Unrelated Blogger Comments April 2014



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  • April's Post:

    MS has been my entire life

    Hello to everyone my name is April I'm 39 years old with rrms. I was diagnosed definitively in 2004. This disease has been a part of my entire life. My mother also had MS. I have no memories of her walking. She was diagnosed in the late 60's when she was 16 years old. She did fairly well until after she had me the disease progressed rapidly (not saying pregnancy caused this). When I was 6 years old she had to be put in a nursing home. I would get to go visit her maybe twice a month. She would always talk about all the things we would do when she got better. She always had hope for a cure. She was so brave and fought the disease until the end. The day before her 41st birthday she passed away from complications of MS. I was 13 years old. I pray to god I will see a cure for this disease in my lifetime. I don't want my children or anyone else to ever have to hear the words "I'm sorry but you have ms" I'm so thankful for you all and all of the support you give. It helps so much to share with others who understand, because we are all in this together and share a common goal. To find a cure and see an end to Multiple Sclerosis!!!

    Dear April,
    Your post is as eloquent as it is touching. Would you mind if I pass your testimony on to some MS researchers who occasionally need encouragement? Thank you, April for perfectly clarifying why research is worth pursuing.

    Thank you for your kind words. You may absolutely pass this on. Hope is all we have and with the support from others like you it helps me to not give up hope. God bless you, you don't know how much your words mean to me.

  • Have the NEDA/early aggressive treatment arguments been aired in the parliamentary MS committee? Could we not do a massive lobby to this body? Or has it all fallen on deaf ears?

  • In a recent post regarding Tysbari you mentioned that in general neurologists have a higher risk appetite that ms'ers. However, as Tysbari carries a high risk of PML the longer you are on the drug, as well as a high chance of rebound-relapse if you come off it, I'm struggling to understand the risk vs benefit equation especially as it is not a cure.
    However HSCT treatments carried out by Dr Burt in the USA, Dr Federenko in Russia and other facilities are showing high success rates for RRMS, with a better success rate than any other treatments for progressive MS. As some HSCT trials now have 10 year + data with a mortality rate between 1-5% (as you have mentioned) is it not time for the neurology world to seriously start to consider this a viable option, instead of focusing on drugs to slow down progression? If this truly does offer a cure, is the risk profile of 1-5% mortality for a cure vs 0.85% PML risk not something you think ms'ers would be more willing to take. (and cheaper for the NHS is the long term)

    • The 5% mortality rate for HSCT was back in the days total body irradiation was used (approximately before 2000). Today, the mortality rate is more like 1% or less. I would definetly opt for this over Tysabri, but unfortunatley it is not on option. I can imagine that it won't be an option for a long time as the pharmaceutical companies cannot make money from this and it is a threat to their drug profit pipeline.

    • Mousedoctor – do the neruology community still believe a cure for MS is out there by using drugs? Or is it an accepted theory that HSCT could be future? Dr G's blog is very informative but rarely mentions HSCT. He last mention said it was the ultimate human experiment. but hasn't HSCT been used for years for other dieeases like Cancer?
      Would you if you suffered from MS consider HSCT as a risk adverse neurologist?

  • After following this blog awhile it has been stated that tolerance induction can be achieved by a one time "vacination" and therapies such as Copaxone should not need continuous administration. But, there is a fine line between activation and tolerance.


    So in reality, Copaxone may function by inducing tolerance. It is amazing a drug like this was developed as it is well ahead of its time and unique in that it may get to the root of the issue in MS. The inventors are true hero's.

  • Esophageal Motility Disorder
    Common in MS, but looking for why? Or is it a cause of adverse drugs?http://www.ncbi.nlm.nih.gov/m/pubmed/20227023/
    Or just another tidbit that has become part of me caused by MS effecting more muscles, those ineeded in swallowing. Taken for granted by everyone.
    Professor G any thoughts, studies, side effects of drugs, or??

