. NHS England does not allow it on the bluteq system. We are appealing this decision. The cost-effectiveness timeline that NICE used for alemtuzumab was 20 years, which is ridiculous. NHSE thinks that frontloading costs with 2 or 3 courses of alemtuzumab will last 20 years. Really? Another factor that was not taken into account was NABs. This as it flies in the face of common sense and the science so we hope NHSE will relent. But at the end of the day, it is all about cost-effectiveness.

      • Hi thanks for the reply

        Is this rule about not being able to be treated with ocrelizumab after alemtuzumab fairly recent as I saw my neurologist who did not mention that?

        There seems to be a reticence in prescribing a third course of alemtuzumab with the excuse that the first two have not worked but surely that is why you have a third?

  • In a Feb 2018 article on the blog entitled ‘DOES YOUR AGE PREDICT HOW WELL YOU RESPOND TO DMTS?’, there was a lively discussion about what the referenced study did or did not show about decreasing DMT benefits with age. Prof G commented that ‘This is meta-analysis of phase 3 trials and does not include long-term follow-up. I have emailed the MS-Base team to get them to look into this question from their real-life data set. The MS-Base data will capture therapeutic lag.’ What were the results of this as I don’t think results were ever added in the comments of that particular post?

  • What about this new study which suggests chocolate, particularly hot chocolate might improve MS fatigue? It mentions flavonoids as the key but might it be that cocoa contains caffeine which is well known for keeping you awake?

    • Done at Oxford Brookes University. Smallish trial. It was all about the cocoa content, no mention of caffeine when I signed the consent forms – for I was one of the twelve that took part. This was c 3y ago.

      It goes to show how the press doesn’t like the detail to get in the way of a good headline.

      http://bfy.tw/MdPb

      Best result being https://goo.gl/hjJU7c

  • A question for MouseDoctor: wondering your thoughts these days on Alemtuzumab and the problematic issue of NABs? (Remember reading your previous lengthy posts on this ‘hidden’ problem).

  • Do the NHS/NICE protocols cover changing from Ocrelizumab to Alemtuzumab?

    If this is possible, please can you describe the processes involved regarding timings, tests and anything else that you feel is important to know?

    Furthermore, how do you think the approach to one’s neurologist wrt this can be made?

    I ask this after reading Dr G’s remarks that he’d take A or HSCT as the most efficacious treatments for RRMS.

    Whilst I still fall in this category, am treated with O, likely to be ineligible for HSCT, (don’t have a spare 80k knocking about to go to London Bridge) it seems that this is likely to provide me the best chances I have when looking to the future.

    Thank you.

      • I see that rituximab treatment is an exclusion criterion for hsct trials in Norway, so I guess anti-CD20 medication (ocrelizumab, rituximab and ofatumuma) may be incompatible or unwise if you are considering hsct. Regretfully no one here at home whants to elucidate this. Maybe ocrelizumab and rituximab are not a clever treatment choices if you may opt for hsct later???

        • Anders Svenningsson thinks that HSCT is not excluded for people that have been treated with Rituximab, but it is extremely rare that it will be needed in that case.

  • Would be interested to know if anyone has read the book ‘Recovering from multiple sclerosis’ by George Jelinek and Karen Law? Please would you be kind enough to share your thoughts? I was seriously considering treatment with Alemtuzumab but have serious doubts now having just read the book and don’t know whether to take the risks of such a potent DMT. Has anyone met the authors or had any positive/negative experiences after ceasing treatments for MS altogether? Thankyou.

  • Trial of AB Science’s Progressive MS Therapy Masitinib to Continue Without Additional Patient Requirement

    Masitinib is an oral therapy that inhibits enzymes called tyrosine kinases. They play an important role in cell growth, differentiation into other cells, energy conversion and death. The drug targets immune system components known as mast cells and macrophages.
    Masitinib’s unique mechanism of action makes it a possible treatment for cancer and inflammatory diseases as well as central nervous system disorders.
    AB Science is also conducting Phase 3 trials of masitinib as a treatment for metastatic prostate cancer, metastatic pancreatic cancer, severe asthma, ALS, and Alzheimer’s.
    Final results of the study are expected in the second quarter of 2019.

    https://multiplesclerosisnewstoday.com/2018/01/08/board-allows-ab-science-to-continue-phase-3-progressive-ms-trial-without-more-patients/?fbclid=IwAR13jBy-DmLJ9OpDubfLAly8QgAJErul7T8JQWVg8vgnZsxGVWVuZCB4sXA

    • Trials are mentioned on MS Society UK and Ms Trust websites

      Prof g if this treatment got approved would it be an add-on treatment to existing treatments?

