Happy New Year Q&A Jan 2018

Happy New Year!

For those who want to say something unrelated to the posts this the place for you.

So whilst ProfG prepares a year that was, it is a two-way street 

This is a message I came across this Christmas from Lucy Woods,  she was 5 years old when she was diagnosed with MS. So as the year turns a message to us.

About the author



  • 2 year study suggests treatment with Gilenya (fingolimod) may limit cerebral gray matter atrophy in relapsing-remitting multiple sclerosis (RRMS) patients

    Assessing brain atrophy by measuring cerebral gray matter has gained particular interest in MS for several reasons. First, the volume of gray matter is less susceptible to external factors such as inflammation; second, gray matter atrophy may precede the onset of MS symptoms, and third, it may help predict some MS clinical disabilities.


    • I have been on holiday; actually a much needed holiday. We are trying not to overload you with too many posts. We also suspect readers are getting bored of hearing the same-old, same-old, stuff. Our aim is to spread things around a bit with other bloggers using the Barts-MS platform. This is why we want potential guest posters to contact us (bartsmsblog@gmail.com).

      I am still experimenting using Medium as a platform. I have bought into Evan Williams' philospophy about how Social Media should evolve. I am one of many who is trying to help keep good quality publishing alive.

      Thanks for the read.

  • Hi quick question alemtuzumab. In some patients if their white counts is 0 at day1 after treatment, Then 0.2 at month 1. 1.2 at month 2. 0.8 at month 3. How can the count go down if the drug alemtuzumab has left the body at month 2? If it's not the effect of the drug then what else can cause the count to go down?

    • The lab tests are highly variable and at month 2 there may have been another stimulus increasing the counts that was not present at month 3; for example an infection.

  • Hi I was wondering if the 'stand up wheelchairs' would be really helpful for some pwMS and help their independence? I can imagine they would be.
    Any thoughts?

  • "We also suspect readers are getting bored of hearing the same-old, same-old, stuff"

    … ineffective, extortionate DMDs.

    • I agree "bearms" with a very stagnant MS research world. Many MSers have become very disenchanted with the current disgustingly expensive, partially efficacious neuroinflammatory treatment model only, particularly in progressive MS patients. I do not feel optimistic about our future unless your MS is caught immediately right now and even then the NEDA is less than 50% with all current DMDs (excluding HSCT in early highly active MSers or disease < 10 years)

      However, I think sometimes we misplace our anger at the researchers at Barts MS for this miserable disease and that is not right either. I do believe that they are trying to help and appreciate learning online from them.

    • MD, do you think that everyone going on a DMD, like Ocrevus, should be tested for JCV status prior to initiating?

    • Do you get involved with MS research, as a person with MS?

      I do and it helps me feel I'm involved and contributing to MS research, I feel more positive about the future. I don't just mean being a participant on a MS drug trial. There are opportunities to be involved.

  • Hi. Has there been a policy shift on Alemtuzumab that 2nd dose is no longer guaranteed if there a been no response to the 1st I've been told by my nhs care provider. My 2nd round of Alemtuzumab will depend on my Mri after 6 months of the first dose

  • I think Luis had mentioned it at the comment section somewhere, so I will try to ask again:
    Is there a way to predict a relapse through B cell blood levels? (I am not referring to monitor the response to anti cd20 therapies). I think its mostly used to NMO patients.

    • You can certainly have a relapse with few B cells in the blood and we have yet to see the results for MS but Kim et al has been using CD27 memory B cell levels to determine retreat mentioned of NMO and has certainly reduced the relapse rate and it also helps reduce the number of rituximab infusions.The Five year data has been published in 2013 and the ten year data was presented at ECTRIMS 2017.

    • Good question

      As you know i had had hsct 1/5 months ago, and i am doing cbc´s and cmv and ebv blood screening every 15 days (hoppefully they are still negative)
      So last time i was with the neuro doc i ask to do also cd3 cell populations and cd 19 and cd27 cell populations to

      (base line from 2 months ago where whitin normal values)

      I ask neuro doc that same question about Nmo and cd19 and cd 27 screening

      He said that since in Nmo you have antibodies against

      auquaporin chanels ,you have to screen the b cell that

      produce those antibodies and keep them in a tight range .