  • Prof G,

    I'm really confused with regard to MS research i.e. the progress being made. As I look to the big research events in the next 6-7 months there is the ANN annual meeting and then the ACTRIMS / ECTRIMS conference. No doubt some more trial results will be announced, but are we likely to see any major breakthroughs? By that I mean a detailed understanding of what causes MS and what drives the disease? I thought research would through various approaches (brain tissue studies, analysis of CNS fluid, pathology studies) lead to a detailed understanding of the disease. However, the approach that has been adopted seems to work the other way round i.e. an approach where therapies are used and then the effectiveness of the therapy is used to try and understand the disease. So Alemtuzumab is being used to text (20 year experiment) whether MS is an auto-immune disease or not. The Charcot project using an anti-viral is being used to assess whether ebv / a retro-virus is involved in the disease. Is this the approach used in other diseases? It just seems the wrong way round to me.

    • I'm not sure what your attention has been focused on, but the consensus is that MS is an autoimune disease. There really is not going to be any big revelations. The drugs being deployed are to modify your immune system, and in the highly effective drugs such as Lemtrada it resets your immune system. Not to mention HSCT which does the same thing without pharma involment.

      Trials to attack EBV such as the Charcot project is in essence the acknowledgement that PWMS have immune systems that react innapropriatly to EBV. Prog. G may try to suggest something else, but deep down he knows this is the case.

      As far a progressive types, once meylin is destroyed your nerves start to degenerate. Maybe there will be advances in nerve repair, but the science behind what causes MS is no longer a mystery.

    • I thought you had invented a new word a "Scangos" turns out its George Scangos Biogen Idec Exec “To put it bluntly, patients will not be able to get access to therapies … if funding and insurance reimbursements dry up"

      Maybe a "Scango or should it be a Scangos" could new term to add to the armoury of MD blog words a money mad exec…. it has a nice ring:-)

    • Great. Another mechanism of action for BG12. Is there anything that his drug doesn't do? I think the fact that it suppresses your white cell count by 30% on average has a lot to do with its mechanism of action.

    • Neutrophils dogma says not alot. However the EAEers will say alot. In NMO neutrophils are common in MS less so

    • Is there anything it doesnt do………..does it get into the brain is a question I am not sure about.

    • It is said to be very similar to Quentiapine and the latter is certainly gets into the brain?
      Looks like nearly any drug that gets through BBB has some effect on the MS, even clemastine, heh

    • I think shift.ms is rubbish. It's a fey, middle-class hang-out that's as bland as they come. They spend more time feeling sorry for themselves than actually pushing things forward. It's like the BBC Three equivalent for MSers.

    • Oh, are you not supposed to have MS if you're middle class? I must be the exception to the rule because neither do I watch BBC Three.

  • Yes i know about this we will report on this when the full paper arrives. Anyway we know too much salt is bad for you but remember we do need salt. So another risk factor may be born and animal studies translate .

  • Prof Mouse,
    Do you have any thoughts on how cladribine has been supposed to work in ms? If it's mechanism is the same as with the alemtuzumab (lymphocyte depletion?), why lymphocytopenia was observed in only 1/4-1/3 of patients in cladribine trials vs ~100% on alem? And still it has shown comparable, if not exceeding, efficacy? Is it due to possible higher chances of the cladribine to get into the cns or something else?

    • We think it works because of it immune depletion, which you correctly say is not as aggressive as with alemtuzumab,but maybe you do not need complete depletion for affect and as you say also it can get into the brain.

      We can't work this in rodents because clabribine does not work in mice.

      I would not say it is better than Alemtuzumab but on the basis of published data looks similarin terms of efficacy. Maybe because you do not get so much depletion this is why you do not get the autoimmune problems associated alemtuzumab.

      A head to head seems in order as cladribine is clearly better from a safety stand point and wins hands down from a cost standpoint I think it was 20,000 euro for the abandonded Merck Serono version. and about 500 for the generic.

