Q & A January 2021

Q

“Happy” New Year, as we trudge into another lockdown.

Got a question?

You know the drill.

About the author

MouseDoctor2

160 comments

  • Is there a preferred Covid vaccine to opt for (Between Pfizer, Moderna, Oxford) for someone on an anti-CD20 who developed hypogammaglobulinemia? Do they all show a good T cell response if we can’t rely on seroconversion on the antibody side?

    • No preferred vaccine. At a population level, the RNA vaccines (Pfizer and Moderna) offer greater protection, but this is offset by cost and logistics issues (cold chain), which is not a problem with the AstraZenca-Oxford vaccine. My advice is simple; take whichever vaccine is offered to you.

  • With everything we know right now about MS, what do you suggest a 5th year RRMS patient on Rituximab do to maximize their chance of staying RRMS (or get better!) and keeping the disease from progressing aside from staying on their DMT? What else can they do? Any decent additive treatments that have a low downside but potential upside?

    • I second this question. Thanks to this blog, we know that lipoic acid, metformin, HAART etc might be useful. There is always this nagging feeling that there might be things we could be doing right to help long term prognosis (along with intermittent fasting and exercise), but might have to wait half a decade to get conclusive proof.

      Must say, it was blissful existence when I did not have to search for “double dose ocrevus” on the clinical trial website 🙂

    • We don’t have data on this, which is why we need to do add-on clinical trials. I suspect we may need an add-on combination therapy to address all the aspects of the pathology that drives smouldering MS.

  • how long is a piece of string question here

    If called by GP and told come for Covid vac within next 4 weeks

    BUT
    3rd dose (so 2nd round) of ocrevous due right at start of March

    what they heck should be done?

    I gather GPs are in charge of Covid vac…GUARANTEED if able to speak with a GP about this they will use the perennial “you need to speak to the neuro, this isn’t our speciality”

    so as always, loads fall through the cracks between the supposed joined up thinking of the NHS.

    What to do?

    • In general, I would have the vaccine (both doses if possible) and wait 3-4 weeks to allow the immune response to develop before having the next dose of ocrelizumab. In the UK this is now complicated by the 8-12 week gap between first and booster vaccine doses. The solution may be the first dose of the vaccine, wait 4 weeks, ocrelizumab infusion and then have the booster vaccine dose when it is available.

  • Does the failed phase 3 high dose biotin study mean that energy deficits in the mitochondria caused by demyelination are not the main drivers of disability in spms ?

    • No. High dose biotin is only one potential way of improving mitochondrial function. I am not sure if it was ever shown in humans that high-dose biotin improves energetics in the CNS.

      • Interesting thank you professor 🙂

        Also i thought this could be of interest in a mouse model they showed it improved mitochondrial function and helped regained healthy axones in a mouse model.

        Title : High-dose biotin restores redox balance, energy and lipid homeostasis, and axonal health in a model of adrenoleukodystrophy

        Link :

        https://pubmed.ncbi.nlm.nih.gov/32511826/

        Wishing you all the best professor and have a nice week 🙂

  • Lockdown and my resulting lack of movement has reduced my mobility even further. I am on the waiting list for physio but have been for months and will be for months. I can’t find a private neuro physio in my area. What should we be doing to try and reduce the physical impacts of lockdown?

  • I read a post recently from Prof G on the processes that drive SPMS and how once they have been established, DMTs will not impact upon them. As patients, or even as neurologists, is there any markers to identify when these processes have set in?

    • Progression starts from the very beginning for all if not most ms patients even with relapsing forms of multiple sclerosis. B cells are the main drivers in ms and when looking at brain samples from spms patients and rrms patients the damage is very much the same.

      B cell accumulate in the brain, spinal cord and in the meninges even before spms. It starts very early on which causes slow neuronal damage even in the beginning.

      The official diagnosis of spms is done retrospectively when you look at your MRI scan and no new lesions have formed from demyelination for a period of time starting anywhere from 6 months to 2 years and you have worsening of symptoms that is when your neurologist will say you have spms.

    • The markers can be clinical (deep phenotyping) to look at worsening function more sensitively. I call this the neurological stress test and should look at cognition, exercise endurance, fine dexterity, etc. Brain volume loss, slowly expanding MS lesions, neurofilaments, etc.