      In neuro doc words ,since Nmo is a very dangerous disease he

      likes to see b cell total in the first year in 0.05 and then as a maintenance therapy no more than 0.1

      Eyestarday in went to do cd19 cd 27 hoppefully tomorrow i will have the results

      Hope that helps 🙂



    • I agree screening for aquaporin 4 specific B cells would be good but I am not sure this is done yet.

      Also not all NMO is aquaporin 4.

  • One more for the black swan 🙂

    Comparative Effectiveness of Rituximab and Other Initial Treatment Choices for Multiple Sclerosis

    This observational study of patients with newly diagnosed RRMS who are new to treatment demonstrates that patients receiving RTX displayed a significantly better drug survival compared with all DMT included in the analysis and a lower risk of switching because of disease breakthrough compared with platform DMT.



  • I see that Prof G is now posting research articles on his Twitter account (he seems to have ditched this blog IE no clinic posts). The posts on this blog have reduced in number and quality. Is it time to close the blog down. After almost 10 years the message has got through (treat early and hard) and we are now aware of the importance of brain health. Thanks for all your efforts.

    • "After almost 10 years the message has got through (treat early and hard)"…………….
      Sadly, I think there is much more to be done before we can say this is widely accepted so IMO there's life in the old blog yet 😉

  • Eu gives full backing to Ocrelizumab. How long now before nice gives backing? And clears the cupboard of ineffective injectibles. In my Opinion. Only the following drugs should be used RRMS. Ocrelizumab, Alemtuzumab, Natlizumab, Caldribine, Tecfidera. Period. Oh yeah daclizumab.

  • An innovative PET tracer can measure damage from multiple sclerosis in mouse models

    In the January 12, 2017 online issue of the journal Scientific Reports, a multi-institutional team based primarily at the University of Chicago Medicine and the National Institutes of Health, describe early tests of a novel minimally-invasive way to assess myelin damage using positron emission tomography (PET).

    These PET scans use a radioactive molecule designed to target voltage-gated potassium channels, a protein found on demyelinated axons. The PET images, based on the detection of this molecule, provide quantitative information about underlying biochemical processes. A PET tracer that can target potassium channels.


    • Yes interesting.

      If we can truly image demyelination
      then remyelination trials get a massive boost.

      It works on principle of targeting potassium channels that are not normally exposed unless there is no myelin.

      One confusion is the colouring. The areas of high myelin code green in the pet images compared to staining but based on the scale red is more intense than green so why are areas of lower myelin coloured red?

      I wonder if the fact that the label accumulates in the kidney will be of concern to use in humans. I don't know enough about PET

  • Ocrelizumab (Ocrevus) gets European licence for relapsing and primary progressive MS

    The European Commission has granted marketing authorization for ocrelizumab (Ocrevus) for the treatment of both active relapsing MS and early active primary progressive multiple sclerosis. This follows a recommendation from the European Medicines Agency in November that a licence should be granted.

    Active relapsing MS means people who are having relapses or showing new lesions on MRI scans
    Early primary progressive MS is defined as people who have had symptoms of MS for 15 years or less, have an EDSS of 3.0 to 6.5 and evidence of MS activity on MRI scans


  • Quick question. When accepting a job am required by law to inform them of my ms. For instance, if I don't and have a relapse. Will company health policy cover me? If I do inform them I suspect i will be turned down for the job. I have 3 interviews which looked promsing but at hr when i informed them inwas turned.

  • MD post last month: Rebound? What causes the emergence of disease after Alemtuzumab
    Having read your posts on neutralising antibodies and depletion, I'd previously asked, and you'd kindly replied to say that I was correct in thinking that it's important to have significant depletion following both rounds of Alemtuzumab.
    This happened for me – round one Nov 2016 and round two Nov '17.
    However, I've just received a copy of my MRI from December and it shows two new lesions, one enhancing and an old lesion that's now enhancing.
    Is there an understanding of rebound on Alemtuzumab that allows for depletion? Before seeing my consultant in March, I'd like as good a grasp as possible as to why depleters show evidence of failing.
    In addition to your posts, I've found information about rebound following other treatments prior to Alemtuzumab, but I was treatment naive.
    Myself and others will benefit from any insight/understanding you can offer.

    • Dear Go
      No treatment is infallible.

      Likewise I would not call this a rebound it could be simply disease reactivating. A rebound is a massive attack more common with the migration inhibitors.

