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MouseDoctor

202 comments

  • ECTRIMS 2021

    What tracks will you be following and why?

    Any Presentation / Poster in particular that you’re looking forward to?

  • Does cladrabine have an effect on plama cells in the brain? I know there’s been a study on this, just wondered if there was any info and when the results be published

  • Prof G, if the brain atrophy data on anti-CD20 is so poor, is it really fair to call it a high-efficacy therapy? Wouldn’t you expect people on Lemtrada/Tysabri/Mavenclad to do much better in the long term even if in the short term they are the same in terms of lesions and relapses? Someone in the UK may not be allowed to access Lemtrada and Tysabri, but would you recommend they go for Mavenclad instead of Ocrevus?

    • Yes, but some can leave with you some end-organ damage, for example, a destroyed thyroid gland that means you have to take thyroid hormone replacement therapy for the rest of your life.

  • With the expectation the UK will begin offering third doses of covid vaccines from September, what advice would you give to people on anti-CD20 therapies about how to maximise their response? Should the wait 12weeks post infusion?

    • I would say from a B cell perspective the longer the better but if you have no B cells then the chances are there will be a poor response

  • If you were going to switch from an anti-CD20 to cladribine, is there anything you would want to keep in mind? Do you have to wait for any amount of B cell repopulation?

  • Regarding exercise, any data oriented way (think sports wearables to target heart rate or something) to go to the edge in training while preventing being almost wiped out the next day?

    I presume we should push as hard as possible…

  • I came across this https://pubmed.ncbi.nlm.nih.gov/22312480/ and it says that CD8 low level somewhat depends on low vitamin D. Is there proof about this? I have seen my CD4/CD8 ratio increase (from 3.3 to 5.2) with vitamin D supplementation (from 21 to 66 ng/mL) so the opposite of the expectation and little CD8 count increase (from 135 to 180). The starting data were taken before starting ocrelizumab. Is it possible that it is not vitamin D that contributes to increase CD8 count but something else that is produced by sunlight exposure?

  • Should the clearance of oligoclonal bands from the cerebrospinal fluid, be considered a target in MS treatments?

  • MD- Came across this in my inbox this morning: “Risk of Severe COVID-19 Not Raised by Immunosuppressive DMTs”, cited and seemingly reviewed fairly well, in Multiple Sclerosis News Today. (A study out of Australia). Does anyone have any comments? This appears on face to be a pretty definitive headline, paraphrased “Hey everyone, don’t worry at all”.

  • Other than the CLARITY trial for cladrabine, is there any other data on brain volume loss associated with oral cladrabine?

        • Cladribine is a “big gun”……and as a rrms patient that is quickly transitioning to ppms that just started clad, I take exception to anyone suggesting otherwise.

          I did my research!

          The safety profile of Clad outweighs any of the additional small benefits one would get by risking Alem or HSCT.

          I would like to keep my thyroid in good functioning order, thank you. And let’s not forget the 2-3% confirmed mortality rate associated with the still experimental HSCT.

          • Myeloablative HSCT might be as high as 2-3% mortality, maybe (although that’d be the upper end of the last estimate I saw). Non-myelo seems to be down around 0.3%.

            (Which is admittedly still way higher than cladribine mortality, and even if it is more effective it’s not *that* much more effective, so preferring clad is an eminently reasonable decision.)

            (The lack of proper comparative trial data really is bloody frustrating.)

          • Thyroid problems caused by alemtuzumab are easily treatable. HSCT is not experimental (it’s basically just bone marrow transplantation), and there have been cutting edge hospitals using it in MS since the ’90s. The mortality rate is not 2-3% but ranges from 0.5% to 1% at the centers which have actually performed large numbers of these procedures (in other words, around the same rate as hip replacement surgery).

    • Not really T time but B time, the treatment makes T cells kill B cells and lupus is treated so this sort of says that Lupus is a B cell driven condition….how long before this is done in MS?……My only problem with this approach is I am not sure they can turn this off, so in this individual no B cells for life….so hypogammaglobulinaemia and infection becons in the future as it is going to be like being on ocrelizumab for ever.. However they should make the effect reversible because if it goes wrong there is no where back. However on the plus side this approach could scrub the brain clear

      • Ok, do you think improving energy state will slow down neurons dying off. What about energy failure related symptoms?