  • CSF biomarker clusters correlate with MS severity

    Patients with multiple sclerosis (MS) have elevated levels of specific clusters of cerebrospinal fluid (CSF) biomarkers related to astrocytes and microglia that correlated with disease severity in a blinded analysis of more than 1,000 proteins from the CSF of more than 400 patients with neuroimmunologic disease and healthy volunteers.

    https://www.mdedge.com/neurology/article/195455/multiple-sclerosis/csf-biomarker-clusters-correlate-ms-severity?fbclid=IwAR1Xy6oJJ0ozJ8nXn8gZCZ8l1cfY4111aEF8Yq1ZlS9n8aDX7O5M4GJYXoE

    Axonal damage in spinal cord is associated with gray matter atrophy in sensorimotor cortex in experimental autoimmune encephalomyelitis.

    https://www.ncbi.nlm.nih.gov/pubmed/30843756?utm_source=dlvr.it&utm_medium=facebook

  • Is there much clinical experience of moving a patient from Ocrelizumab to Alemtuzumab?

    Where would you suggest that one looks for guidance on this?

  • I’d be grateful for an an answer to this question.

    Is loperamide, aka Immodium, safe for people with MS, considering people with MS may have a leaky blood-brain barrier?

      • Read some of profGs post as you can have leakage around a constipated bowel. So a laxative would be of value in tjis circumstance

        • My concern is – is loperamide not neurotoxic if it accesses the CNS? So a leaky BBB would make this medication unsafe?

          • Immodium is a low opioid drug, safe for use under prescription. Opioids cross the BBB anyway. In very high amounts (not the prescription amounts) it can be toxic to the heart.

  • Does Cladribine affect sperm count?

    The neurologist this morning informed me that new info about Mavenclad has just recently been found that with men wanting to have children in future are urged to have sperm frozen as it affects sperm counts.

    • As part of our due diligence DrK has offered this as he has taken a safety first approach As cladribine can get into DNA you have to take contraception for 6 months after last dose. There is some data in animals of altered testis effects however cladribine has different affects in animals. Deoxycytidine kinease (killing mechanism) expression is very low in sperm suggesting that it should be affected as much. This is coupled with a potentially high level of NT51B which could counteract.cladribine. This needs to be formally shown.

      Did you know that sperm express CD52 but alemtuzumab is not reported to shrink the you know whats

  • I’m a student with MS looking to study for a degree in the UK. It was dawned on me that SENCO’s (Special Educational Needs Co-ordinator) of the further education colleges that I’ve come into contact with have very limited knowledge of MS and how MS can impact on reading, writing and studying in general.

    How can we raise knowledge of MS among SENCO’s?

    • Having just finished 6y at University in the UK I found quite the opposite. SENSO is a term usually used in compulsory schooling. My wife is a school teacher and they have several SEN teachers there.

      In university, it is usually referred to as something like the Disability Service. Not only a central function but also each faculty had designated coordinators. They liaised with the central function.

      It depends on what university you are applying for I suppose. What have you discovered by going on their individual sites to read about how they manage it?

      • Hi and thanks, I have a SENCO currently as I am at a further education college not university. I know the SENCO’s need to be qualified teachers.

        I’ve also got two degrees (an undergraduate and a masters) from UK universities already but having to go back to college to get something for the third degree.

        May be I’m greedy going for the third degree but hey….

        • Not at all greedy! I go pre-armed with information. Have given up on the idea of educating all and sundry that I meet. I just ask them for what I need. I find they are generally quite compliant as I am not asking for something I am not entitled to.

          It is such a time-consuming bore to agonise over the paucity of knowledge in some people that ought to know better.

          Good luck. What are you reading this time?

  • Leptomeningeal Contrast Enhancement Is Related to Focal Cortical Thinning in Relapsing-Remitting Multiple Sclerosis: A Cross-Sectional MRI Study.

