About the author



  • The announcement was made in various media that a search would have confirmed the cause, as suspected, the Amyotrophic Lateral Sclerosis. They studied cases of ALS linked to mutations in the SOD1 protein and realized that SOD1 creates a temporary cluster of three molecules – the trimer. This trimer is very toxic to motor neurons, which leads to the death of these cells … I know they are different pathologies, but this study have any implications for MS, especially progressive forms? Because we know that the two conditions hold in common is the neurodegenerative factor. It has been researched enough on oxidative stress in MS then the SOD1 would have "something to say" about MS as well, since the SOD1 acts in apoptosis and destruction of free superoxide radicals?



  • MD: I know it happens (in Australia anyway), but my question is *should* it happen? Is it essentially risking brain reserve & wasting time?

    • It was a metaphorical place I was thinking about not a country:-), in places like New Zealand I understand they don't bother with the CRABs anymore, somone can correct me, becuase they are not that cost effective

  • New question.
    As MS progresses and neurons die do positive symptoms improve?
    Comments please, thanks for your time.

    • I assume you're talking about sensory symptoms which result from dysfunction of specific sensory neuronal pathways and therefore the symptoms largely remain. Negative symptoms i.e. loss of power, are the result of dysfunction as a whole in the motor pathways.

  • Any chance of a post on what we might expect to see in 2016. I'm not expecting Mystic Meg, just six things we might hear about in 2016 e.g results of key trials.

    • MaybeG will do it, the headline results of a number of trials have been leaked in 2015 and are negative maybe we will see the publications

      1. Siponimod in secondary progressive MS…success here and academic trials are wasting their time,but if fongolimod failed in PPMS what can they do to make it work. Trials due to finish summer 2016. Expect results to shareholders by end of 2016 maybe

      2.Ocreluzimab will get licence for RRMS, what will happen in PPMS more trials?

      3. Repair trials reort

      However the MS Society made a list on 1 December 2015


  • Last month there were a few posts about bladder issues in MS. I would like to see some research around the area of diet and night time urination in MS.

    I was reading that sugar – refined, honey and artificial sweeteners can irritate the bladder. Also coffee, tea, acidic fruit and that cranberry juice on the one hand it can help but on the other hand it can still irritate the bladder.

    Yesterday I had quite a bit of natural and refined sugar all through the day and evening and I was up in the night urinating three times. That's quite a bit for me.

    If I stop having sugar after lunch say from 1pm will that help? I will try it out.

    • Speaking personally, I find the worst thing of all for my bladder is salt. Salty food can inflame my bladder to the point of mimicking a serious bladder infection. (I've never had any evidence of a bladder infection through testing and – touch wood – no more problems since cutting out salt.)

    • If they are trolls why not just delete their posts and filter what is deemed non troll by Team G? Or is it that every comment was a troll? The latter must be the case.

    • We still have to read the mushroom food that these idiots write to decide if they are worth going public. So rather than be a magnet for these vile comments, sometimes it is easier simply to turn things off.

  • I have PPMS. One thing I remember about my teenage years was having persistent cold sores inside my nose. Could there be any link?

    • I'm cutting and pasting a comment from an epidemiological study by the Danes: "Neither age at infection with measles, rubella, varicella, mumps, pertussis and scarlet fever (upper age limit, 14 years) nor the cumulative number of these infections between the ages of 10 and 14 years was associated with the risk of multiple sclerosis." Paper is entitles Childhood infections and risk of multiple sclerosis, http://brain.oxfordjournals.org/content/127/11/2491

  • MD I forgot to mention that when I read the publication on the Daily Race to try to approve Cladribine automatically came to mind the movie "Extraordinary Measures". Not wanting to be "socialist, or even demagogic" but maybe Hollywood not overdo both portray Big Pharma …

  • Could you please tell me – in your opinion, purely in terms of the implications of hormones for MS – is a woman of childbearing age with MS better off on the contraceptive pill?

    • Extremely worrying. Apparently the drug is a "cannabis-based painkiller", which in itself is disturbing as you certainly wouldn't expect to see this with a conventional cannabinoid. I'll be checking as more details emerge.

  • "A case of progressive multifocal leukoencephalopathy (PML) associated with natalizumab (Tysabri, Biogen) therapy has been reported in a patient with multiple sclerosis (MS) who had tested negative for JC virus (JCV) antibodies just **2 weeks** before symptoms developed…

    The patient in this case, a 70-year-old woman with MS, had been taking natalizumab since January 2010, had never received immunosuppressants, and had had several negative JCV antibody test results, the most recent of which was just 2 weeks before the onset of PML symptoms."