    • I think it’s been shown to raise cellular energy levels in the brain by increasing ATP

      Hopefully a phase 3 goes ahead and clinical benefit can be found.

    • Looks like they are not moving on to Phase III but are instead doing another Phase II… I guess we will have to wait another ten years to see it in the clinic even if it does work… Sigh…

  • A question for Prof G if he is around. I thought his recent news letter on anti CD20 was excellent. Switching from this therapy is certainly a hot topic. However, previously I have read posts that considered the switch from Ocrevus to HSCT to be relatively safe. In the news letter, Prof G highlights the potential for long term lymphopaenia if b cells are not allowed to reconstitute first. Why is this any more of a risk than starting on HSCT given that the treatment generally takes out bcells anyway?

  • Happy Sunday

    I find there is there such little information about switching from tysabri to cladribine.

    Does anyone have any personal experience? Did you take meds prior to sleeping or in the morning?

    Is rebound common during the switch, and what are the backup protocols of cladribine fails?

    Is cladribine a highly effective treatment?

    Thanks

  • Do we know if melatonin benefits pwms? I’ve had trouble sleeping, it’s a new problem and coincidently, perhaps, an incidental less than cm pineal cyst seen on my recent brain mri. Possible harm if i try melatonin? Other ways to soothe my third eye???

  • Are BTK inhibitors classed as immunosupressant drugs?

    Also, does continual long term blocking of BTK cause a dampened response to a virus or is it as simple as stop the BTKi and your immune response is back to usual?

    If that makes sense

  • Does anyone else (pwMS) find it very difficult having an MRI scan? I was having a open MRI scan recently and had to abort after 15 mins, I couldn’t take it any more, it’s still claustrophobic and very loud. Open MRI scans take longer to do than in a standard MRI scanner. I don’t want to take sedatives.

    I read an article today about PTSD caused by an MRI experience causing claustrophobia. There are open upright scanners and I will need to try this next year.

  • https://www.tmc.edu/coronavirus-updates/daily-new-covid-19-positive-cases/ . No guidance here in Houston Texas USA area for pwms on anti cd20 with a very steep increase of cases and lot of apathy. Even our chart dial had to be adjusted for increase I just cancelled my infusion for ocrevous this week. Although my entire household is vaccinated, they must interact with people at high school, college and work. I can’t self isolate sufficiently. What is guess for timeframe of this surge so I can reschedule? Completely left to figure it out on my own.

    • I recommend that you at least get your B-cell counts checked regularly and don’t delay your ocrevus infusion by any longer than it takes for repopulation to begin. I would be much more worried about undertreated MS than COVID.

    • Not an MD but unless you are banking on getting a few b cells back to get a better vaccine response ocrelizumab delay probably won’t help much if at all. Depletion seems take somewhere between 12 and 30 months to recover to low normal…

      Yes, it SUCKS.

      Having said so, it seems covid is mostly survivable even on anti cd20 given you are otherwise in reasonable shape.

      • Or is it? Antibodies against covid have a half-life of around 3 months only and people on anti-CD20s seems to mount a stronger T-cell response. It doesn’t seem to be that big of a deal..Just get vaccinated.

    • Update, neuro feels up to 2 month delay for ocrevus infusion ok for me because of my inability to completely self isolate during this latest wave here. Contact tracing? Did we give that up? And govt focusing on treatment instead of prevention , setting up 8 monoclonal antibody centers in Texas. Ads are on tv. only 150 patients can be treated at center a day and need to be accepted after dr referral. life saving care.should not be luck of the draw. Is there data on outcomes for MSers treated with Regoneron monoclonal antibodies? https://abc13.com/covid19-antibody-infusion-center-montgomery-county-texas-department-of-state-health-services-judge-mark-keough/10955171/

  • Hi MD,

    Can you please help confirm what a “reasonable” antibody protection against Covid is? The test I am being offered is an IgG test against SARS CoV-2 which has a reference of =7.1 BAU/ml as positive.

    Would you say, for example, that 15 BAU/ml would be a reasonable level of protection? I know some people who had Covid have BAU/ml results over a 100.

    If the units are an issue, BAU/ml = 0,142 AU/ml in this Abbott test.