    CONCLUSIONS:Focal leptomeningeal contrast enhancement is associated with reduced thickness of the surrounding cortex in patients with relapsing-remitting MS, but not in those with secondary-progressive MS. Our results suggest that pathology associated with the presence of leptomeningeal contrast-enhancement foci has a stronger, localized effect on cortical tissue loss earlier in the disease.

    https://www.ncbi.nlm.nih.gov/pubmed/30872420?utm_source=dlvr.it&utm_medium=facebook

  • Structure-based design of small-molecule inhibitors of EBNA1 DNA binding blocks Epstein-Barr virus latent infection and tumor growth

    These inhibitors selectively block EBV gene transcription and alter the cellular transforming growth factor–β (TGF-β) signaling pathway in NPC tumor xenografts. These EBNA1-specific inhibitors show favorable pharmacological properties and have the potential to be further developed for the treatment of EBV-associated malignancies.
    http://stm.sciencemag.org/content/11/482/eaau5612

  • Interesting (it’s all about B cells)

    New rat model recapitulates disabling grey matter damage in multiple sclerosis

    Introduction of the β-synuclein-reactive T cells into wild-type rats caused severe neurological disease that differed from traditional EAE. Symptoms included paralysis, stereotypical scratching movements and ataxia.“This came as a surprise because most neuronal antigens tested beforehand had induced only very weak disease signs, if any,” explains Francesca Odoardi, the co-senior author of the study. “The biggest surprise, however, came when we analysed the animals histologically. Almost exclusively, the CNS grey matter was inflamed, in particular the brain cortex.”To confirm that the effects of the T cells were indeed mediated by their reactivity against β-synuclein, the researchers also made a T cell-receptor transgenic rat in which >95% of T cells were reactive against β-synuclein. T cells from these rats caused extensive grey matter lesions, and more than 80% of the transgenic rats developed disease

    To assess the relevance of the animal experiments to humans, Flügel and colleagues also examined reactivity of T cells to β-synuclein in healthy people and individuals with MS. Reactive T cells were observed in both groups, but their levels were higher in people with MS. Interestingly, levels of β-synuclein-reactive T cells were particularly high in people with chronic progressive MS.

    https://www.nature.com/articles/s41582-019-0168-2

    • Introduction of the β-synuclein-reactive T cells into wild-type rats caused severe neurological disease that differed from traditional EAE. Symptoms included paralysis, stereotypical scratching movements and ataxia.“

      So, they have developed an autoimmune model of Parkinson’s disease, not MS.

      • ” levels of β-synuclein-reactive T cells were particularly high in people with chronic progressive MS.”

        Progressive MS patients have Parkinsons after all?

  • Any pwMS addicted to prescription painkillers? That would be interesting MS research.

    ‘From April 2019, the government has announced that pregabalin will be reclassified as a Class C controlled drug under the Misuse of Drugs Act 1971 and be placed in Schedule 3 to the Misuse of Drugs Regulations 2001. This follows concerns over the drug being misused.

    Doctors will only be able to provide 30 days’ supply of pregabalin on one prescription
    (MS Trust website)

    • Both pregabalin and gabapentin will become Class C controlled drug on the 1st April 2019.
      Any pwMS stockpiling these?

      The law change will mean the drugs are still available for legitimate use on prescription, but there will be stronger controls in place to ensure accountability and minimise the chances of pregabalin and gabapentin falling into the wrong hands or being stockpiled by patients. (gov.uk)

  • I see NurOwn are signing people up with progressive MS to MSC stem cell treatment trials. The stem cells are taken from bone marrow and put back into the CSF. Is the aim of this to treat the disease, or repair axons or prevent further axonal damage or regenerate myelin. What do the team at Bart’s think of this treatment.

  • Rumour has it you are using Mavenclad instead of generic cladribine for the Chariot-MS trial. Is this correct? Isn’t this against the underlying principles of why you are doing this study in the first place?

    • It is not a rumour it is the current plan.

      Maybe DrK will comment.

      The aim is to give people in wheelchairs an option.

      To do that we have to get a funded trial…having a donation of product and support for the study means it is more likely to occur.

      A tablet means three to four less hospital visits per dosing round and so significantly reduces logistical issues and several thousand taxi fares. This reduces the cost.

      It may be of interest but the trial was given a ceiling cost and significant cost savings were required.