      The questions are how hard do you want to look if we have no treatments for these processes and also how do we deal with premature or early ageing?

      • Yes, I agree. Not very hard I suppose is the answer as it’s not going to help treatment options. The reason for my question is about risk. For instance, if the processes which drive spms have already set in, is is even worth upping your DMT risk i.e. to lemtrada or HSCT. Where would the potential benefits lie?

  • 🙋‍♀️🙋‍♀️ I have a question! It’s not for me but for a fellow MS friend who developed PML whilst taking Tysabri. He is very concerned if he can & should be getting the vaccine. We are in the states. Only Mederna & Pfizer are currently out & just began.

    • Yes, PML is due to a different virus and having had another viral infection does not change the safety profile of the vaccine.

  • I was listening to Dr Robert Cywes talking on youtube about how carbohydrates interfere with the vitamin D pathway. I hadn’t this before and wondered if you had an opinion on this?

    • Why would carbohydrates interfere with anything to do with vitamin d? What possible mechanism did he give that makes him believe this and what evidence did he give? He appears to be a bariatric surgeon not an endocrine specialist. As vitamin d is an endocrine system stick to what either endocrine doctors say or vitamin d researchers with a long track record. The main reason people have too little vitamin d is 1) not enough UVB exposure, 2) the RDA is wrong.

    • Not aware of the link between carbohydrates and vD biology except via obesity. Will look into this.

      Cheap, widely-available and excessive consumption of carbohydrates, in particular processed and ultra-processed carbs, are no doubt behind the obesity epidemic that is partially to blame for the rising incidence of MS. How carbs and/or obesity is doing this is unknown at present, but it could be via vD mechanisms.

      • The only obvious effect is the amount of fat in the body and that is not a direct effect of carbohydrates, it is what is eaten and how much. The vitamin d is ending up in fat cells not in the blood as 25(OH)D, so the person ends up deficient. It would help if the RDA actually allowed for how much a person weighs. The RDA for a 5kg baby is 400IU a day, and for a 100kg adult 400IU a day. That cannot be correct. If the baby is correct the adult should be about 8,000IU a day.

      • Could vit D deficiency also be a consequence of the promotion of a low fat diet as it needs cholesterol. Is it not now widely accepted that low fat/high carb way of eating is wreaking havoc in our bodies?

  • In your opinion Should my ocrevus infusion have been cancelled purely because lockdown was imposed? It was due on 3rd Feb?

    • No. Not at our centre. It may, however, have to do with the reconfiguration of the NHS and redeployment of staff to COVID ward etc. The latter is what happened earlier this year.

  • More a topic wish than a straight up question : Would love to read about a comparison of anti spasticity medications – from the normal ones (gabapentin, pregabalin, baclofen) to more special ones (tizanidine, benzos, possibly even cannabinoids).

    • I have taken myself pretty much off all because they don’t just relax the affected muscles but all my muscles & I was beginning weaker and weaker. I ended up getting botox in affected area that was helpful. However, I stopped going because of Covid & high rate of positive cases within bldg Dr was in. Resorted to something new. Friend was making his own tincture (MJ is legal now in our State). I asked what he was doing with the plant material after he extracted from it. He gave it to me. I used it in a skin formulation I made & tried it dermal. I have never smoked, never will – but the topical I made is the best stuff I’ve ever used on my pain & spasticity! I am going to be lost when it is gone as it may be legal in my State, but it is so expensive to purchase from a dispensary plus high tax rate on it. Even with a Medical card it’s still too expensive.

    • This is the best review I’ve found. It doesn’t pay much attention to botox though. There are some comparisons of botox with placebo and other agents but they’re small and of course hard or impossible to fully blind. Being a symptom, spasticity is not a glamorous object of study, even though it’s among the top 3-4 things PwMS struggle with.