    • I am sorry no-one knows what these values mean in terms of protection. Abbott does loads of differnt tests double background is not high I think. do some searches there are humdeds of papers on each test

  • If your lymphocytes are are the 2.0 mark with out meds. You take something like DMF for a year where they hover around 1.0 mark.

    Then you start cladrabine. Will you lymphocytes head back to your normal range of 2.0 in the next few years or will they head and stay around the 1.0 mark where your lymphocytes where before initiating treatment of cladrabine?

    • My experience is that DMF switchers to cladribine have lower lymphocyte numbers than expected and are more likely to get Grade 3 or 4 lymphopaenia. DMF’s effects on lymphocytes get carried over.

  • Treatment Escalation vs Immediate Initiation of Highly Effective Treatment for Patients With Relapsing-Remitting Multiple SclerosisData From 2 Different National

    This study suggests that escalation of treatment was inferior to using a more effective disease-modifying treatment as initial treatment for multiple sclerosis

    https://jamanetwork.com/journals/jamaneurology/fullarticle/2783261?guestAccessKey=5cf8818e-aa09-482a-82ca-a5aada612484&utm_source=silverchair&utm_medium=email&utm_campaign=article_alert-jamaneurology&utm_content=olf&utm_term=081621

    Dont we all know this allready?

  • On average, in percentage, how much higher are NFL levels for people with RRMS? Than healthy individuals

  • Early High Efficacy Treatment in Multiple Sclerosis Is the Best Predictor of Future Disease Activity Over 1 and 2 Years in a Norwegian Population-Based Registry

    https://www.frontiersin.org/articles/10.3389/fneur.2021.693017/full?utm_source=F-AAE&utm_medium=EMLF&utm_campaign=MRK_1665889_a0P58000000G0Y2EAK_Neurol_20210623_arts_A

    The immunomodulatory treatment guidelines should be updated to ensure early, high efficacy therapy for the majority of patients diagnosed with MS.

    Dont we all know this allready? (part2)

    😉

  • Well maybe inflammation is not that bad

    Increasing evidence shows the benefits of the inflammation phase (4). At the early stage of injury, microglia, monocytes, macrophages, neutrophils, and T cells can collectively orchestrate a response that preserves neural tissue

    Microglia/Macrophages and CD4+CD25+ T Cells Enhance the Ability of Injury-Activated Lymphocytes to Reduce Traumatic Optic Neuropathy In Vitro

    https://www.frontiersin.org/articles/10.3389/fimmu.2021.687898/full?utm_source=F-AAE&utm_medium=EMLF&utm_campaign=MRK_1706117_a0P58000000G0YLEA0_Immuno_20210817_arts_A

    Or is it?

  • So you get EBV as a child, 20 years pass, a few unknown conditions are met, and then you get MS. Why do most people present in their 30s? What happens then to trigger the autoimmune attack in your 30s and not 10, 20 years prior when initially infected with EBV?

    • “Why do most people present in their 30s? What happens then to trigger the autoimmune attack in your 30s and not 10, 20 years prior when initially infected with EBV?”

      It takes awhile…to go throught the disease events…people with higher CD8+ Tcells probably
      have better EBV control and postpone the disease more.
      Childhood ms does occur but it’s very rare.

      “It is postulated that autoimmunity evolves in the following steps: (1) CD8+ T-cell deficiency; (2) primary EBV infection; (3) decreased CD8+ T-cell control of EBV; (4) increased EBV load and increased anti-EBV antibodies; (5) EBV infection in the target organ; (6) clonal expansion of EBV-infected autoreactive B cells in the target organ; (7) infiltration of autoreactive T cells into the target organ; and (8) development of ectopic lymphoid follicles in the target organ”

      https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3270541/

  • Is anything being looked at as a treatment after an IRT? Particularly Cladrabine. Rather than waiting for a possible relapse?

      • I think the idea would be a sequence of treatments to get the best possible results for pwMS. Something like alemtuzumab initially to nuke the periphery, then cladribine to mop up any long-lived cells still lingering in the CNS, then maybe teriflunomide as maintenance to prevent the MS coming back. Of course, no MS neurologist is going to sign off on this due to fear of “side effects.” It’s hard enough getting them to prescribe any IRT as it is.