      As such unbelievably DrK had to remove imaging from the main study. It was considered by the funders to be expendable and.non essential

      By the time the trial finishes oral cladribine should be out of patent, therefore their will be sources available for the drug and so would help uptake for the project.

    • Yes, and no! Again the reasoning behind the use of cladribine is complex and has to do with CNS penetration. Saying that rituximab is our most favoured DMT for our SALVAGE trial.

    • Would Roche supply the drug for free. Probably not… so for every hundred people in trial that would be a million quid. So the maximum budget has been exceeded before you do anything.

      Next up would Roche give us drug…they are funding study oratorio hand with ProfG being a PI. If successful they will be seeking market.rate.

      Meither ocrelizumab or rituximab proably get in the CNS mavenclad does

      Continued b cell depletion gives a safety risk for infections such as uti urti lung

  • COMBAT-MS on RTX – Patients questions

    How efficient is the treatment?

    3A. Is there any statistic on the frequency of reduced number of relapses at clinics using Rituxan?
    Anders Svenningsson:
    There is a lot of data from Swedish MS centres showing that the relapse frequency is extremely low for patients treated with rituximab. We have published that in a couple of studies already, but presently running a controlled trial with relapses as endpoint. In all, it is far below 1 relapse per every 10 years on average which is as good as any of the highly active treatments on the market. Only autologous stem cell transplantation beats it regarding efficacy, in my opinion.

    3B. Can one after some years of treatment with Rituxian have a slowdown of MS disease (that is what my doctor is telling me)?
    Anders Svenningsson:
    If you mean with slowdown that the disease activity is turning less active permanently it is probably true, but still too early to say if it has “stopped” to be active. With time the disease becomes less active by itself to be almost completely inactive by the age of 55-60. So these two mechanisms might work in concert to reduce risk for further relapses over time.

    3C. Is it right to give Rituxan to patient when the disease is not so active anymore?
    Anders Svenningsson:
    I would say it is a matter of age. Around 55-60 (maybe youger!) the combination of a prolonged treatment effect and natural cessation of disease activity makes treatment of very low value, but you still retain the risks. So I would say as a rule of thumb that if you are over 50 and have had a not so active disease anytime it might be worth trying discontinuing all therapies. Of course keep yearly MRI controls.

    3E. Does Rituxan have a better effect than Tysabri (natlizumab)?
    Anders Svenningsson:
    I would from clinical experience say “no”. Tysabri is exceedingly effective that is hard to beat, but I think rituximab is equally effective. I wanted to do a comparative study between the two drugs some years ago, but realized that we should never get a “winner”. So, the difference between the two drugs does not lie within efficacy but rather convenience (1 infusion per moth vs 1 infusion per 6 or 12 months) and safety (primarily the risk of PML and herpes infections for Tysabri vs probably slightly higher risk of other infections for Rituximab). It is up to the discussion between the doctor and the patient to decide which “profile” fits the best in each individual case.

    4. What dose interval should be used and why?

    4A. After three years on the drug and if the disease is stable you shift to 1 time per year, at least this is how they do it at Danderyd hospital, right?
    Anders Svenningsson: Yes, that is the normal procedure we use and it is as well used regularly in Umeå where I started to use this treatment in 2008.

    4B. Do all hospitals follow these treatment regimens?
    Anders Svenningsson:
    I am not sure if all do, but this protocol becomes more and more common since we do not see a clear tendency of recurrence of the disease from doing so and we surely increase safety by it. To get the “final” answer to this question, we are now in Sweden running a large trial (RIDOSE-MS) where we randomize between treatment every 6 and treatment every 12 months after initial 1 – 3 years of treatment every 6 month. It is a long trial of totally 4 years (thus end by year 2023), but it will eventually tell us very well which regimen is giving the best benefit vs risk ratio.