    • Thanks, Mouse Doctor.
      >"wins hands down from a cost standpoint"
      From this standpoints almost any drug is inferior to arzerra, around 200 euro per dose. Can't even imagine how much will they charge if they ever get the indication for ms. 🙁

    • Ofatumumab = Arzerra.
      You can guarantee it will not cost 200 Euro in MS look at example of Lemtrada and Alemtuzumab 🙁

    • P.S. In terms of cost that also could be 500 a lifetime (assuming it works) for generic cladribine not per dose. 10mg is £165 in UK this is not the NHS cost, I have seen it for $32 elsewhere.

    • Do you know why the Cs at Cambridge went for IV alemtuzumab in the 90's rather than IV cladribine? Was it because they knew they could get pharma on board if it worked?

    • No. They did it because alemtuzumab was invented in Cambridge i.e. CAMPATH-1H and at the time Hermann Waldmann and Greg Winters and co. were using this antibody in quite a few different conditions in humans and quite a logical thing to try in MS.

      Success in developing this agent no doubt has brought rewards to Cambridge University, cladribine.

      "They knew they could get Pharma on board"…..Ask the C's the story of CAMPATH and its relationship with pharma…it was anything but an easy and straight forward road to success and the drug was parked quite a few times along the way…credit to the Cs for being persistent and uncovering some interesting biology

  • Hope to see you Good Peeps later, how apt and timely the IJV reconstruction paper you've posted today is,
    Thank you for that, if I hadn't had to pop into work to print tickets off for MS Life may have missed it. 🙂
    Regards as always and see you later pal.

  • Could you please post the link to the ms life sessions recordings on youtube on the blog
    I think this would be useful for the people who was unable to attend the event

  • Professor G,
    Question about MS and the muscles of the throat, known as Dysphagia. As disease progresses will swallowing eventually become impossible? Dysphagia Seems like a problem… I know they are trying to treat the symptoms and slow the disease, but is there a progression you are managing things to here, or is it all case by case and we hope for the best? I tried looking this up, but the internet answers seem very vague, or nonspecific… get into bands of this and that, or this or that symptom, and not into any progression discussion -which may indicate it is always unique?

  • I would be grateful if someone in the know could answer the following question for me:
    What is the NICE/ABN definition of high risk for MS.

    I've been told the SPC definition if high risk when considering to use rebif and avonex following a CIS states at least 9 T2 hyper intensity lesions on initial scan and at least one new T2 or one new GAD-enhancing lesion on follow up scan.

    I can not find any information on this. Is this correct? What criteria do people with a CIS have to meet to be considered high risk of converting to CDMS? Is it subjective? I would be really grateful if you could provide clarity in this area.

    Thank you.

    A confused CIS'er.

    • Dear Confused CISer

      The info you require is the NHS England "Clinical Commissioning Policy: Disease Modifying Therapies for Patients with Multiple Sclerosis (MS)" document from April 2013  Reference : NHSCB/D04/P/a:


      It states:

      * Neurologists may, in certain other circumstances where the evidence for efficacy is less secure, also consider advising treatment after discussion with the patient concerning the risks and benefits. For example;

      (i) Patients within 12 months of a clinically significant clinically isolated syndrome when
      MRI evidence predicts a high likelihood of recurrent episodes (i.e. development of MS).
      This is on page 7 of the document.

      I hope this helps.

    • Thank you for your reply.

      I am aware of the policy you refer to and the quote above. What I'm trying to establish is what evidence on an MRI predicts high likelihood. Is there a certain quota of lesions needed. I've been told high risk is defined as quoted in the SPC for Rebif which is 9 T2 hyper intensity lesions on initial scan and at least one new T2 or one new GAD-enhancing lesion on follow up scan. Apparently this is recommended guidance from the DOH when considering if to start Rebif following a CIS.