    • “ Rather than waiting for a possible relapse?”……IMO this is already the benchmark for all DMTs, not just cladribine. They work until they don’t work anymore.

      What is the main benchmark in most MS drug studies……no evidence of new lesions or relapses, so how is that any different than the efficacy data from the cladribine studies. The only difference I can see is you take clad in a short pulse while the others are constantly suppressing, which seems to lead to more concerning issues in the long term.

      Your neuro is probably like the rest and have thrown Clad in the trash bin with Alem, due to initial black label concerns, which now seem a bit over blown.

      I agree, not knowing what to do if a clad patient relapses in day year 5, is frustrating. However, if clad gives me 5 relatively “stable” years, that would be better than what I experienced on OCR.

    • Thanks but with rare events we have to ask are they causal or chance and until they appear again and again then they are difficult to interpret

    • “Are EBV anti bodies 100% present in any other auto immune disease?

      Yes..All of them.
      Even in a very rare AI disease like aplastic anemia that destroys the bone marrow.

      “How can infection with the Epstein-Barr virus EBV lead to aplastic anemia?
      Conclusions: Aplastic anemia may be associated with Epstein-Barr virus more commonly than suspected by history. Localization of the virus in the bone marrow supports a causative role for Epstein-Barr virus in bone marrow failure.”

      “CD8+ T-cell deficiency is a feature of many chronic autoimmune diseases, including multiple sclerosis, rheumatoid arthritis, systemic lupus erythematosus, Sjögren’s syndrome, systemic sclerosis, dermatomyositis, primary biliary cirrhosis, primary sclerosing cholangitis, ulcerative colitis, Crohn’s disease, psoriasis, vitiligo, bullous pemphigoid, alopecia areata, idiopathic dilated cardiomyopathy, type 1 diabetes mellitus, Graves’ disease, Hashimoto’s thyroiditis, myasthenia gravis, IgA nephropathy, membranous nephropathy, and pernicious anaemia. It also occurs in healthy blood relatives of patients with autoimmune diseases, suggesting it is genetically determined. Here it is proposed that this CD8+ T-cell deficiency underlies the development of chronic autoimmune diseases by impairing CD8+ T-cell control of Epstein-Barr virus (EBV) infection, with the result that EBV-infected autoreactive B cells accumulate in the target organ..”

      https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3270541/

    • In mice. And fed a “Western diet” which is basically 75% pure sugar and fat. To say that this translates to humans is a stretch.

      • Really?

        . In rodents fed a high-fat diet, TRF attenuates body weight gain, reduces body fat accumulation, improves glucose tolerance, and restores diurnal rhythms of core clock transcripts compared to high-fat ad libitum diets4,9. Moreover, TRF protects against high-fat diet-induced obesity, fatty liver, dyslipidemia and glucose intolerance in mice with ablated circadian clock machinery10. In humans, time-restricted eating decreases body mass by reducing energy intake11,12, but improves whole-body insulin sensitivity and beta cell responsiveness independent of daily energy intake8. Collectively these results suggest that the interplay of energy intake timing (including time spent fasting), and whole-body circadian rhythmicity have a profound impact on whole-body metabolism and metabolic health.

        Time-restricted feeding alters lipid and amino acid metabolite rhythmicity without perturbing clock gene expression

        https://www.nature.com/articles/s41467-020-18412-w

      • Intermittent fasting (IF) improves cardiometabolic health; however, it is unknown whether these effects are due solely to weight loss. We conducted the first supervised controlled feeding trial to test whether IF has benefits independent of weight loss by feeding participants enough food to maintain their weight. Our proof-of-concept study also constitutes the first trial of early time-restricted feeding (eTRF), a form of IF that involves eating early in the day to be in alignment with circadian rhythms in metabolism. Men with prediabetes were randomized to eTRF (6-hr feeding period, with dinner before 3 p.m.) or a control schedule (12-hr feeding period) for 5 weeks and later crossed over to the other schedule. eTRF improved insulin sensitivity, β cell responsiveness, blood pressure, oxidative stress, and appetite. We demonstrate for the first time in humans that eTRF improves some aspects of cardiometabolic health and that IF’s effects are not solely due to weight loss.

        https://pubmed.ncbi.nlm.nih.gov/29754952/

    • This was our first time studying female mice, and we weren’t sure what to expect,

      Sexism evident even in the study of wee mice eh?!
      No wonder we don’t know the ideal dosage and impact of the majority of meds on women!