      Pharmacological management of spasticity in multiple sclerosis: Systematic review and consensus paper

      Susana Otero-Romero, Jaume Sastre-Garriga, Giancarlo Comi, Hans-Peter Hartung, Per Soelberg Sørensen, Alan J Thompson, Patrick Vermersch, Ralf Gold and Xavier Montalban

      Multiple Sclerosis Journal

      2016, Vol. 22(11) 1386–1396

      DOI: 10.1177/ 1352458516643600

      © The Author(s), 2016. Reprints and permissions: http://www.sagepub.co.uk/ journalsPermissions.nav

      Abstract

      Background and objectives: Treatment of spasticity poses a major challenge given the complex clinical presentation and variable efficacy and safety profiles of available drugs. We present a systematic review of the pharmacological treatment of spasticity in multiple sclerosis (MS) patients.

      Methods: Controlled trials and observational studies were identified. Scientific evidence was evaluated according to pre-specified levels of certainty.

      Results: The evidence supports the use of baclofen, tizanidine and gabapentin as first-line options. Diazepam or dantrolene could be considered if no clinical improvement is seen with the previous drugs. Nabiximols has a positive effect when used as add-on therapy in patients with poor response and/or tol­erance to first-line oral treatments. Despite limited evidence, intrathecal baclofen and intrathecal phenol show a positive effect in severe spasticity and suboptimal response to oral drugs.

      Conclusion: The available studies on spasticity treatment offer some insight to guide clinical practice but are of variable methodological quality. Large, well-designed trials are needed to confirm the effectiveness of antispasticity agents and to produce evidence-based treatment algorithms.

  • Does any of the approved DMTs require that pwMS have to be re-vaccinated more frequently than people w/o MS?

    • The general advice is that all people with MS and other diseases about to start immunosuppressive therapies should have the pneumococcal vaccine.

      For HSCT which is approved by the NHS to treat MS, revaccination with childhood vaccines happens in some BMT units usually towards the end of year 2.

  • When will the covid antibody study start now that funding has been secured? How does one get on the study?

  • I’ve read that it will be possible to tweak the current vaccines in a matter of weeks to make them effective against any new strain of the virus (especially relevant in the light of what Prof G has posted today). But is that true of the Oxford vaccine, which is not of the same type as the Pfizer/Moderna ones?

    • The oxford vaccine was designed over a weekend the design is not the problem the isue is if safety studies have to be be done before mass use

  • Opinions on the gut microbiome and MS? Columbia is holding a small trial using a probiotic visbiome/vivomixx. While I doubt it’ll cure MS, it could be an effective addon therapy.

      • I’m not expecting it to be a cure of the week kind of this. But, from a scientific standpoint its a really interesting brand as there’s a number of different studies in different areas using the same brand. Helps with reproducing findings rather than a sensationalized cure of the week trial.

  • Promted by the whole covid19 thing, I wonder how many CIS are actually undiagnosed post infectious enchephalitis’ or ADEM patients. What do you think?

  • Why are cd20 drugs called immunosuppressive if they do not immunosuppress fully? E.g not be called immune modulating like some of the other DMTs?

      • Oh interesting. But I’m still prreeeettty baffled! Quite confusing really, ‘immunosuppressive ’ makes it sound worse than it is

          • Immunosuppressive National Institute of cancer. Treatment that lowers the activity of the body’s immune system (Beta intereferon Yep). This reduces its ability to fight infections (beta Interferon Yep) and other diseases. Immunosuppressive therapy may be used to keep a person from rejecting a bone marrow or organ transplant (Beta intereferon no, ocrelizumab no I suspect) . It may also be used to treat conditions in which the immune system is overactive, such as autoimmune diseases and allergies (Beta interferon yep).

            See

            Immunosuppressants are characterized by a low therapeutic index (narrow window between the therapeutic and toxic range)
            and significant intra- and interindividual pharmacokinetic variability.

            (Beta intereferon gives flu like symptoms)

            These shortcomings are circumvented by precise drug dosing (based on ideal or lean body weight) as well as by screening for end-organ toxicity and, in some cases, close monitoring of plasma drug levels (parent or metabolite peak and trough levels).

            This does not make sense if the toxicity is not driven by an effect of the immune system being reduced then it is a nonsense

            Immunomodulators, by contrast, have a wider therapeutic index, a greater safety margin, more predictable pharmacokinetic properties, and less interindividual variability.