    4C. For how long do one stay on once a year infusions (my neurologist does not give me any clear answers)?
    Anders Svenningsson: I understand he or she doesn’t because none of us know that for sure yet. It might be a decision made of several parameters where our age definitely is one of those. The key question we do not have the answer to yet is whether the repeatedly depleted memory B cells eventually have “lost their memory” for the disease and thus you could say if you would be immunologically “cured”. Even that might be individual, so we really would need a specific way to measure the individual response to whatever autoantigen that is most relevant in order to safely quit treatment permanently. In a practical sense, one could use different algorithms out of which this one is quite practical (completely pragmatic from my own practice): After 3 years (this might be possible to shorten by the way) 6 monthly interval, increase the interval by 6 months every other infusion. Ex, after the 7:th infusion (3-year time-point), go on with intervals of 12, 12, 18, 18, 24, 24 months and so on. If you have had no recurrence of the disease by 50-55 years of age you could probably quit permanently. Remember, this is my practical approach that is not tested scientifically, but builds on real-world experience on using the drug for over 10 years. It might be modified in the future.

    4D. If you stop Rituximab treatment, will you be without disease modifying treatment then? And if so, are there any studies supporting this? How is it going to be monitored?
    Anders Svenningsson: Please see my answers above, which basically deal with this question. Formal studies have yet not been performed regarding stopping treatment. Being “without” treatment could be a good thing to be if you do not need treatment and possibly repeated treatments with rituximab will make your disease milder so you don’t need treatment any longer (OBS! Hypothesis!). If you are above 50 years of age the need for treatment is going down rapidly and in this category of individuals I cannot remember any recurrence of disease activity when we have stopped treatment. It is important that you are followed continuously with yearly MRI scans, however, since we never know for sure in the individual case.

    4E. Do they take into account individual variations when they prolong the intervals?
    Anders Svenningsson: Yes, we do. Someone with initially low disease activity and small number of brain lesions could be increasing intervals earlier.

    4F. I want to know why some doctors say that the treatment is for three years and other says that there is no limit for how long you can be treated.
    Anders Svenningsson:
    Do not know what they mean when saying that it is a “3-year treatment” and that’s it. Possibly if you are above 50 years of age it would make sense to me. Otherwise I would advocate an individual approach on that issue, but in any case taper off the treatment somewhere between 50 and 60 years of age, no longer than that is needed.

    4G. Why do doctors have different protocols?
    Anders Svenningsson: I think that is because the treatment has not been licensed for MS by a company, which otherwise prescribe specific protocols in the product label. But it is not at all unique that treatment schedules are individualized in medicine and in many ways that is ideal. You never have “one-dose-for-everybody” when it comes to hypertension or diabetes therapy. We need to be better in measuring disease activity in real time in MS to do that systematically, but you could definitely see the changing protocols of rituximab as a way to adapt the treatment after the need for treatment, which I think is quite exciting.

    4H. Why do some get 2 infusions back to back in 2 weeks and others start with 1 and then go 6 months?
    Anders Svenningsson: It is an old protocol inherited from rheumatology that was used more in the beginning of rituximab treatment for MS. We found it unnecessary high and have successively lowered the dose to make the treatment safer.

    4I. How long can you stay on rituximab treatment?
    Anders Svenningsson: I think you will find the answer to that question above. As a rule of thumb, until the age between 50 and 60 years, depending on individual factors. It will not be needed any longer as far as we can conclude from what we know about the disease and the drug today.

    4J. Is there a set time and when one can say that you are close to being cured?
    Anders Svenningsson:
    I wish I could have an answer to this thrilling question. The day we can measure the relevant autoimmune phenomenon and we see that it has disappeared and not come back for many years without treatment, then I would say “cured”. A “wholly grain” for MS treatment is to get rid of all signs of inflammation in the cerebrospinal fluid (CSF), that could be an intermediate goal. More than half of very inflammatory active patients that will be treated early with autologous bone marrow transplantation will lose every sign of inflammation, including in the CSF. I think those individuals are cured.

    4K. What is the longest time that someone has been on rituximab for MS?
    Anders Svenningsson: I would say almost 10 years, but in those cases the intervals have been successively increased so I need to do some deeper checking what the infusion scheme actually look like for those persons.

    4L. What is next if I fail on rituximab?
    Anders Svenningsson: It completely depends on why you fail. If it is because you have developed anti-drug antibodies (ADA), Ocrevus or ofatumumab will work fine to switch to. If it is because of other side effects, Tysabri would be a good alternative if you are anti-JCV antibodies are negative, otherwise possibly Lemtrada or Mavenclad. If it is because of hypogamma or a lot of infections, it is trickier – if you are JCV+, the one safe alternative would be Copaxone. The most unlikely reason would be return of disease activity and no ADA and if that would happen I would consider autologous bone marrow transplantation. In my practice, it has never occurred, however… (with hundreds of patients for many years on rituximab).