      Still, good to see some more positive evidence for IF in its new identity of TRE.

    • Breakfast 8am. Lunch 12noon. Evening meal 5 to 6pm. This means fasting for 14 to 15 hours and is doable…..

  • OK – a follow-up reminder for Prof G to keep his promises……..
    Posted on July 18 in last month’s Q&A was the question “A weekend musing question for Prof G. At what point should a PwMS in their early 60s go, “Hmm, not too sure if my worsening cognitive and memory problems might NOT be MS but might be some form of Alzheimer’s kicking off. I wonder if I should see my doc and get some form of testing done……..?”

    To which the Prof replied “Good question for me whilst on holiday. I will be back on the 2nd of August with an answer.”
    So, the Prof is now back, but no answer yet.

    And now there a Part B which could use a response as well.
    “How is a differentiation made between loss of function (i.e. significant deterioration in walking ability) arising from MS spinal lesions and a loss of function arising from pinched nerves and/or other MRI confirmed lumbar spine problems, especially when alterations in skin sensation in the legs match with dermatome maps of the legs for the affected nerves?

    There are far too many stories from patients where they raise issues with their docs but problems go un-investigated and/or untreated because their concerns are met with the far-too-frequently-used brush-off statement of “Oh, it’s probably due to your MS.” (with the unsaid part being “so go away and stop bothering me”). How should patients deal with these brush-offs when options for additional opinions don’t exist?

  • I tried to get my neurologist to consider switching me from rituximab to cladribine and got this response:

    “We do not recommend cladribine over rituximab as it has an inferior safety profile and long-term data remains limited. While the manufacturer promotes it as a single-course of therapy, questions remain about its long-term efficacy and if/when another course is needed. In a recently published long-term follow up study, ~40% of patients started another treatment within 1 year, ~50% within 3 years within 70% after 5 years. Comparative efficacy data also suggests that while it is more effective at preventing relapses than other moderately effective therapies such as glatiramer acetate, interferons, or dimethyl fumarate, it is only about as effective as fingolimod and is less effective than natalizumab (and by extrapolation, rituximab).”

    I’m doing fine on rituximab for now, but I’m not sure I agree about the safety profile. It doesn’t seem like covid’s exactly going away, so how safe is it to keep your MS patients permanently immunocompromised? Curious about your take on the efficacy.

    • It is obvious to me that some people with need another course…about 50% of people with alemtuzumab do, in terms of inferior safety profile not so sure but this is how the SH1 sticks and shows the problem the manufacurers have in educating neuros

      • Inferior safety profile…. Yep SH1 sticks and also Shows me that neuros also need to learn to read the literature outside of their own discipline and extrapolating a bit.

      • So neuro didn’t like cladribine because they were worried that the patient might need another course… And then they put her on rituximab instead? Because they think rituximab is going to need fewer courses than cladribine? That seems like a surprising hypothesis.

          • This is how it goes down…

            “Mavenclad…What’s that..?”

            “Oh..Cladribine..hehe..you don’t to risk cancer…do you..?”

          • I assume so. Unfortunately this is not just this one doctor’s view, as he took my inquiry to the “regional experts” and this is what those experts told him.

  • Do you think targeting HMBG1, to inhibit pro inflammatory cytokines could or possibly will be a good treatment against MS and other auto immune diseases?

  • If brain volume loss can be affected by how hydrated you are why is there no standard level of hydration before an MRI scan for clinical trials measuring brain volume loss ? This could reduce the potential error margin for brain volume loss.

    For example the individual must not eat or drink anything for 8 hours before his MRI scan and one hour before his scan he has to drink 750 ml of water. This could be a simple way to reduce the error margin and get a positive outcome quicker.

  • Is blood in urine, but no UTI an MS symptom?

    I am aware of a pwMS that has severe ongoing frequent UTI ‘type’ symptoms (of pain mainly and weak bladder sometimes), but only in occasion infection and blood in urine.