            If they have lower toxicity of course you will tolerate a wide range…nonsense

            In addition, although immunosuppressants appear to globally impair the host immune response typically in a dose-dependent fashion, immunomodulators may act more selectively by targeting only specific portions of the immune system and therefore pose a lower risk of complications related to immune dysfunction.

            Selective verses non selective immunosuppression

  • What are your thoughts on covid 19 neurological effects ?

    Im on the long covid group on social media and alot of the people are exhibiting common ms symptoms some even relapsing months after diagnosis. I myself had covid in march and was hospitalised i came out in april but was back in hospital in may when i went numb head to toe and had transverse mylitis. An Mri and lp later and i was diagnosed with ms with no previous symptoms or health issues.
    My atack seems to have been alot rougher than most especially the rapid disability that i have gained after it.

    Do you think covid 19 could be causing a neurological disorder similiar to ms ? Or the onset of ms ?

    https://www.sciencedaily.com/releases/2020/12/201217154046.htm

    • Yes, famciclovir is a pro-drug and is converted into penciclovir in the body. Penciclovir is probably the best anti-herpes simplex virus encephalitis antiviral we have and is the go-to drug in the USA. Sadly Novartis were too lazy to license it outside the USA when the purchased the drug from SKB as part of the merger requirements when SKB and Burroughs-Wellcome became GSK.

      So yes very good CNS penetration.

      • Veryy happy to hear that. I think you made a good selection for choosing famciclovir to target ebv both in the peripheral blood circulation and within the cns.

        Can’t wait to see the results of your trial 🙂

        Have a good day professor gavin giovannoni

  • Prof G,

    In people who experienced worsening walking with Ocrevus, do you know whether those people improve after discontinuing the drug or does it cause irreversible damage / triggers progression?

    As one source for reference, https://www.drugs.com/comments/ocrelizumab/ocrevus.html
    It looks like 50% of patients online also experience worsening of balance and/or walking or some form of worsening. From your experience do things go back to pre treatment baseline after Ocrevus is discontinued?

    • Unfortunately, no, not in my experience.

      You also have to be concerned with rebound activity after stopping Ocrevus. Had to stop after an adverse reaction in January 2020. Began repopulating in September, bad relapse in October. Teri kicked in November and began regulating my CD19, and the relapse stabilized in December. Started Teri in August.

      • I haven’t heard of rebound activity after discontinuing Ocrevus… So we are saying that, we took a gamble and for those who had worsening due to Ocrevus, we have a choice between discontinuing Ocrevus (and risking a relapse) or continuing Ocrevus (and continuing worsening).

        That sounds insane?

        • Welcome to my personal hell, membership is free; however, once you are in, you can never leave!!

          Look, I am not saying my experience is the norm. There are very few individuals who stopped the big O, so there is not much data.

          Yes, rebound risk is real. Mine left me with excruciating daily pain and mobility issues, requiring the use of a cane.

          To complicate my situation further, I didn’t have any cold sores for the past five years. However, when I relapsed in November, it coincided with a bad cold sore…….EBV????

          The interesting part of my recent experience is that Teri effectively regulated my CD19 b-cells. Since they were already depleted from Ocrevus, once Teri started working, my CD19 dropped and the relapse stabilized. Went from 0/ul, to 2/ul, up to 32/ul, then dropped back down to 10/ul and has remained at that level since🧐

    • Are these people worsening because of ocrelizumab or despite of it? How could we untangle those two options?

      Need to dig into this, have a neuro appointment soon and am less than convinced ocrelizumab really works for me.

      • I remember one of the MDs wrote in a post that an hypothesis for worsening after ocrelizumab could be related to the cytokine release after the drug kicks in after the first infusion(s). I had a very very small worsening for my slightly heavy leg while visible improvement for others small things (tingling disappeared in less than 24 hrs from infusion). It made me imagine that ocrelizumab killed the cells that were poking my brain… just fantasy. I would have preferred to see improvements elsewhere (eye) but that’s fine anyway for me, I am still functioning. I am due the first full dose in March so I will be able to tell more. Maybe ProfG wants to start a survey?