    5. About using drugs off-label:

    5A. How close are we to recommending Rituxan as MS treatment?
    Anders Svenningsson:
    Oh, that is a tricky question where Big Pharma is doing everything they can to prevent that, and regulatory authorities in my opinion are weak and more sensitive to the economic rules set up to protect pharma than to the best need for patients and society of effective medication for reasonable prices. We work actively on the matter in Sweden, but are not there yet. Hopefully something will start to happen this year.
    We can of course informally “recommend” the treatment between doctors and that is what is happening in practice from gaining more and more positive experience of the drug. More formal “official” recommendations in, for example, national guidelines provided by national authorities has been prevented from aggressive actions performed by Big Pharma companies.

    5B. What will be the consequences when Ocrevus (ocerlizumab) is approved?
    Anders Svenningsson:
    That will vary a lot from place to place. In Sweden, it will be used in very little amount for obvious reasons and in the USA, I think it will depend on individual doctors and insurance policies.

    • (For MD)

      C. Some says that MS is caused by EBV and that this virus infect B cells. Is this why Rituxan works? Because it clears all the infected B cells?
      Anders Svenningsson: This is a very interesting theory that I have given a lot of thoughts but we have still not had the time to look deeper into this question, but I hope we will be able to study that theory in the future. However, it is unlikely that this is the main mechanism since autoimmunity when developed involves a lot of other cells than B cells, which are not infected by EBV. We will definitely have this question in mind while planning future studies.

  • Exercise 0- backgorund

    I used to be a keen cyclist, climber, swimmer, rower etc. I have had MS for 26y, on Ocreluzimab and am now out of the habit of regular exercise. I have had several bad experiences with exercise in the last 2y. What I consider light exercise has entailed me doing it and then suffering a feeling of being wiped out for the next several days.

    This exercise has not been of the training variety but light. Nevertheless, it has been progressively rolled back to no avail.

    The Question for the Doc(s)

    I know exercise is good for MS. What I cannot get anywhere is what is the minimum amount of exercise is required to have a positive effect on brain health?

    If I can get an idea of minimum, I’d rather do that as a minimum target so I know if I am doing the correct minimum amount. If there is a minimum amount then how can I measure it? I can’t run, cycle or row on the water now. No easy access to a pool at the moment.

    I use a Concept 2 Ergometer so there are a variety of measurement options I can use. Is it heart-rate, a percentage of VO2 max, power output on a Concept 2 Ergometer (rowing machine – can set display for split time or watts)? (I did a VO2 Max in a lab 3y ago, so it is prob well out of date)

    Please don’t just say exercise. I want to be able to understand the bare minimum if it has been studied.

    My latest crappy experience was 5km on the Concept2 at a very meagre split time – takes v little effort – of 2:30min per 500m. That saw me flat on my back for the remainder of the day, so rather off-putting.

    Any specific help or advice on minimum levels to positively affect brain health is v. welcome.

    Thank you.

    Dominic

  • A drop in the number of young children diagnosed with type 1 diabetes could be associated with the introduction of a routine rotavirus vaccination of Australian infants since 2007 – the year that rotavirus vaccine was introduced. This is the first time the rate of type 1 diabetes in young children in Australia has fallen since the 1980s. The discovery builds on earlier research suggesting natural rotavirus infection may be a risk factor for type 1 diabetes.

    https://www.wehi.edu.au/news/illuminate-newsletter/march-2019/rotavirus-vaccine-type-1-diabetes?fbclid=IwAR3KGPEPVHxDk7tk7H8P08iNWvXt1G6q-LreNZhuaD5tanieupn69bM-lMU

    Note: Both MS and Diabetes t1 are hypothesised to be linked with the HERV-W env (are investigated by Geneuro). Also, both have positive results from the BCG vaccine trials.

  • Access Arrangements for pwMS, at college not uni. Regarding reasonable adjustments in exams and 25 percent extra time. College request written evidence from MS consultant not nurse, that MS impacts on working speed. Consultant not able / willing to give written evidence to help student. JCQ will only speak to teachers not students.

    How do students with MS proceed in getting extra time in exams?