    Lupus can cause blood in urine, so I wonder if MS can?
    The PW patient has been advised by several nurses including an MS nurse to have an appointment with the Continence Team. But the patient informs that the Continence Team in the area only offers advice on pads and catheters, not diagnostic investigations (other than urine retention ultrasound). The patient has requested a referral to a Urologist.
    The NHS website has a link which informs: no infection but blood in urine merits a ‘two week fast track’ referral to Urology.

    • It depends on what the trial is about for some easily over $100,000,000 academic trails tend to be less than £2-4,000,000 but this is not the full cost. Think you may have 600 people in the control arm on an active drug which has to be bought, so that is 600 (people in the control group) x $50,000 (drug cost per person but for most MS drugs their cost is closer to $100,000 = $30,000,000

  • Given your teams experience with cladribine, are you aware of any heart issues associated with taking Clad? Increased heart rate and consistently high blood pressure?

    These are not side effects listed in the drug pamphlet or any of the published studies.

    Thank you in advance for your time and consideration to my question.

    • I should clarify…..any heart issues with clad, other than the one reported patient that experienced heart failure.

      I know “one patient” is not statistically relevant…..unless you are that one patient!!

  • Why does a course of high-dose steroids shorten recovery from a relapse. But it does not seem to impact long-term disability?

      • The inflammation itself damages the myelin sheets, why does stopping the inflammation earlier not prevent more damage from occurring?

          • When I was diagnosed with optic neuritis and was asked if I wanted steroids, in my research I read that if you took steroids for your optic neuritis, it would have the effect of delaying the onset of MS (this is in the aggregate and assuming you don’t already have MS, which I did). So I would think it does prevent damage and no doubt some long term disability as well. But of course you wouldn’t want to take a lot of steroids all the time.

    • Because relapses are not the disease…many people have very few relapses and so never
      had steroids…and still their ms turns progressive…and this sp stage is what leads to
      disability not the relapses from the rr stage.

    • Common sense would tell us that it does have some impact, since of course the quicker you shut off acute inflammation the less tissue damage that particular bout of inflammation should cause. However I think the impact is probably really small and I assume you would need to monitor a large cohort for 10-20 years to actually tease it out.

      • – “Because relapses are not the disease…”
        – “I think the impact is probably really small and I assume you would need to monitor a large cohort for 10-20 years to actually tease it out.”

        Then do neurologists grossly overvalue the absence of acute inflammation (GD enhancing lesions on MRI) as an indication to stay on a certain DMT?

        • this is pulsed high dose which is the high dose used monthly, what im suggesting is that it would make a difference if used long term continuously

          • I indeed saw that they were monthly administering 1g of methylprednisolone (is that good for your bones). This could also work preventative or hit the inflammation at such an early stage that it is not really comparable to the single high dose that you might get after a relapse. Studies with this kind of single pulse have not shown any long-term benefit to my knowledge.

  • I am right handed but with the increasing weakness in that arm I am thinking of the future and beginning to train my left hand to carry out tasks my right hand usually takes care of. I will keep working and exercising the right arm to keep it going as long as possible but some things are close to becoming unmanageable. I was wandering if anyone has any advice on working towards becoming ambidextrous.

  • Is there much investigation into cannabinoids and multiple sclerosis? I know cannabis is now a treatment for spasticity,

    However acting on CB1 and CB2 receptors. Would cannabis show potential to slow down MS in some way. Acting on both sides of the immune system and possibly calming inflammation

    I know it’s a sticky subject as cannabis is illegal in a lot of country’s.

    • Experimentally, yes, loads of it, chiefly by us, who initially identified the anti-spastic properties and also its neuroprotective capacity.
      Despite the one trial investigating cannabis as a neuroprotectant “failing” due to a combination of factors, there was a definite positive effect on slowing of disease in a sub-group of pwMS with less severe impairment at the start of the trial.
      However, the trial was reported as a failure and despite our repeated prompting for another better dw esigned trial. I’m afraid it has fallen on deaf ears.
      Everything we know about the biology of cannabis and the cannabis receptors tells us it has to have a neuroprotective effect in a nimber of neurological conditions, not just MS.

      • MD1 says no, MD2 says yes, haha

        There has to be some effect, such an interesting plant

        THC also however it’s surely neuroprotective, if microglia do play a role in progressive MS.

        I’ve been thinking about a CBN supplement to help me sleep, I’ve tryed cannabis but the THC just doesn’t agree with me it makes my mind race.