      Is this correct? I cant find any information in NICE documents confirming this only what you quoted above. I've looked at the SPC for Rebif in regards to a CIS and it says there is no definite definition of what is high risk but a conservative approach would be the 9 lesions etc. I have read the EMA policy and it says they do not develop treatment guidelines yet I am told this is what neuro's base their decision on when considering Rebif following a CIS.

      Can you shed any light on this please?

      Many, many thanks.

    • Is anyone able to answer this please? I think I'm being told incorrect information and I'm really trying to establish the true facts.

  • Prof Mouse,
    to the best of your knowledge, is there any theoretical possibility, that occasional recreational psychedelic drug use (or abuse) can cause MS (or MS-like disease) in some person? Say tryptamines/phenethylamines/extasy for instance

    I found following abstracts, but maybe you are aware of something in more relation to neuro disease?

    Tryptamine induces axonopathy and mitochondriopathy mimicking neurodegenerative diseases via tryptophanyl-tRNA deficiency.

    Acute administration of 3,4-methylenedioxymethamphetamine induces profound hyperthermia, blood-brain barrier disruption, brain edema formation, and cell injury.

    Many thanks.

    • This sounds a bit like "reefer madness". (A film to demonise pot)

      MS. risk is the domain of ProfG and DoctorRuth, so I don't know for definite but would say probably not from occasional use. MS has been around a lot longer than Ecstasy.

      However, recreational drugs generally all mess with your brain and some in a bad way, and some in a very bad way. Because the drugs are elicit then there is not a lot known about them and the long-term consequences……so just say "No"..I never inhaled.

      I had a look at some of the references you pulled out and see these are in mice and not humans,

      Anything that stops an animal from moving causes hypothermia and you need to look at doses to know if they are relevant to human use often they are not

      If you look hard enough you will see the dangers of toothpaste or salt (easier to find).

      If you asked David Nut (ex drug Tzar)t..he would say the most dangerous and damaging recreational drug is alcohol.

    • Thanks Prof Mouse.
      By the way, do you have any general rule of thumb when it comes to dose translation from rodents to human?

  • Are you involved in one or both of the Laquinimod progressive trials?


    When will recruitment start to ARPEGGIO?

  • Dear Prof G & Prof Mouse,
    Sorry for asking advice there but…
    I'm tired with palinopsia which coincided with my last MS attack and does not seem to improve. Also my neuro does not believe that this is MS related and refers me to ophthalmologist which does not believe this is eye related and sends me back to neuro and so on.
    Is this complication actually so uncommon in MS? The data I can find myself is inconsistent, in some sources this is stated to be retinal or cortical feature, few say that this could be MS related.
    But there are few case reports I able to find on pubmed that suggests that lamotrigine may be of help with this at least in migraine and HPPD. I'm planning to insist on Lamotrigine prescription on my next appointment with my neuro. Is it wise to do so or may be anything else?

  • http://www.jaoa.org/content/114/5/368.full
    Wikipedia vs Peer-Reviewed Medical Literature for Information About the 10 Most Costly Medical Conditions

    >Conclusion: Most Wikipedia articles representing the 10 most costly medical conditions in the United States contain many errors when checked against standard peer-reviewed sources. Caution should be used when using Wikipedia to answer questions regarding patient care.

  • Professor G, can you elaborate on repository corticotropin injection, known as Acthar?
    Is it worth $36,000 USA for a 5ml vialto be injected?
    I only see vague reports from ACTHAR, but thought it may be worth try. And how much injections would be needed 10-20-30ml?
    Or should on just buy stock in Questcor , the manufacturer of Acthar, or Mallinckrodt, who is trying to buy Questcor?

  • ProfG and team, I am struggling to understand how NICE calculates a QOLY brought about by taking Fampyra to be £150,000 – can you please explain or point me in the direction of somewhere else to find this information? The cost of a private prescription for 4 weeks supply is c£190.

    Thank you in anticipation :

By MouseDoctor



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