Sunday, 1 May 2016

Unrelated Blogger Comments-May2016



Sometimes you want to say something unrelated to the threads . This is the place for you

52 comments:

  1. Some may feel this was covered with MDs post a few days ago. And in part it was. But Prof G, if you could comment on the recent Alemtuzumab data it would be much appreciated.

    I had my first course of Lemtrada a couple of months ago after two years of research. Not once was the idea of retreatment based on T cell levels mentioned. How is this linked at all with the success of Lemtrada? Couldn't T cell levels rise without causing a problem?

    One reason why I chose this treatment was because it offered the chance of long term remission. Smashing the immune system repeatedly can't be good in any respect!

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  2. I have SPMS otherwise in perfect health. Assuming nothing else gets me first, how will I die?
    Not being morbid, just interested to know what lies ahead.

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    Replies
    1. I don't think SPMS kills people, if I understand correctly? Only a small minority reach EDSS 8 onwards, I think most people plateau under or at EDSS 8 and progression seems to slow or stop thereafter, and they go on to die of other causes. Correct me if I'm wrong though.

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    2. Dear Judy, this is a morbid question - unless it's something that's has been on your mind? In a majority of cases it is by natural causes. Since the introduction of DMTs the high EDSS (with greater disability) are not common, i.e. being bed bound. Here the risk is with acquired infections esp when there are breathing problems.

      Previous posts:
      http://multiple-sclerosis-research.blogspot.com/2015/03/breathing-problems-in-ms-unseen-entity.html
      http://multiple-sclerosis-research.blogspot.com/2015/06/clinicspeak-co-morbidity-and-ms.html
      http://multiple-sclerosis-research.blogspot.com/2015/06/clinicspeak-ms-comorbidities-and.html
      http://multiple-sclerosis-research.blogspot.com/2014/08/causes-of-death-in-msers.html

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    3. why are conversations about death morbid? they're not and it's not at all a morbid question. it's quite natural. According to google, morbid means being "characterized by an abnormal and unhealthy interest in disturbing and unpleasant subjects, especially death and disease." I don't see how a question about the future and death of a patient with a disease is not an abnormal or unhealthy interest. Unless you meant to say "this is NOT a morbid question - unless it's something that has been on your mind?"

      Bojana

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    4. Call it a medic thing, when you spend most of your career dealing with this question from your patients it becomes a defensive mechanism.

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    5. Thank you for response. Sorry, but MS patients (and people) deserve doctors who are not defensive. i'm really distraught that a natural and logical question about death from an ms patient would be 'labelled' morbid (aka shutup and don't think about it cos it makes me uncomfortable). what if you were an oncologist - would the question still be morbid?

      Bojana

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  3. Is this blog stuck in a rut and running out of relevance?

    I ask this because reading material here has become like a Smiths song: Every Day is Like Sunday

    It's the same old, same old. There are no new ideas. No mind-blowing vision. It's become institutionalised.

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    Replies
    1. I don't think it has run out of relevance. I have relapsing MS and this blog gives me a little shot of hope each day when I open it up, that there might be some new study or new discovery or new drug in the pipeline for me to read about. Most days there aren't exciting trial results or investigations for them to report on, but when there are new drug trials I think this is the best place to get interpretation and context. If you don't like this blog please just stop reading it and please don't encourage them to shut this blog down because I still find it useful and I think several others do too.

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    2. What new idea do you want?

      T cells are the cause of secondary progression?

      HSCT is the way to go?

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    3. Something good. For everyone.

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    4. Look I follow this blog for almost 02 years, every day, and every day I learn a little more, I'm sure that I'm exercising my brain to read subjects that aren't of my daily practice.
      And I see the commitment of people seeking solutions to our problems. And I recognize and am grateful for it.
      See the announcement of Daclizumab and Cladribine done in recent days. For those who have MS Progressive perhaps the scenario begins to be changed when Ocrelizumabe begin shipping in bulk.
      Only time will show, I know time is also our problem, but nothing comes of a sudden is not exhaustive work.