    • Have you asked your nurse for advice? The Consultant’s secretary? They are quite likely to have a rough pro-forma on file as you won’t be the first.

      • The EDSS is not fit for purpose, it needs to go in the bin. I am being referred to a clin psychologist for assessment via the nurse. They are aware if my opinions.
        But the evidence needs to come in letter from neuro.

        The EDSS is discriminatory, it has severe limitations which mean I am not able to be fairly assessed by the neurologist. Disability discrimation.

        Campaign to bin the EDSS!

  • Just arrive at the
    45th Annual meeting of the European Society for Blood and Marrow Transplantio n
    In Frankfurt
    Will be reporting all the highlights

    Obrigado

  • Wanna laugh and cry over Biogen’s Alz drug failure. For how long can pharma invest on treating the symptom and not search for the cause?

    • The sad thing is this blind faith in antibodies to treat CnS diseases. The simple truth is very little gets into the brain

  • Fasting

    “They saw that when p38 was totally inactive, caloric restriction failed and had no impact on innate immunity. When it was active, but at lower levels than normal, it triggered the genetic pathways that turned down the innate immune response to an optimal level.

    That this immune-regulating response was activated by nutrients, rather than bacteria, was also surprising. This adds to a growing body of evidence tying metabolism to the immune system.

    “This is really an emerging field in mammals now, so called immunometabolism—the idea that there are ancient links between metabolism and immunity,” says Dr. Blackwell. “We were able to show in this really very primitive immune system that it is regulated metabolically, and affects lifespan and health independently of an anti-pathogen function. That is when I started calling this a primitive immunometabolic pathway or an immunometabolic regulation.”

    https://medicalxpress.com/news/2019-03-evidence-links-lifespan-extension-metabolic.html?fbclid=IwAR0TkT43SrpgUiOr6TCvgTSCyOSooUFg-GgwRWbUJ89X2xFs3kvpQY-zmo8

  • As mentioned above, HSCT may increase the probably of malignancy; alas, also do antibodies like rituximab, ocrelizumab and alemtuzumab. Are there any approximate numbers for differences between the respective treatments when it comes to frequencies of secondary malignancy? Thanks 🙂

  • Brain stem cells age faster in multiple sclerosis patientsttps://medicalxpress.com/news/2019-03-brain-stem-cells-age-faster.html

    Rapamycin will it work?

    Better to fast

    • Does this mean there’s advice as to how to stop this aging process? Fasting is spoken about a lot recently – is there any real evidence that it would help? If so, how long, what can you drink and do you need to do this for life?

      Also, you mention a possible drug to help – please share more info and why aren’t these types of meds given to MS patients along with DMDs and Neuro pain management?

      Thanks –
      Curious, impatient patient

      • You dont like to read?

        If so watch

        https://www.youtube.com/watch?v=4UkZAwKoCP8

        Well well well
        In 2016 just heard this Dr talk about diet and ms and he said that NO diet is efective in ms
        BUT
        FASTING

        Well 3 years past and no word on fasting anymore

        https://youtu.be/KQe57Dl1VLg

        (min 45. 50)

        Wonder if he forgot

        Obrigado

        Pavan Bhargava
        March 13, 2019 at 8:48 pm

        Hi Luis,

        I absolutely still feel that a fasting diet will be beneficial in MS.

        There are multiple studies in animal models and now some early data from human studies that a fasting strategy might be beneficial in MS patients. Some of the studies in MS patients are still ongoing.

        The focus of this post was not diet and hence I have not mentioned this research. The effects of fasting on the metabolic profile in MS patients are currently being studied at our institution and hopefully will be reported soon.

        https://multiple-sclerosis-research.org/2019/03/guest-post-studying-metabolic-abnormalities-in-ms/

        Its a Barts Blog guest neurologist

        🙂

      • ADWP-3 – Randomized autologous hematopoietic stem cell transplantation versus Alemtuzumab for patients with relapsing remitting multiple sclerosis: the Scandinavian RAM-MS trial Anne Kristine Lehmann, Norway
        09:35 – 09:50

        ADWP-4 – CIBMTR autoimmune disorders update: BEATing-MS and other developments Marcelo Pasquini, United States
        09:50 – 10:10

        https://www.ebmt.org/annual-meeting/scientific-programme

  • On tuesday 26 of march at the Ebmt 2019 had the pleasure to atend the talk of Prof Paolo Muraro from the imperial college london

    About AHSCT in MS and autoimmune diseases: how does it work?