      The failure rate of Alemtuzumab is about 50 percent.

      Likewise of there are two lesions there could have been four or ten without treatment. Hopefully they are clinically silent. Please don't answer that as I don't need to know.

      The question is were the lesions in December set in motion before the second cycle of alemtuzumab. I
      If you look at current papers they rebaseline to two to three months after treatment onset to account for this. So perhaps were you a good depletes in sept Oct Nov. Again please don't answer.

      Next were you a good depleter. The paper above does show that they can't predict this from looking at CD4 CD8 or CD19. However they are not looking at disease causing cells

      I have asked for the memory B cell data from Genzyme upteen times but have got nowhere. However even if the disease causing population is in there it may not be specific enough to see an effect.

      There question is can you get a third dose. This takes the unresponsive rate up. You will have to wait for your neutralising antibodies to hopefully disappear before December when you could have another infusion.

      If not you may have to switch if more lesions appear.

    • Morning and thanks so much Anon and MD for your replies.
      I did spend more time searching online last night and found and looked at the nih paper.

      I appreciate the additional clarification MD and was very pleased to have picked up last night on your point about rebaseline at 2/3 months post treatment. I actually found reference to rebaseline via a video from Aaron Boster. He makes very clear that the two rounds 12months apart constitute the full infusion and proposes a scan at 6 months following the second round to rebaseline. I am very pleased therefore that my consultant has a scan planned for me in six months.

      Whilst I can still wait on the impact of Alemtuzumab, it is beneficial to have your posts MD to know that 50% fail and that such a high percentage of us develop neutralising antibodies. I will most definitely be raising this with my neuro if needing to discuss a second lot of Alemtuzumab or having to switch.

      In addition to not having the memory B cell info from Genzyme, I think you've also referenced previously the limitations of the monthly blood tests, as well as your informing me yesterday that they can't predict from CD4,8 or 19. As a lay person, I have solely concentrated on lymphocytes. They fell through the floor and were slow to rise across the 12 months between the two rounds. I know this is important.

      I really hope that this communication between us is of benefit to others having or considering having Alemtuzumab. Every time I think I've a handle on it, I find I'm needing to enhance and refine my knowledge. This site and everything you provide on it is invaluable. The dedication and motivation you show individually and as a team is beyond compare, and consequently I really can't comprehend, and even resent those seeking to run you down or even abuse you!

      Btw I have to own I don't know what mitigation inhibitors are

      Have a good weekend
      With appreciation,

    • Thanks for posting 🙂

      Your post is of great insight and very helpfull

      I am also worried because my cd4+ are coming back

      129 Cells/ul , 1/2 months after hsct

      "Btw I have to own I don't know what mitigation inhibitors are"

      I think Md is refering to does Dmts that trap lymphocytes in

      the lymph nodes (Fingolimod,natalizumab)

      Ps: correct if i am wrong 🙂

      Obrigado Luis

    • Thanks luis for the support about my posting + explaining what mitigation inhibitors are. Now I fully comprehend what 'rebound' means.

      I've read the article you've kindly added, and understand it in very basic terms, as someone who is not at all medically or scientifically trained or knowledgeable.

      I am so sorry you have worries after your HSCT – especially as I, along with others on here, were wishing you every success with the treatment! I hope we, along with many others go forward well into the future!

      I may not be able to follow and understand a lot of the scientific posts, but I do understand that you make valuable contributions to the exchange of knowledge and opinions.

  • PS to my Rebound, Alemtuzumab question
    Do I recall ProfG posting that MRI shouldn't happen very close to having received treatment?
    What timescale does apply to assessing the efficacy of Alemtuzumab following both treatment rounds?

  • Deep grey matter volume loss in the brain drives multiple sclerosis (MS) progression and disability, and is particularly evident in people with progressive forms of the disease, a retrospective multi-center study suggests.


    However, a recent study found that Gilenya halts grey matter atrophy

    However, Gilenya is less effective than Tysabri in delaying progression

    The risk (assessed as hazard ratios) to convert to SPMS among patients treated with injectables was 0.31 (follow-up of 7.9 years), 0.23 with Gilenya (follow-up 4.6 years), 0.50 with Tysabri (follow-up 4.9 years), and 0.60 with Lemtrada (follow-up 7.2 years), compared to matched untreated patients. The higher the hazard ratio, the lesser the risk.