      Again I say no longer live in the period of "scientific epiphany", all currently requires a lot but a lot of money to be put into practice, we created the "monster" to the "save us" but this same monster devours us the little bit...
      So if you really want to see something happening and live in the UK, and is able to look for such part of the study MS-PROXIMUS on neuroprotection.
      More still if you have Progressive MS, this will be a big step for all, we need Neuroprotective. And the addition of anti potent inflammatory (Cladribine, alemtuzuLook I follow this blog for almost 02 years, every day, and every day I learn a little more, I'm sure I'm exercising my brain to read subjects that are not of my daily practice. And I see the commitment of people seeking solutions to our problems. And I recognize and am grateful for it. See the announcement of daclizumab and Cladribine done in recent days. For those who have MS Progressive perhaps the scenario begins to be changed when Ocrelizumabe begin shipping in bulk. Only time will show, I know time is also our problem, but nothing comes of a sudden is not exhaustive work. Again I say no longer live in the period of "scientific epiphany", all currently requires a lot but a lot of money to be put into practice, we created the "monster" to the "save" but this same monster devours the little bit ... So if you really want to see something happening and live in the UK and is able to look for such part of the study MS-PROXIMUS on neuroprotection. more still if you have AT Progressiva this will be a big step for all, we need Neuroprotective. And the addition of anti potent inflammatory (Cladribine, Alemtuzumab, Ocrelizumabe, Natalizumab, etc.) more neuroprotection can change the destiny of us all, and allow science to focus on remyelination...

      And I'm convinced that the search investigations the genetic relationship + vitamin D + EBV infection will bring us many answers...

      If you don't think any of this then stop reading the blog and left for those who really appreciate science the only work done here...

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  4. Why have you not featured the rituximab vs fingolimod after tysabri study published recently

    http://www.news-medical.net/news/20160426/Rituximab-outperforms-fingolimod-after-natalizumab-switch.aspx

    Very interesting study !

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    Replies
    1. Why have you not read

      http://multiple-sclerosis-research.blogspot.com/2016/04/researchspeak-rituxumab-vs-fingolimod.html

      Maybe do some reading.

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  5. psychoactives to treat everything would be a nice way to go

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  6. Men are genetically more likely to develop MS and women may be more susceptible to developing MS due to gene-environment interaction, or not?!

    http://bmcneurol.biomedcentral.com/articles/10.1186/s12883-016-0575-6

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  7. Fluorosamine seems to promote remyelination. In what scale it would be compared to Clemastin and Anti-LINGO 1?

    http://www.nature.com/ncomms/2016/160426/ncomms11312/fig_tab/ncomms11312_F6.htm

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    Replies
    1. The work presented in this paper are very preliminary and need to be transferred from mice into humans. The focus is on reducing the scar formation in lesions to allow myelinating cells to grow.This is a different presumed mode of action to anti-LINGO 1/Nogo 66 and clemastine. We'll see how it does in humans in a Phase II study - I assume they'll be testing it in optic neuritis like remyelinating agents before it.

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    2. Thanks NDG!

      I'm even glad to see another substance is ascertained to promote remyelination, even in mice, because "hope is the last to die"...

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  8. Dear NDG,

    Follow on from your 'use it or lose it' piece, just opened my first real padlock without the key!

    When I did the 9 peg I was told I was slow so I bought a clear padlock and pick set in January. The clear padlock allows you to see the pins move into place so it is good training. It's taken a while but I finally just opened a real lock! Whoo hoo.

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    Replies
    1. Each to their own! I personally jump over fences in such situations - which I did last w/e having locked myself out ;)

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  9. I was once told that high signal T2 lesions seen on MRI showed areas of demyelination. If follow up scans show no high signal in that area does that mean that remyelination has occurred. Also does this only happen in RRMS or can it happen in PPMS and SPMS too.

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    1. Up to 30% of lesions have been reported to disappear on follow-up. If these were demyelinating lesions, one must assume remyelination has occurred as part of the repair process. However, even remyelinated lesions may appear hyper-intense on T2 weighted MRI, so it can be difficult with standard MRI techniques to make a judgement call. Here is where so-called quantitative MRI techniques, such as relaxation time and magnetisation transfer mapping, and diffusion MRI can sometimes help as these are able to detect tissue changes in areas that look normal on standard scans, for example in areas where previously a lesion had been spotted. Remyelination & repair are less likely with increasing age and disease duration, hence you will find "vanishing" lesions much more often in people with (early) relapsing rather than progressive MS.

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    2. Thankyou, on a scan 2 years ago I had 2 spinal cord hypertense T2 lesions. On my last scan there are now no hypertense T2 or T1 lesions. GP has given me the report so am waiting on what neurologist has to say.

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    3. Sounds good. T1 hypo(!)-intense lesions are much less common in the spinal cord than in the brain. Not sure it has been assessed systematically (probably has), but my feeling is one finds more "disappearing" lesions (on T2 weighted scans) in the spinal cord than in the brain. This may not have anything to do with pathology but rather with the more challenging environment (vertebral column) for image acquisition of the cord.