        • Fabio/Aanon,

          So in my case I have had this MS thingy for circa 10 years and have not been on any DMTs. Relapses occurred after illnesses (colds) and never following anything else. My current walking/balance issue occurred 1 day after the 2nd half of the first dose, i.e. this is not a coincidence. Fortunately we did think this was due to “cytokine storm” and indeed the issue went away after 1-2 weeks. BUT…

          I had peace and quiet for 1-1.5 months and then persistent walking/balance issue reappeared since 3rd November and are present till today. I am quite confident in saying this was something to do with the Ocrevus (my last cold was in January 2020). Also a lot of people on the link I included seem to have this type of worsening.

          Prof G – any thoughts? MRIs most likely won’t show enhancing lesions since Ocrevus is good at dampening these, but how can we assess whether to continue treatment (and risk worsening) or stop treatment (and risk relapse due to rebound activity)?

          • This issue is raised in each Q and A session but I have not yet seen a response to it, unless I have missed it (sorry in advance if I have). It is very pertinent given the amount of patients now being treated by ocrevus. Any chance of a post on this topic MD?

            Personally, i am due my first full infusion next month. I’ve had a miserable time since my last one with persistent sensory symptoms, a relapse, and generally feeling ill every day! I was very optimistic about starting treatment but i am less than confident now

          • What is the specific question?

            The sensory symptoms and the the relapse are neurological, one asks why this was not stopped

    • Sorry MD, i could not reply to your post of 11.15 (maybe maxed out no. of replies) so have used this one instead as the original post. The specific question from Coronakon was whether those who experienced walking difficulties following ocrevus would return to their previous level of capability after discontinuing treatment? to expand on this, is there a theory as to why the drug has this affect? it does not seem uncommon in the various ocrevus groups and i have said before, for a drug not to be effective is one thing but to actually make things worse is another. Yes, MS is a degenerative condition so some worsening is inevitable but the cases that i am talking about appear directly attributable given the short timefarme between commencing the drug and experiencing walking / leg issues. Thank you

      • I am not a neuro and have not experience.

        The suggestion is that a brake is being removed, I can see in the literature their are cases and some signs may improve after but not sure of the cause..time for some reading

        • OK thanks for the reply MD……sounds like going to a dodgy mechanic. Fixes your gearbox but a month later your brakes fail and you’re back in the chop shop :-). Happy to do some reading if you can point me to the right place. I have looked before but probably in the wrong place. A number of patients say that persistence is required and things improve after 2 years but its obviously hard to hold your nerve for that long….particularly when they are already frayed

          • I meant reading for me…A cytokine release syndrome from cell destruction could cause
            worsening but one would think it is transient.

            One for the neuros to discuss and explaain

    • https://multiplesclerosisnewstoday.com/news-posts/2021/01/19/besides-b-cells-ocrevus-targets-pro-inflammatory-t-cells-in-primary-progressive-multiple-sclerosis-ppms-study-finds/

      However, some subsets of pro-inflammatory B-cells were increased, indicating that some B-cells can “promptly arise” after Ocrevus treatment and that “anti-CD20 treatment does not reconstitute a fully healthy immune system or re-establish immune tolerance in all patients, supporting the need for retreatment,” the team wrote.

      An explanation?

  • Best wishes to all!
    I have a question about EBV and MS/DMTs.
    Given the possible/probable anti-EBV effects of various DMTs (notably glatiramer, teriflunomide, B-cell depletion), and given the association between EBV reactivation and MS relaps, could it be hypothesised that if a patient has one or more EBV reactivations using a particular DMT, that DMT is perhaps not quite so effective for that patient, even though no new lesions appear on MRI? I realize it’s speculative, but I would like to read some thoughts on that.

  • i always find mri results very basic, they never mention brain volume loss or anything significant ie lesion count, types, they normally just say when there is new damage.

    my question is, are these measurements taken and not included for a reason ? if so how would one get the results and please dont say your neuro as most of them are barely contactable.

    • There are time and costs attached to every thing even if it is an internal cost, I am not sure these are standard measures and part of standard reporting. I am not a neuro.

    • If you are in the US, try having the MRI performed at a major university with a MS center. I have found the experience to be night and day.