  • A question on cause of MS. Can taking protein supplements that have been broken into individual amino acids for quicker uptake trigger MS? As they would be small enough to breach BBB. Its popilar supplement amongst body builders. I notice my ms appeared when I started taking these supplements.

    • To which supplements are you referring to specifically, if I may? The issue with amino acids is not clear, but Copaxone is made from amino acids too. NAC has been mentioned here in the past for potential benefits and L Lycine is supposed to control EBV. Some patients also use L cysteine.

    • Their generally mixture including gultumine, carantine, alanine, etc. Sold as BCCA brand. Just not sure if any of these can mimic myelin proteins and trigger immune response once they cross BBB. I'd steer clear of.these hydrolysis proteins. I'm sticking to food sources for my protein sources.

    • Hello various Anons
      All proteins are broken down into amino acids in the digestive tract and hepatic portal. Individual amino acids are then absorbed into the blood for distributing and assembling into proteins as required by the body. As first anon said absorption might be quicker if you take individual amino acids. So peptide sequences that might resemble myelin protein cannot leap from the gut to the brain, which is why glatiramer has to be injected. I threw the OMS book across the room at the point where it said drinking milk is probably linked to MS and (quoting a rubbish paper) a protein in cow's milk strongly resembles myelin protein.


      Sorry gone off topic! First anon just stick with great food 🙂

    • Thanks AM, thanks Anon1. I had read that for milk too, lol. I dont know who indirect is the digestion to the brain, oral ALA significantly reduces brain atrophy (Class I evidence). NAC also seems to help neurological conditions such as autism and maybe MS. These cannot be achieved with just food. You want the good parts but not the bad parts :/

    • Multiple Sclerosis and Amino Acids

      As the essential building blocks of protein for the body, amino acids are receiving increasing attention for the important metabolic role they play in modulating health and disease. Recent studies have uncovered several crucial amino acid imbalances in patients with MS that may shed new light on how the disease develops and progresses.

      Relapses of MS are associated with periods of increased stress, and this stress is believed to increase the body's metabolic need for the amino acid tryptophan, a precursor to the crucial brain neurochemicals such as serotonin, melatonin and dopamine. One researcher has linked lower availability of tryptophan in the blood in MS patients with greater susceptibility to stress, and hence, increased vulnerability to progression of MS.1 Several amino acids play crucial anti-inflammatory anti-oxidant roles in the body, such as cysteine, glutathione, and taurine, which may safeguard against the neurodegeneration in MS.

      Patients with multiple sclerosis and other demyelinating conditions also commonly show critical deficiency of vitamin B12, signaled by high levels of homocysteine, which may exacerbate symptoms and/or hinder recovery.2,3 Westall and colleagues reported "extensive amino acid abnormalities" in MS patients. They noted that relapses of MS are preceded by gradual rises of glutamate, a month or two before each relapse, with levels peaking during the relapse and declining slowly thereafter.4 Other amino acid abnormalities reported in MS patients include elevated glutamine, asparagine, glycine, alanine and arginine.5,6

      Underscoring the significance of amino acids in MS disease conditions are numerous clinical trials that show treatments with copolymers of amino acids (e.g. glutamic acid, lysine, alanine, and tyrosine) greatly reducing relapses in MS patients, without incurring serious side effects.7,8

      Great Smokies' Amino Acids Analysis is the most comprehensive and sensitive assay available for urine or plasma analytes. Commentary is thorough and provides clear guidelines for possible treatment interventions.

      Related Information: Multiple Sclerosis and Oxidative Stress

  • Good debate MD on HSCT. Everyone had their say. But good call to Stop the debate also. No need to keep repeating same arguments. I notice from your comments that you were manually checking comments before publishing them. You do know there many apps which can auto filter spam. Matching on word patterns. I'm sure there are plenty of I.T people with MS that read this blog and would gladly help/advise.

  • An interesting report from an Ocrevus patient

    I received my half doses of Ocrevus in August. I have seriously had one infection or another since then and have felt like crap. In getting blood work for my next round next month, looks like I'm actually getting pulled from Ocrevus and won't be taking it anymore. My immunoglobulin levels are critically low. I have to do IVIG treatments ASAP. My wonder drug I waited to take for 2 years is not so wonderful for me. My neuro says he has had to pull a lot of his patients off of it. He thinks its too strong of a dose. He is suggesting going back to Rituxan only using the Swedish standards of 500mg every 6 months instead of the US 2000mg but it will be awhile before I can even do that.