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  10. When I had my first MRI scan I was not given contrast. I have been informed it is normal not to give contrast on first scan. The second scan six months later I was given contrast.

    Why do they not give contrast on first scan? thanks.

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    Replies
    1. It depends, a basic protocol doesn't include contrast (for example, for headache). If ?demyelination was in the request then most protocols include a post-contrast scan. Sometimes, if there is no kidney function result on the system, the radiographer may decide not to give contrast as it's unsafe in those with abnormal renal function.

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    2. Thanks. I had vertigo and double vision when I had my first scan but I did have a bout of severe vertigo, sensitive eyes and fatigue three months before (recorded by GP).

      I just wondered because if I had my first scans done without then with contrast it may have shown lesions in time. I had multiple lesions on the first scan in brain and c spine. I do think I would have fitted the MS criteria then. Old lesions and new enhancing lesions.

      If I had contrast with the first scan I could of been diagnosed with MS instead of CIS. Meaning I could have started DMT ten months earlier.

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    3. early after my partner's ms diagnosis, we stumbled on a conservative neuro. we caught an enhancing lesion at my insistence on gad MRI - he wasn't going to do it. (of course, he subsequently forgot to request the gad on the MRI, which led to a new referral and a repeat MRI 2 weeks later which caught the enhancing lesion). The enhancing lesion was important at the time because the conservative neuro had labelled her with PPMS without waiting for a year of progression, on the basis of my partner reporting she had no recognisable relapses (at the time I doubt either one of us even knew what a relapse was). I've found that we've had to fight for most of the things my partner got from the MS neuro world - nothing's come easy. There are days when I'm so angry I want to scream from the mountain top - luckily I don't have MS and my partner's neuros can't blame my anger on MS messing my emotions. They tried that with my partner when I threw a stink about a botched LP then botched LP headache hospital admission in her name lol. I wrote the email that caused the stink and sent her from her account. She was lying in the neurology department 10 hrs after presenting to ER for LP headache and vomiting, without having received any hydration or coffee or pain killers at all (the drip the ER tried to put in blew her vein and the drip was then abandoned). In response to the stink I created in her name (she was wilted and sprawled on the bed, was in no shape to write anything lol), they accused her of being unreasonable angry and wanted to know if it was a symptom of MS lol. She has had other medical issues throughout the years and we've had a fair bit of contact with doctors - this was the first time I felt I walked into a tea cup party from Alice in the Wonderland. I wish the story ended there, but I could go on and on and on about what we call the royally mucked up hell.

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    4. For suspected MS patients having there first MRI scan I would have thought having contrast would be useful to show old lesions and new enhancing lesions.

      I think this needs to be added to the protocol.

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  11. I'm looking forward to the next MS case study put on this blog (when you get time to do it). These do help self manage my MS. I've been thinking of possible ideas...

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  12. I just ran across the article in New York times on studying Zika virus in mini-brain organoids (three-dimentional cultures of brain cells):
    http://www.nytimes.com/2016/05/10/science/a-window-into-the-workings-of-zika.html?hp&action=click&pgtype=Homepage&clickSource=story-heading&module=second-column-region&region=top-news&WT.nav=top-news&_r=0

    The virus kills neural progenitor cells; this correlates well with brain damage in fetuses. Killing of glial cells was also observed, and this is proposed to be responsible for viral damage in adults.
    Another important message: rapid drug screening is possible. The path from discovery to translational studies does not have to take decades.
    So, seemingly slow-moving MS research may also pick up speed dramatically when/if the key experiments are performed. Science is not predictable...

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  13. As per your UK guidelines is there any age limit for alemtuzumab or any other DMT? Are you ever too old?

    Is age a factor in decision making about DMTs?


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  14. Perhaps Prof. G has an interest in this case report: "Young-Onset Adult Hodgkin Lymphoma Diagnosis Associated With Multiple Sclerosis"

    http://lymphomanewstoday.com/2016/05/09/multiple-sclerosis-risk-young-adult-onset-hodgkin-lymphoma/

    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4841639/

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  15. Just a few questions about Tecfidera and monitoring
    Obviously bloods being checked regularly because of PML risk but does having a lymphocyte count between 0.5-1.0 mean you are open to other viral infections?
    Has the baseline MRI (recommended by EMA) become standard or do some people think this is overkill? What about those who were on Tecfidera before the recommendation came in?
    Are many centres checking sub-groups of lymphocytes? How does this help?
    thank you

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  16. I'm on Tecfidera and my lymphocyte count has been between 2 and 2.4 every three months. Been on it 18 months.
    Some information implies a way Tecfidera works is because it reduces lymphocyte levels. Mine have not reduced, does that matter?