    The article suggests more regular MRI monitoring, so I wondered,
    1- if NHS funding was unlimited, how regularly would you like to monitor via MRI each patient on Tysabri?
    2- accepting that NHS funding is NOT unlimited, how often should a person taking Tysabri be monitored via MRI?

  • Not wishing to be ageist but why is a 70 year old receiving Tysabri? Cannot see how it can add up in the patient's interests. Crazy prescribing!

  • Any thoughts or comments on this:
    New TSRI Study Shows Path to ‘Dial Down’ Autoimmunity without Compromising Immune Response

    LA JOLLA, CA – January 18, 2016 – A new study led by scientists at The Scripps Research Institute (TSRI) shows how dangerous autoimmune responses, seen in diseases such as lupus and multiple sclerosis, might be “dialed down” without compromising the immune system’s ability to fight viruses and bacteria.

    The new study, published this week in the Early Edition of the journal Proceedings of the National Academy of Sciences, defines an unexpected mechanism at work in an anti-autoimmune drug candidate called ozanimod


    • Well this seems to be interesting, they looked at the S1PR1 agonists targeting the dendritic cells plasmacytoid. Changes in S1PR2 seem to be more common in women … Fingolimode acts in S1PR1 … Fingolimode has been tested for Lupus and Rheumatoid Arthritis?

  • You may have already covered this. But what is the science behind Cladribine? Does it focus on B cells or T Cells or is it an inhibitor of some kind.


    • I realize this is anecdotal but I checked my EBV-VCA IgG level when I was diagnosed and the titer was relatively high (1:1280 ;this is a dilution factor). Dysfunctional B-cell response to chronic EBV infection……good luck to Charcot 2.

  • MD remembered one of the last publications made here on the Blog on the role of antibodies to lipids in the CSF (I see it more as a result of the attack against to oligodendrocytes). Anyway, a friend who is doing a doctorate in Chicago sent me this link published late last year, in which the author argues not be MS an autoimmune disease.
    Although I disagree with the argument I find it interesting to discuss, since as MS is a disease with more questions than answers research up on everything that may or may not be related to it.


    • In the eight edition of Immunology Male et al, MS is listed under Autoimmune diseases with a ? Mark along with atherosclerosis. Until the pathology is worked out and autoantibody (ies) are ided then there should be discussion such as EBV as the culprit.

    • I hope Prof. G does comment on the Corthals article – it has been fairly widely discussed in the MS patient discussion boards, so that fact may also interest him.

  • For patients with PPMS, no relapses, should it be presumed that a sudden increase in nerve pain that then persists without diminishment (increasing the level of burning pain from, say, a 3 to an 8 on a scale of 1-10) mean that the next step may be more rapid loss of function? Is pain part of the process of nerve damage that then will lead to loss of function?

  • I would like to know the answer to this question as well. I have had a similar experience where my onset of MS two years ago was burning pain on the right side of my face and rather mild and not constant (my doc called this a relapse). Then a month or two later the burning pain moved predominantly to both legs along with severe aching and was constant and borderline disabling. I started taking 75 mg pregabalin and the pain has improved significantly. That was about 18 months ago and I haven't noticed any rapid loss of function although I developed bladder urgency/frequency (but it is manageable at this point with no meds). I sometimes notice subtle changes in proprioception in my right foot after walking for a long period of time without sitting down and very very subtle balance issues (no falls). My doc has not told me what type of MS I have. I'm curious do you have any spinal lesions? My spine is clear. I have 5-10 lesions in my brain (supratentorial and superior cerebellar peduncles), 3 of which are "mild" black holes per my MRI. Never had a new lesion or GD enhancement or relapse since diagnosis.

  • Yes almost all spinal. Interested to know about research re. worsening pain, nerve health, and loss of function. From posts here, it seems pain is less studied – at least compared to other features of MS.