    This is his presentation

    https://ebmt2019.abstractmgmt.com/uploads/ebmt2019/81-presentation.pdf

    Last but not least James Lindsay, United Kingdom from Barts and The London School of Medicine and Dentistry

    ( yes i talk to him we know all of barts blog team 🙂 )

    Presented HSCT for Crohn’s disease: ready for primetime?

    https://ebmt2019.abstractmgmt.com/uploads/ebmt2019/83-presentation.pdf

    Obrigado

  • I see on your Twitter account ProfG that you’ve highlighted a report that concludes that those PwMS who refuse PASAT are more likely to be cognitively impaired (you missed the ‘be’ out of that sentence btw, which provided a wry smile)

    For a moment or two I responded by feeling vulnerable to irrational thinking in knowing that I would refuse any cognitive testing, and concern as to whether this rejection reflects the extent of my cognitive impairment.

    Then I came back to the critical consideration for me: where is the distinct evidence of benefit to routinely testing and what provision of support, if any, is available? In a nutshell: why put people through the agony of tests (who doesn’t stress at tests or exams) if there’s little that can be offered, and surely focussing on lifestyle and neuroplasticity would be far better?

    This question appears even more pertinent when routine cognitive testing is not a requirement for people with Alzheimer’s/dementia here in the UK. This is taken from the ‘Dementia Revealed: A Primer for General Practice’
    ‘follow-up may include periodic assessment of cognition, as in a memory clinic, but should be omitted if it upsets or intimidates the patient.’ It also adds that ‘an assessment of well being and functioning is more important.’

  • Hello.
    I have been suffering from multiple sclerosis for about 10 years. But I have been confirmed for 6 years, when the course of the disease became aggressive.
    In 2013, I had 40+ active lesions in the brain and 2 lesions in the spinal cord and 4 exacerbations. I had alemtuzumab therapy in 2014 and 2015. I recovered well , my EDSS about 2 -3 points .
    But since 2018, I have slowly become more tired. I have not had any additional focus on MRI since 2014, but I was assigned Ocrevus.
    I love wild walks in the wild forest and taiga. And this is part of my life. But ticks bite me sometimes. I want to be vaccinated against enzifalita but my neurologist forbade me. He says that any vaccines are prohibited in multiple sclerosis. In Russia, this opinion was taken by neurologists.
    What do you think about encyphalitis vaccination when I’m on Ocrtvus therapy?

  • An NHS story

    “Multiple Sclerosis Awareness Month
    Day 30 – Time Is Brain

    Neurologists routinely advise people with MS that their condition is mild and to adopt a “wait and see” approach.

    The problem is that MS is always mild or benign until the day you wake up blind, or unable to walk, or incontinent or with any number of other symptoms. When that day arrives, it is too late. The damage is done. Damaged nerves can’t be fixed.

    Multiple Sclerosis means Multiple Scars. Those scars are in the brain and on the spine. The central nervous system controls everything the body does including breathing.

    So why are people with MS expected to wait and see before they are offered the most effective treatment available ?

    People with other conditions are offered effective treatment, so what makes MS different ?

    My brain and spine were damaged beyond repair when my neurologist took this approach and refused to let me have the most effective treatment available. I asked him directly; I asked for a second opinion and was refused an appointment with a different neurologist.

    6 months later I transitioned to Secondary Progressive MS and deteriorated rapidly from a disability score of 1.5 to 6.5

    The neurologist now hasn’t seen me in 3 years, I have permanent disability and can’t work; I don’t see family and friends much; my daily life is dull and about 80% spent in bed.

    Am I bitter ? You bet I am. One man’s laissez faire approach robbed me of the opportunity to try to slow deterioration before it was too late. He gets to live his life still.

    Sadly I am not alone, this is the situation for 100,000 people and their families in the UK, with an average 100 diagnosed every week.

    It’s time for change”

    • Hi Prof Gavin, as a 54 (nearly) do I fall into funding issues? Which are more costly 1. Tysabri or 2. Ocrelizumab? Would the costings be the same nationally? How do you fight your case? Sorry for all the questions but it is really important for me at this moment. Thanks for reading 🙂

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