      MRI performed at my local hospital has a general radiologist performing the test, the report is vague, 1.5 magnet, and I am lucky if my neuro even mentions the results at my next appointment.

      Compare that to my MRI at a university MS center (5 hour drive from my house). T3 magnet, MS specific radiologist, report is very detailed about lesion load and brain volume loss, includes cervical spine, plus the neuro meets with me directly after and goes over the results.

      Best of luck!

  • Discontinuation of certain DMTs is associated with rebound relapses. Is there evidence on what drives those rebound relapses (e.g. infections,…)?
    Discontinuation of other DMTs would seem to be possible without fear for (severe) rebound relapses. Is it known why?
    And are there prognostic markers that could help assess the risk of rebound relapses in individual cases?

    • see above. The wrong approach is to use peptides when the approach can make protiens, but people will buy it. We did DNA vaccines the approach wasn’t good enough maybe we should restart the tolerance approach s it is a way tomake protiens/

    • I am wondering how one designs a vaccine without knowing what pathogen to target.

      Maybe shooting at EBV would be an option?

  • Hi,
    Any new updates regarding deaths / how pwMS fare who are taking Cladribine now with new variants of Covid?
    Thanks

  • Are there any neurologist/doctors in Canada that have arrived to the same conclusion on EBV and ms that i could maybe have as my treating neurologist ?

  • Would you be able to shed any light on the significance (if any) of Virchow-Robin-Spaces in MS? They were on my first MRI report at diagnosis and although the doctor didn’t mention anything to me during my appointment to get the results of my latest scan yesterday, they were talked about on the print-out I got to take home. I googled (sorry), but saw the words “Alzheimer’s” and “small vessel damage” and decided not to go there. Thank you!

    • Sometimes better not to google, but then here is your top Google result: https://radiopaedia.org/articles/perivascular-spaces?lang=gb which provides a good overview. VRS are are part or nornal brain anatomy, and even most of the “enlarged” VRS are seen in otherwise normal healthy brains. There is some discussion around whether they can be used as an imaging biomarker in MS or other diseases (like atrophy/loss of brain volume or lesions), but it’s rather a niche science, and I personally don’t expect it to play a major role predicting anything in MS any better than other (MRI and non-MRI) measures already do. Prove me wrong!

    • It is an anatomical space found by Vichow and Robin, on the report you may have seen brain is is an anatomical entity…Google brain and you may get alzheimer google blood vessel and you may get CCSVI. A blood vessel is in fact a double skinned vessel and the space between that skin is the virchow -robin space. A perivascular space, also known as a Virchow–Robin space, is a fluid-filled space surrounding certain blood vessels in several organs, including the brain. When a white blood cell tries to get into the brain it has to get through two layers. The blood vessel cells and the membrane below the blood vessels cells. Cells get through layer one and accumulate around the blood vessel as a perivascular (around the vessel) cuff. The cells can try and get into the brain tissue (Parenchyma) or they can move up and down in the space between the blod vessel wall and the brain tissue.

  • There’s an article on Sky News website, about long covid and includes neurological symptoms. The article mentions three medics that are suffering from long covid, and one is suspected to have damage to their spinal cord due to covid.
    This does concern me, that getting covid could trigger an MS relapse.

    Has this been the case? Thanks.

    • Thanks isnt it interesting that the
      autoimmunity is not against myelin proteins…every healthy person has autoimmune cells in them

  • Odd question…..any cases of Teri causing brittle bones? I have found cases of hair loss and finger/toe nails falling off. However, I could not find any case reports of brittle bones due to Teri.

      • I had the same thought; however, most RA patients have existing bone issues and also take methotrexate, so the data is somewhat skewed.

        I did find some articles related to tooth loss in MS patients on Teri. https://pubmed.ncbi.nlm.nih.gov/29982109

        Hair, nails, and teeth are bone related, so it is reasonable to assume when a 39 y/o pwms coughs and fractures 6 ribs…..it is most likely related to recently initiated use of Teri, when all other factors are excluded.

        I also found the following article during my research and thought it was interesting.

