Multiple Sclerosis Research

A comment on the Multiple Sclerosis Research Blog

In a world where it is easier to be lost than discovered, dissonance is the word of the day. When you have a serious medical condition, your day to day life is suddenly uncertain and unpredictable, your mood, a narrative from the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition – DSM-5 for short, and its 186 footnotes. Being ill is a profound life experience, but not a fait accompli.

What does it mean to overcome adversity? The answer is yours to discover.

Sometimes, it’s the small gains that stand between obscurity and discovery.

This year alone there have been 2807 individual publications listed in PubMed for Multiple Sclerosis. This has been increasing steadily, year upon year. Thousands, upon thousands have participated around the world to create these figures and these dots in themselves hide the life story of MS.

  • The dawn of the therapeutic area in MS began with the approval of interferon-β-1b by the FDA for the treatment of RRMS in 1993
  • Natalizumab, the first monoclonal antibody therapy was published in two papers in 1999.
  • In 2005, natalizumab is withdrawn as the risk of Natalizumab-associated PML is revealed.
  • Three oral therapies are approved between 2010 and 2013: fingolimod, teriflunomide, dimethyl fumarate (DMF).
  • The highs and lows of monoclonal antibody treatments: alemtuzumab and dacalizumab were approved between 2014 and 2016, but dacalizumab was unsucessful and alemtuzumab is temporarily under Article 20 restriction by the European Medicines Agency (EMA).
  • Cladribine is revived in June 2017 as the EMA gives approval.
  • Targeting B cells becomes a priority; 2017 sees the publication OPERA I and OPERA II Phase III trials of ocrelizumab in RRMS.
  • Clinical dilemmas on best treatments as the number of choices for RRMS rises (in 2018 ECTRIMS/EAN and AAN formulate treatment guidelines for MS).
  • New frontiers emerge in Progressive and Aggressive treatment of MS; ocrelizumab for PPMS is published in 2017, and siponimod for SPMS in 2018. Autologous haematopoietic stem cell transplantation  (aHSCT) enters as a potential treatment option for aggressive and progressive MS between 2016-2018.

You can read about all of these milestones in Nature Reviews Neurology. The developments listed to date are a tribute to those who participated, and is something to be proud of.

This week Francesca (my Post Doc), informed this week that ‘X’ was here from Oxford for their lumbar puncture and MRI head scan for the alemtuzumab neurofilament study. A few months back, an MS Specialist nurse from Preston contacted me to ask if one of her MSers who’s interested in the SIZOMUS (anti-plasma cell drug) study could come all the way from Preston to London to participate. Now, what is unique about these two individuals is that they initiated first contact.

So, go out there and do your own piece of research. For those of you who have never participated in clinical research, a good starting point is

About the author

Neuro Doc Gnanapavan


  • This is amazing! Thank you for the context. It shows MS is increasingly a priority for research, which is great news! Question though – is there any correlation to outcomes/prognosis in MS? Curious if time to disability charts would should a correlation between increasing research (or more DMDs) and decline in time to disability….

  • Comments from article about secondary p. research…puts that publication chart into perspective.

    “My son has secondary progressive MS. He is 58 years old.and lives with my husband and I. His legs barely move and is mostly wheelchair bound. I see his brain slowly deteriorating. How does one get into a clinical trial? My son, Stephen, has been on Gilenya for several years. I see no future for him and no good news for people with his form of MS. My husband is 82 and I am 79. I see my son needing a feeding tube soon and I don’t know if I want to be here to see that, or not.”

    “Please help me. Someone I love deeply has secondary progressive MS. He’s been bedridden for a couple of years. I don’t think it has to be that way but his caregivers really haven’t cared. He’s an easy paycheck. Instead of waking him to eat, he is allowed to continue sleeping, which is primarily brought on by sleep inducing meds. No food = No nutrients = your body begins to waste away. It’s his pain that makes him want to sleep… from the ms and non stop urinary tract infections. What can I do to ease his pain without making him sleep from Meds? If I can ease his pain, he will decide to live again. If not, he will die! He is only 56. I love him and want a life with him! Please….. please help me.”

    • I agree, no one should have to face that level of suffering. There are a lot of symptomatic treatments for the progressive stages, at times it’s about withdrawing treatments that are ineffective and where side effects outweigh benefits. The neurodisability teams and MDT rehabs are critical for this

      Just to point out that Sub cut Cladribine will be starting to recruit at EDSS 6.5 and going up to 8. STAT-2 up to edss 6.5 is currently recruiting, and SIZOMUS (anti plasma cell drug) will be up to EDSS 8.0!

  • Apart from aHSCT, there is no other trials for PPMS in the UK. Any chance that the ORATORIO-HAND study will be recruiting anytime soon?

  • Hear Hear.
    I had an improved MRI on rituximab, but insisted on an LP to check CSF NFL(knowing both through this blog and my own reading that anti-CD20 is very good at stopping MRI but not necessarily disease activity). LP showed an elevated level of NFL and elevated CXCL13(so evidence of on-going inflammation).

    Now I am about to have leukapheresis for HSCT. I had been feeling “stable” and if I hadn’t been informed I would have been happy with the MRI results and left it at that. Who knows what that would have resulted in long-term.

    • Interesting that your CXCL13 level in particular as well as NFL was still elevated, tells you that not every treatment works the same way in everyone!

      • ” tells you that not every treatment works the same way in everyone!”

        NDG peripheral B cell depletion doesn’t work for any one according to S. Hauser….So the emperor has no clothes.

        “Our findings raise the possibility that IMTs, which effectively reduce clinical and MRI relapses, may not sufficiently target CNS-compartmentalized immune mechanisms that have been associated with gradual and relapse-independent MS worsening in relapsing MS and progressive forms of the disease”

        Similarly he says they don’t affect long term disability.

        “The appearance of silent progression during the RRMS phase and its association with brain atrophy suggest that the same process that underlies SPMS likely begins far earlier than is generally recognized and support a unitary view of MS biology……Moreover, as relapses and focal white matter lesions are brought under excellent control by disease‐modifying therapies for RRMS, the effectiveness of these agents against silent progression is likely to represent a key determinant of their relative value.”

  • Thanks for this post. I was excited to see references to the alemtuzumab neurofilament study and the SIZOMUS (anti-plasma cell drug) study.

    I still think that too many research papers focus on EAE (poor model for MS), the older less efficacious treatments (eg Copaxone), or are concocted for the benefit of PhD students not for the benefit of MS patients.

    While MS research has come some way, there are no metrics to measure the progress made for patients (in contrast to cancer research and treatments which can show improved survival rates etc.). When I was diagnosed 20 years ago, I read that MS reduces average lifespan by 8-10 years, 50% of RRMS patients will become SPMS after 20 years, after 20 years 50% of patients will need a wheeelchair. I wonder if the research and treatments have impacted on these metrics?

    Good luck with the two projects you mentioned.



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