Unrelated Blogger Comments – February 2013

Sometimes you want to say something that is unrelated to the threads. This is a spot for You. Previous comments can be got at on the posts on the right of the main page.
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About the author

Prof G

Professor of Neurology, Barts & The London. MS & Preventive Neurology thinker, blogger, runner, vegetable gardener, husband, father, cook and wine & food lover.


  • 1. How EBV/HERV-W theory fits with Na+/K channel blockers? Aren't they completely different approaches?
    2. Is Charcot project aiming same target as H. Perron? If does, do you think that your drug could be approved sooner than GeNeuro treatment?
    Thank you!

  • Yese they are different approaches one aims to go at a potential cause of disease the other is to deal with a consequence of disease.

    HERV are one target of the charcot project which is what peron is targetting but we have a broader view.

    Could our drug be approved sooner than the GeNeuro tretment it depends if they work first of all.

    The difference is type of drug if antibody needs to get in cell and in brain it is a hard ask compared to a chemical drug but antibodies have their advantage. If they both work equally well would you prefer a pill or an infusion. Answer is a no brainer.

    The drug for part of the charcot project is all ready approved for human use, this is just a repurposing and has a big pharma compnay backing the study.

    • I don't think the pill/infusion answer is not a no-brainer. There are enough reasons to prefer either one over the other

  • This is a basic question I could look up but I think you will probably give a better answer in the context of MS.

    I'm under the impression that myelin only exists on the nerves in the brain and spinal cord because nobody ever talks about demyelination in the arms and legs of MS patients. Is that correct? If so, how are the nerves in the rest of the body able to function without it and why can't the brain do the same? Also, where are the borders of where myelin stops coating nerves?


    • There is myelin on most peripheral nerves which is made by Schwann cells (similar to oligodendrocytes in the CNS). Not sure if there is demyelination in these in MS but will have a search to see what is known.

    • Hi Matt,
      Just had a quick look and it seems that peripheral nerve demyelination is not a great problem in MS which begs the question why CNS myelin is lost and not peripheral. Suggesting that the purely autoimmune hypothesis may not be robust?

      Clin Neurophysiol. 2008 Aug;119(8):1829-33. doi: 10.1016/j.clinph.2008.04.010. Epub 2008 May 20.

      Peripheral nerve demyelination in multiple sclerosis.
      Misawa S, Kuwabara S, Mori M, Hayakawa S, Sawai S, Hattori T.

      Department of Neurology, Graduate School of Medicine, Chiba University, 1-8-1, Inohana, Chuo-ku, Chiba 260-8670, Japan.

      To elucidate the frequency of peripheral nerve demyelination in multiple sclerosis (MS). There are a number of case reports describing MS patients associated with demyelinating neuropathy, but its frequency in a whole MS population is unknown.

      Extensive nerve conduction studies were prospectively performed in 60 consecutive patients with relapsing-remitting MS. Multiple excitability measurements using threshold tracking were also performed in median motor axons and superficial radial sensory axons.

      Nerve conduction abnormalities suggestive of demyelination were found for 3 (5%) of the patients. Two of them developed clinically evident neuropathy, whereas the remaining one had only generalized areflexia in addition to MS symptoms/signs. In all the three, MS preceded demyelinating neuropathy by several years. Excitability testing showed that supernormality and threshold electrotonus at the tested sites (median motor axons at the wrist, and radial sensory axons at the mid-forearm) were similar in the normal and MS groups.

      MS patients do not generally have peripheral nerve demyelination, but approximately 5% of patients develop demyelinating neuropathy. The association could result from a common pathogenesis possibly due to epitope spreading during the long course of MS.

      Association of chronic inflammatory demyelinating polyneuropathy with MS is not frequent, but needs to be recognized as a treatable condition.

    • "begs the question why CNS myelin is lost and not peripheral."

      The obvious answer is that it may have to do with the fact that different kind of cells perform the myelination (Schwann vs Oligos). However, a careful observer would find another major difference: CNS is compartmentalised within the scull and the vertebral column with no room for anything redundant, whereas the rest of the human tissue sits more comfortably around the bones.

    • BTW VV don't take that as an endorsement of your pet theory! Also did you get the email from MD? We'd really like to see your response so please reply.

    • I find it a little disturbing that this isn't a bigger question. If there is also peripheral nerve demyelination it would seem to change the game dramatically. One obvious place is that PPMS might be more peripheral.

      It also seems those nerves are more ready to lower risk direct observation on a living organism than the nerves of the brain and spinal cord.

      I'm kind of freaking out a little bit. I just don't understand how or why only very few people are asking this question.

      I also have one giant piece of circumstantial evidence for peripheral nerve demyelination: legs always seem to go first (with the longer nerves more prone to damage from peripheral demyelination).

    • In MS the dominant response is in the CNS you get damage in eye where there is no myelin but it could reflect effects in optic nerve which is myelinated.