    • Here in Brazil we are facing an outbreak "kind" of Chycungunya virus, Zika virus and virus of Dengue.
      The vector for the 3 virus are female mosquitoes of Aedes Gender, especially Aedes Aegypti and Aedes Albopictus.
      Dengue we turn to face about 20 years, and little has been done about it (no anti-viral against the four types of dengue virus, no vaccine, no combat the mosquito from the people and the state, etc.).
      Already outbreaks of infections by Zika virus and Chycungunya Fever are very recent in the country.
      No one knows yet say when and how it started, only began to realize a stratospheric increase in the number of cases of children born with Microcephaly, originating from mothers who had symptomatic infection by Zika virus.
      They realized also that the ZV was related to the increase in the number of registered cases of Guillain-Barré Syndrome, particularly in the northeastern states.
      Only national research organizations found that both the Zika Virus as CHIKV were "causing outbreaks" of Guillain-Barre.
      These entities this week the press reported the case of an indian girl of 17 who at first had died as a result of Guillain-Barré Syndrome caused by CHIKV.
      But the neurologist who treated the girl if requested an autopsy the autopsy; found this to CHIKV infection just that he had not caused Guillain-Barré, but Miosis. "I suspect" that alone the Ministry of Health and the Brazilian Government have failed to address these epidemics without cooperation with other countries, despite the efforts of research institutes and national health as FioCruz …

      But the Guillain-Barré Syndrome is characterized by immune attack to the Peripheral Nervous System, while MS with respect to the Central Nervous System…

    • Re while MS with respect to the Central Nervous System…

      Though I have RRMS and have peripheral nervous system damage. It is known MSers may have peripheral nervous system damage including those who have had MS a long time.

      [The role of the peripheral nervous system damage in clinical picture of multiple sclerosis].

    • Ops now I saw, went wrong, the new infection registered in Brazil that seems to be related to Chycungunia Fever is the "Myositis" (correct name)…Phone broker only disturbs sometimes ….

    • Team G can best answer this question of MS and GBS …
      I know that MS affects the peripheral nervous system, but as you said as far as I know is the evolution of the disease (I also have RRMS)…

      But as the number of cases of Guillain-Barré increased significantly in Brazil until layman noticed a very distinct difference between it and the IN: within 24 hours the person can no longer move or speak and starts you can not breathe, is all very fast even …
      And maybe the other similarity is that infections may trigger the disease 2, in the case of MS EBV is the most suspect, but from what I see of GBS various pathogens may be involved …
      Outside I know it is done tests to detect the presence of GBS antigangloside antibody…

  • http://journal.frontiersin.org/article/10.3389/fnins.2016.00016/full
    This article looked into the cells that most likely are primary drivers of complex neurological diseases i.e. cells that highly express genes involved with MS. Alzheimer's and MS were determined to be primarily driven by microglia. What s keeping microglial cells activated? Are T-cells that are still present driving microglial activation? As microglia have a "good" side and a "dark"side hopefully microglial gene studies will lead to therapies for progression. Does team G have any opinions on targeting microglial activation?

  • Linkage of Multiple Sclerosis and Guillain-Barre Syndrome: A Population-Based Survey in Isfahan, Iran

    4. Discussion

    In this paper, we described seven patients who suffered from both MS and GBS during their lifespan. In our study, six subjects (Cases No. 1–6) had been diagnosed with MS after development of GBS. Our analysis may provide evidence for an increase in the development of MS following GBS.


    This I find interesting – with the rise of GBS cases could some of these lead to MS cases?

    • Probably this warning was made as a result of what is happening in South America due to the epidemics caused by Zika and Chikungunya Virus… Chronic infections caused by two viruses are related to the absurd increase in cases of GBS in Brazil, which is in Colombia the Ministry of Health said there had been 3 deaths this week related to infection by Zika Virus and GBS.

      "The Guillain-Barre Syndrome (or Polyradiculoneuropathy Acute) is an autoimmune illness initiated to viral and/or bacterial infections, where the immune system has an aberrant response to these infections and ends attacking the myelin sheath of nerve nervous system peripheral, and sometimes the proximal nerve roots and cranial nerves.

      In many individuals the onset of the disease is preceded by infection of upper respiratory infections, acute gastroenteritis (Campylobacter) and a history of acute infections by a number of viruses such as Epstein-Barr virus, Cytomegalovirus, HTLV-1, HIV and many respiratory viruses.

      In 2010, a survey conducted by UFRJ (Federal University of Rio de Janeiro – Brazil), found that the Dengue Virus can be one of the causes of GBS (as 1-4% of people with dengue developed the syndrome).
      The Zika and chikungunya Virus also seems to trigger GBS, given the absurd increase in the number of cases of GBS in persons who have infections by ZV or Chikungunya".


      And in Portuguese: https://pt.wikipedia.org/wiki/S%C3%ADndrome_de_Guillain-Barr%C3%A9

By MouseDoctor



Recent Posts

Recent Comments