        I might try hemp flowers next

        • It is the THC element that makes you sleep.THC is neuroprotective in my eyes it is how you show it in ms. Neuros are not interested in THC

          • When you say neuroprotective how does that equate with the known risk of long term mental health problems. Is there a difference in quality/strength/variety with clinical use and recreational use?

          • “how does that equate with the known risk of long term mental health problems. ”

            Yes….long term it causes paranoia and other
            mental/psychological distortions

    • I’m sure the number of deaths and the total amount of harm done by fewer people being able to access timely care for non-COVID related issues (especially cancers and neurological diseases like MS) will end up being greater than the amount of harm prevented by lockdowns, however I agree that there is nothing imprudent about individuals being extremely cautious. I seems clear at this point that vaccines are not going to be enough to really end the cycles of lifting and reimposing restrictions so I hope that the research being done into finding an effective anti-viral treatment for COVID is successful.

  • Hello MD, lots of questions:
    1. Are OCB antibodies? Do we pwMS make all different OCBs to one and another?
    2. What would Ixazomib do to plasma cells in the blood and bone marrow?
    3. How do other DMTs say Ocrelizumab clear OCB (some % of patients gets clears after x years)?

  • Hi Doctor G and MD, what do you think? Should we be concerned about sildenafil? I think they are quite a few male MS patients who take sildenafil for its original indication regularly and quite often.
    Sildenafil Inhibits Myelin Expression and Myelination of Oligodendroglial Precursor Cells.
    https://journals.sagepub.com/doi/full/10.1177/1759091419832444
    However, in the past there were quite a few animal studies which reported benefits rather than harm like the study from Spain ( http://diposit.ub.edu/dspace/bitstream/2445/172838/3/Diaz-LucenaD.pdf )

    • “what do you think? Should we be concerned about sildenafil? I think they are quite a few male MS patients who take sildenafil for its original indication regularly and quite often.”

      Really doubt it….If you have concerns just switch to cialis..which is actually better…more convenient.

      • Both of them are Phosphodiesterase 5 (PDE5) inhibitors. So, very similar issues and/or benefits according to these and other studies. However, I am not sure how reliable any of these studies are. I would assume that the in-vitro and in-vivo animal experiments have quite different relevances for human MS.

        • If PDE5 is bad, the longer half-life of cialis would presumably be worse.

          Personally, I am not worried, in vitro results are usually of very little consequence. Mice are only vaguely relevant to humans. That sildenafil beats ms study in mice is a favorite example of mine.

  • Hi,
    I am on Ocrevus (ocrelizumab) – last infusion March (but also debating switching meds). I was thinking of getting an anti-body test.
    Should I get one now?
    Should I wait until after Booster vaccine (presuming we get offered one).
    Also should I also get a test that measures T-cell response? (I have seen them advertised).
    Thanks

    • Hi, you of course will want to consult yout HCP, but you may first want to check the status of your B cells to determine whether they have repopulated so that you can mount antibodies from vax. Can unfortunately take anywhere from 5.5 months to 3+ years but varies from person to person.

    • If you get one now (Ab test) it is likely to be low as antibody levels are dropping in a few months, do a blood spot.
      It lookes like most people on ocrelizumab make T cell responses

      • Hoping for T cell response! On Ocrevus and 4 months post Pfizer vaccines, I was negative for spike protein antibody on Roche Elecsys Anti-SARS-CoV-2 S semi-quantative test. I got a .4 u/ml. .8 u/ml is needed for positive. My friend vaccinated and tested at same time as me got 1400 u/ml.

  • I wonder if could answer this please. Unfortunately the ( UK) hospital I am under the care of has decided to switch the provider for my DMF. It looks very likely that I will run out of tablets before I will get the next 3 month supply. Do short (hopefully) breaks in DMF for non medical reasons cause an increase in relapses? Also, how long does DMF stay in your system? I am also worried about side effects again as when I started on the tapering dose I had stomach issues, Diarrhea and bad flushing, will I get this again as I will be straight back on the higher dose with no taper. To say I am not impressed is an understatement. But, hopefully you can clarify these points for me please. Thanks

  • Prof. G, would Ocrevus work in PPMS with no active lesions? If yes, how? Would it treat smoldering MS in such cases? If yes, how? Thx.

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