      The peripheral nerve and central nerve myelin is not identical in the peripheral nerve there is one schwann cell to one nerve segment. In the CNS there is one oligodendrocyte to many nerve segments so it has to work alot harder,so vulnerable to cell stress, which is a trigger factor. In addition the peripheral nerve myelin is not the same the myelin basic protein can be different because there are alternative ways the DNA can be read to make myelin of differnt sizes and CNS nerve has a variant of proteolipid protein and produces myelion oligodendrocyte specific protein and other proteins that are not found in peripheral nerve. When peripheral nerve demyelinates it results in a condition called Guillain Barre Syndrome, this can result is cessation of breathing.

      So if you immunize an animal with spinal cord you get CNS disease and if you do the same with peripheral nerve you get peripheral nerve disease (called EAN neuritis not EAE-encephalomyelitis). It shows that the immune system can recognize the difference between CNS and periheral nerve myelin. In MS and EAE you sometimes get schwann cells entering the CNS to remyelinate this could expose the CNS to peripheral nerve myelin and so peripheral nerve involvement could occur but it is limited.

      I am off to the gym will comment on other stuff when I get back.

    • This is such a big piece of information I didn't have before. It just shows the need for blogs like this. I am still surprised though that I have never heard of the differentiation between these two types of myelin. I wonder if I'll look back and start to see it (The Sixth Sense style) or if MS sorts do really tend to talk about "their" myelin as if its the only type.

      I just re-read the basic description of MS on Wikipedia. It sort of defines MS as a disease involving the myelin of "the brain and spinal cord" therefore future references to myelin technically only refer to that area of the body. It is odd in reading the article you would have no idea there is another type of myelin. I think that's what other MS documents do too.

      I just noticed the article also says the white matter of the brain is mainly composed of myelin. I guess this means on a percentage basis. If this is true it might help explain the dramatic brain shrinkage pictures posted. (Is this a correct conclusion?)

    • Not quite right about the legs and peripheral nerve. The problem is essentially all in the brain and the spinal cord. Wecan show that there is not a problem in the nerve trasmission through the periperal nerve using electrophysiology were we send electrical impulses down the nerves and measure responses the problem is in the central nerves and the altered nerve impulses occcur there. Now why the legs wellthis is the furthest the nerve impulses have to travel from the toes up to the brain and back again to the toes. Now imagine the spinal cord with nerves peeling off along the way so the ones that peel off at the neck control the arms and the ones that peel off around the peel off around the bottom bit of the spine control the legs. Now if you randonmly put holes in the spine from top to bottom you will see that are less chance of the pathways are the top being block but at the bottom there is much more chance that the nerve with have a break somewhere in the pathway. I'll do a diagram and show you were I'm going. Prof G may have a neurology teaching post. Tomorrow at the research day Marija will talk about the nerve impulse travelling and in health and MS and it may help abit alos when here video is shown.

    • This picture is a random picture of a London scene in the rain. I not sure if they have MS or any other disease to be honest. I will take the picture down if it offends you! I surprised you can identify the subjects in the picture; their heads are covered by umbrellas. The picture is from a TimeOut a London rag on what is happening in London.

    • The sad things about such petty comments is that we may be forced to switch off the comments feature. There are always people in the world who have an axe to grind and there are always people in the world who like to spoil the party! C'est la vie!

    • These are people in a street, where any paparazzi could stirke. There is no confidentiality issue here, the pictures posted here are all in the public domain

    • MD & Prof G this person is another killjoy and likely to be a troll. I can almost imagine the post in capitals. Please ignore them the pictures are fine.

    • Dear Anonymous (Friday, February 01, 2013 7:13:00 pm) or Killjoy

      We would prefer it if you didn't visit this site; you are spoiling it for me and the others who are genuinely interested in the posts.

  • I am so impatiently waiting for the Research Day videos – had to make do with Richard III and his bones for now – hurry up plz!

    • Hi Andy,
      Difficult to comment as the paper is not visible yet, need to see the details. When it is will have a look. This is a rat study and the relevance to MS may be slight as most of the rat models ain't great compared to our mouse model.

      You're right it is axon loss that's responsible for loss of function both in mice and humans and we need to find ways of slowing this down/stopping it.

      Good to meet you on Saturday.

    • Had a look at the post it is first, first, first, first

      What the study is getting at is that once myelin come off the nerve it doe not mean it is doomed to death at least not a quick death, I think it is reported something that we know must occur. Will do a post on this

  • "Had a look at the post it is first, first, first, first"

    Ian Duncan overselling his results? Surely not!

  • Anybody listening to the Today programme on Radio 4 this morning? A bloke with MND talking about how he would be willing to take a trial drug and accept the side effects and not sue rather than wait- he doesn't have the time. 2 big guns in medicine talking about the ethics, but one at the end said about a monoclonal antibody for MS that had gone through phase 3 trials in 2006 but just about to be licensed now, and thousands of MSers had missed the boat of opportunity in that time. Presume he was talking about alemtuzumab.

  • Hi.. I am a QMUL student, and currently deferring for a year, coz i got diagnosed with MS on Oct 2012..:(.. Is there any research that can be done on MS in Medical Engineering??