        Bone loss and fractures in multiple sclerosis: focus on epidemiologic and physiopathological features https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3150171/

    • Sure…my first though when I saw interleukin 6 as the treatment was bugger as anti-interleukin 6 is a treatment for arthritis and NMO and so it should be bad but it is not really about IL-6 but some nerve growth factors. Now one thing to be said mice are quite resilient when they have spinal injuries but interesting.

  • I’ve been reading about upright MRI scanners and what they can detect that a standard MRI scanner can’t. It’s interesting the patient can tip the head forward and back in the upright MRI, when sitting up and show CSF, fluid flow issues. I’m interested to know how this relates to MS and there does seem to be a little amount of literature on this.

    I know upright MRI scanners are less clear than standard MRI scanners.

  • How can someone be diagnosed with MS, in particular progressive or advance M, if they have no lesions. As MS means multiple scaring or many scars.

    But I know of some pwMS who have no lesions and were given the MS diagnosis. Hmmm..

  • Has anyone watched the following?
    BBC 2, Silenced: The Hidden Story of Disabled Britain. Available on BBC iplayer.
    https://www.bbc.co.uk/programmes/m000rh1g

    ‘For more than a century, one group of people in Britain has been shut out of society, denied basic human rights and treated with fear and prejudice.
    Now, in this shocking, moving film, writer, actor and presenter Cerrie Burnell is going to uncover the hidden story of how disabled people fought back – and won their freedom.’

    • Yes, overall very good, but like all history, she didn’t interpret it in context. Historians tell me what separates out card-carrying professional historians from amateurs is the ability to contextualise history. Unfortunately, Cerrie Burnell is an amateur historian; it is a pity she didn’t allow the professionals more airtime.

  • Marron 5
    Sugar, yes please
    Would you come and put it down on me?

    :^)

    Parkison disease

    Question Is use of glycolysis-enhancing drugs, such as terazosin, doxazosin, and alfuzosin, associated with decreased risk of Parkinson disease compared with use of tamsulosin, a drug prescribed for similar indications but which does not enhance glycolysis?

    Findings In this cohort study of 147 248 propensity score–matched pairs of terazosin/doxazosin/alfuzosin users and tamsulosin users from Danish nationwide health registries and the Truven Health Analytics MarketScan, the use of terazosin/doxazosin/alfuzosin was associated with a 12% to 37% decrease in Parkinson disease risk compared with use of tamsulosin.

    Meaning Use of terazosin/doxazosin/alfuzosin may lower the risk of developing Parkinson disease.

    Association of Glycolysis-Enhancing α-1 Blockers With Risk of Developing Parkinson Disease

    https://jamanetwork.com/journals/jamaneurology/fullarticle/2775976?guestAccessKey=d1ca62a0-ad21-42ce-bfee-1ecdedc5c10c&utm_source=silverchair&utm_medium=email&utm_campaign=article_alert-jamaneurology&utm_term=mostread&utm_content=olf-widget_02082021

    PPMS

    Together these data suggest a condition of ‘virtual hypoglycosis’ induced by the CSF of progressive
    patients in cultured neurons and suggest a critical temporal window of intervention for the rescue of the metabolic impairment of
    neuronal bioenergetics underlying neurodegeneration in multiple sclerosis patients

    A metabolic perspective on CSF-mediated
    neurodegeneration in multiple sclerosis

    https://www.researchgate.net/publication/334492625_A_metabolic_perspective_on_CSF-mediated_neurodegeneration_in_multiple_sclerosis

    Als

    ALS patients may benefit from more glucose

    The study revealed that when ALS-affected neurons are given more glucose, they turn that power source into energy. With that energy, they’re able to survive longer and function better. Increasing glucose delivery to the cells, then, may be one way to meet the abnormally high energy demands of ALS patients.

    “These neurons were finding some relief by breaking down glucose and getting more cellular energy,” Manzo said

    https://medicalxpress.com/news/2019-06-als-patients-benefit-glucose.html

  • Why in your opinion is Ocrelizumab more effective than Cladribine if Cladribine depletes a larger variety of cells?

    I would like to go on Cladribine as I have failed Copaxone and Tecfidera, and Clad look attractive, but I am wondering whether going on Ocrevus would offer a potential for a more long-term remission.

    Looking forward to your reply.

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