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  17. Hi. Any chance someone could do a post about what mild MS is? I'm hearing from a lot of people with MS that they are being told they have mild MS while their experience of MS on their quality of life is the opposite of mild. A lot of the time this can involve symptoms such as pain, fatigue, toilet functions and similar. If someone who has relatively few lesions and/or relapses but a lot of symptoms relating to pain, fatigue etc and a low quality of life, what's "mild MS" referring to and how is this related to DMD treatment options?

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    1. Bozo Forgot the Docs can surely be better explained to you, but here in the Blog there are some publications on "Benign MS", who like many neuros call individuals who have a course of slower disease, with few relapses, injuries and sequelae.

      However it does not mean that the called Benign MS is 'free' symptoms of the disease, paroxysmal symptoms ...


      Prof. G, so it has already expressed in a publication, see the term "Benign MS" as a fallacy, since the "Benign MS" has nothing ...


      http://multiple-sclerosis-research.blogspot.com/2015/12/researchspeak-more-benign-than-benign-ms.html

      http://multiple-sclerosis-research.blogspot.com/2012/08/research-benign-ms-is-not-so-benign.html

      http://multiple-sclerosis-research.blogspot.com/2012/04/research-benign-ms-is-not-benign.html


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    2. Hi cinara. Thank you for your response, but I'm not asking about benign ms,I'm asking about 'mild' ms

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    3. In aus, all dmds are available to ppl with Ms as first line. Therefore, they must have basis to give some ppl say lemtrada over gilenya and vice versus at diagnosis. There is a paper currently on peer review that I talks about treatment algorithms and perhaps addresses the issue. But until that paper is released, I'm wondering what constitutes mild Ms. It may be that it's an off hand term to explain to patients that has no generally accepted meaning... But it's not the same thing as benign -mild Ms patients are receiving gilenya or cpoaxone etc. Is it mild because it hasn't hit dangerous areas of CNS (v someone who has a brain stem enhancing lesion) - as just one example. Is it mild because, while symptoms progress, the Ms doesn't appear hugely inflammatory (mildly inflammatory? Lol) - which is what dmds work on, etc.

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    4. At least here in Brazil neuros classify "Mild" MS as "Benign" ... Anyway, at least here and I think that in some countries is also well if the treatment is the public health system you start by DMDs 1a line (interferons and Copaxone), even if "Mild" MS ...

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    5. Type of clinical symptoms such as motor symptoms and brain stem symptoms. These would not be classed as mild MS.

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  18. Germany Study of Immune System response to Viral Infection "revives possibility of link between MS and Viruses", more specifically EBV and Cytomegalovirus...

    http://www.mdpi.com/1999-4915/8/4/105/htm

    http://multiplesclerosisnewstoday.com/2016/05/17/virus-derived-activation-of-the-immune-system-may-enhance-multiple-sclerosis-progression/

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  19. I think the following are important in the MS world. It's Mental Health Awareness Week this week.

    And it's International Clinical Trials Day tomorrow/Friday.
    "It provides a focal point to raise awareness of the importance of research to health care, and highlights how partnerships between patients and healthcare practitioners are vital to high-quality, relevant research." HIHR

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  20. hi, how do they give mice, rats and monkeys ms?

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    1. In the vast majority of cases you have to inject the animals with myelin antigens to generate an immune response against myelin which then causes an MS-like disease. Some are more realistic than others, our own model in the Biozzi ABH mouse is a shining example here ie it relapses and remits then becomes secondary progressive. allowing us to study several aspects of MS in the same model.
      Hope that helps.

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  21. Forgive me if I have not looked in the right place: Are you / have you commented on this?

    http://www.nature.com/ncomms/2016/160518/ncomms11626/full/ncomms11626.html

    http://www.n-tv.de/wissen/Ausloeser-fuer-Multiple-Sklerose-identifiziert-article17785466.html

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  22. I have been thinking that a low white blood cell count may cause fatigue. So I looked into it and yes symptoms of a low WBC may include weakness, fatigue, shortness of breath and recurrent infections.

    Those pwMS on DMF some have a low WBC and may have fatigue. It could be difficult to know if the fatigue is mainly caused by the MS or a combination of MS and having a low WBC.

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  23. All scientific papers to be free by 2020 under EU proposals.
    The Guardian.
    https://www.theguardian.com/science/2016/may/28/eu-ministers-2020-target-free-access-scientific-papers

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