    • According to post, data is published in BMC neurology which show higher than incidence in MS than controls. This post suggests that this was removed from COSMO study. There is little merit in me investigating this, the data has been published and will appear here on last saturday of month. The COSMO study is out there also, but it matters not until the blinded analysis comes in. The AAN abstracts throws in more questions.

  • Concerning the Phenytoin trial, do you know if IV Corticosteroids will be administered on top of the phenytoin? If so, I guess both effects will be confounded, don't you think? Honestly spoken, this trial looks like the most appealing to RRMSers, as corticosteroids have a modest (if any) effectiveness

  • I will leave this to prof G to answer, but I thought that people would be given option of steroids as this is standard line of treatment, maybe not I do not know the final protocol

  • Well well the Troll seems to have won the day again. Can I please ask for the sake of balanced argument you take your stupidity to somewhere more suitable, perhaps a jury service given the debacle we've witnesed in the news.

    Re, Dr Reid and Dr Gilhooly, whilst I may or may not agree about operating out of their fireld of expertise, but before we go down a character assasination route, as I understand it, the Essential Health Clinic were trying to get a small study running in collabaration with Sterling uni re ccsvi, but found funding the obstacle.

    EHC led by Dr Tom Gilhooly are also at the forefront of Omega 3/6 balance and it's relationship to neurological disorders, Vit D and have are partneship with Stirling Uni looking closely at this relationship with MS.


    Whilst I understand the arguments of a vested interest and evidenced based medicine, some people do have passion to help others first and I would put Dr Gilhooly in this list, which given our experience over the last couple of months re Hospitals, rehab neuros, pain clinics, etc etc and the total lack of willingness to do anything other than tick boxes is a most refreshing change.
    There are others on this list, but to save anyone's embarrasment shall remain nameless and btw the invite to guest speak, the glass house proverb comes to mind.

    This probably makes no sense at all thanks to the comments being switched off under the vdeo posts. Once again thanks to Mrs Troll

    Regards as always

    • Thanks for the response Andy and I'll accept it that I do not know Dr Gilhooly and maybe I tarred too quick. I'll shut up and remove the comments

      By the way I wrote Franz schelling re guest post but the email on his tone did not deliver

    • If you are serious about guest posts, what about Dr. Fox of the Cleveland Clinic? He did that autopsy study on MS veins vs healthy control veins.

    • We could do this but i can tell you the answer that he does not believe there is a vascular cause , the troll Will arrive. you just have to read the blog about his views.
      What is the precise question you want an answer to. Make sure it is not leading with respect to answer.

    • Ok here are my best questions.

      Since the jugular veins were prepared for the study in a fixing material, how does that affect the ability of the researchers to see if the venous valve leaflets are stiff and unable to move? Could the silicon used to fix them hide the abnormality? Is there any other way to prepare them?

      Will your autopsy research continue beyond the ten MS patients and ten healthy controls currently studied? Are you interested in looking at any differences in intraluminal abnormalities between different subtypes of MS or different durations of MS?

      Your abstract conclusion stated that, "Although vein wall stenosis occurred at similar frequency in MS and non-MS controls, the frequency of intraluminal abnormalities with possible hemodynamic consequences was higher in MS patients compared to healthy controls." Can these intraluminal abnormalities be reliably identified noninvasively using Doppler ultrasound? Should there be imaging studies done that ignore vein wall narrowing and look only for these intraluminal abnormalities?

    • OK the answers to your question are now in and a guest post is waiting However we have agreed to wait until after the AAN March 16-23.

  • It is well known for spinal injury patients to recover limited use of their limbs that were initially paralysed. For example Melanie Reid, she writes a weekly column in the Times every Saturday, is now able to take a few steps using a rollator even though she was paralysed from the neck down because of spinal compression

    If and when there is a cure for MS, in other words when there is no further progress, would it be unrealistic for MSers to start to see some functionality restored to limbs that had been rendered useless by the disease.

    • I think this is a realistic possibility. However to go back to where yoi were before it started without some form of repair is a hard ask with what we know at the moment.

  • But who knows what is round the corner just heard this great talk from a guy from Harvard talking about an organ in a chip.
    The technology was ace. He got a prize well done and nothing to do with our discoveries who said i only think our stuff is good.

  • Sorry to bring this up again. What are the optimum Vitamin D levels for an adult and child of 12 years. My levels have come back as 35 despite taking Vitamin D and having had a week in the sunshine without sunscreen in December. My daughters levels were 19 and father 4 months treatment and a week in the sun also it is now 69. Is this satisfactory? Seeing GP this morning so would be grateful if anyone on the team could answer.

    • The levels should be above 75. However our ancestors on the African plains had levels consistently above 100 as do people with outdoor jobs.

  • I see that the Karolinska Institute have just published a paper in PLOS ONE on the use of imatinib (gleevec) in rats which they hope to translate into a trial for MS. It's a drug used in chronic myloid leukaemia, is taken orally, and is a pharmaceutical rather than a monoclonal antibody like alemtuzumab (a treament for chronic leukocytic leukaemia). It seems to prevent blood brain barrier leakiness and suppresses the autoimmune reaction. Another possible drug for re purposing?

By Prof G



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