    • I am not surprised with the FDA's decision. The evidence at present is simply an association and could be due to reverse causation. We need controlled trials to make this call.

  • Discovery may advance neural stem cell treatments for brain disorders

    "Being able to maintain viable stem cells in the brain could lead to regenerative therapies to treat injury and disease," says Jing Crystal Zhao, Ph.D., assistant professor at SBP. "Our study reveals a previously unknown but essential function of an mRNA modification in regulating NSC self-renewal. As NSCs are increasingly explored as a cell replacement therapy for neurological disorders, understanding the basic biology of NSCs—including how they self-renew—is essential to harnessing control of their in vivo functions in the brain."


  • Scientists supported by MS Research Australia have found that stimulating nerve cells in the brain promotes the laying down of myelin around these nerve cells. This protective layer allows neurons to work effectively and is often damaged and depleted by the immune system in MS.

    Pharmacogenetic stimulation of neuronal activity increases myelination in an axon-specific manner

    Mounting evidence suggests that neuronal activity influences myelination, potentially allowing for experience-driven modulation of neural circuitry. The degree to which neuronal activity is capable of regulating myelination at the individual axon level is unclear. Here we demonstrate that stimulation of somatosensory axons in the mouse brain increases proliferation and differentiation of oligodendrocyte progenitor cells (OPCs) within the underlying white matter. Stimulated axons display an increased probability of being myelinated compared to neighboring non-stimulated axons, in addition to being ensheathed with thicker myelin. Conversely, attenuating neuronal firing reduces axonal myelination in a selective activity-dependent manner. Our findings reveal that the process of selecting axons for myelination is strongly influenced by the relative activity of individual axons within a population. These observed cellular changes are consistent with the emerging concept that adaptive myelination is a key mechanism for the fine-tuning of neuronal circuitry in the mammalian CNS.


  • Ultrathin needle can deliver drugs directly to the brain

    MIT researchers have devised a miniaturized system that can deliver tiny quantities of medicine to brain regions as small as 1 cubic millimeter. This type of targeted dosing could make it possible to treat diseases that affect very specific brain circuits, without interfering with the normal function of the rest of the brain, the researchers say.

    Using this device, which consists of several tubes contained within a needle about as thin as a human hair, the researchers can deliver one or more drugs deep within the brain, with very precise control over how much drug is given and where it goes. In a study of rats, they found that they could deliver targeted doses of a drug that affects the animals' motor function.


  • Monash University researchers are set to conduct a large study into a drug that may thwart the progression of Multiple Sclerosis (MS).

    The drug, a small molecule called DITPA (Diiodothyropropionic acid), may offer protection to nerve fibres damaged by the disease in the brain, spinal cord and optic nerves, as well as enhancing their repair.

    DITPA was approved by the US Food and Drug Administration (FDA) for use in clinical trials to treat a rare disorder called Allan-Herndon-Dudley syndrome (AHDS), which severely affects movement, and has been used in larger trials for cardiac problems.


  • Here we go again 🙂

    Removing obstructions in large neck veins reduced multiple sclerosis patients’ headaches for several years and reduced fatigue, British and Italian researchers have demonstrated.

    It was only about 10 years ago that researchers suggested that many MS patients have obstructed blood flow from the brain. The condition, called chronic cerebrospinal venous insufficiency, can be treated by inserting a catheter into the veins, draining the brain and spinal cord. The catheter carries a balloon, which is inflated to open up the blocked blood vessels.

    The method is called balloon angioplasty. Despite its common use, it is considered controversial, researchers said — partly because studies are not in agreement about its benefits.


    • The dead horse being flogged is so far gone, it's skeletal 🙂
      No doubt this will be hailed as great news in the believer community.

  • Is there any correlation between dmd efficacy and activity location?
    For example would cervical/thoracic activity influence choice of drug?

  • And non-hispanic whites, especially females, are more likely to die from multiple sclerosis (MS) than any other racial group, though blacks tend to die earlier, concludes a study by researchers at the University of Southern California's Keck School of Medicine.

    What would ethnic differences also have to say?


By MouseDoctor



Recent Posts

Recent Comments