Posters Galore @ECTRIMS #MSParis2017



How would I describe this year’s ECTRIMS/ACTRIMS?

With 10,000 participants and more than 2000 abstracts this year, it is undoubtedly one of the worlds largest neurology/science conferences. On Twitter, alone @ECTRIMS reached a total audience of 2.9 million, with 6.2 million impressions worldwide (stats from @ECTRIMS). Walking along the halls of Le Palais des Congres de Paris (venue), I felt a sense of awe and wonder. With the conference now over, the keynote messages will soon move from memory to history; immortalized in reports, seminars, blogs and tweets the world over.

Every year there are a vast number of posters to review, and this year was no different. They were of a very high quality this year, each adding more to our knowledge and our understanding of MS than ever before. Below, I have tried to pick out some of the quirky ones for you!!!


Does it truly exist?; defined as those with an expanded disability status scale (EDSS) of  <3 from symptom onset after 10, 15 or 20y.

S. Marinez-Yelamos’s team [Hospital Universitari de Bellvtage-IDIBELL, L’Hospitalet de Llogregat, Spain]: “Benign multiple sclerosis: does the initial outcome predict a favorable long term evolution?

Of 485 PwMS evaluated in 1996, 82 were felt to be benign. At 2006 (taking into account those lost to follow-up) 62 PwMS were evaluated of which 51 had benign MS. They found that for every 10y of MS evolution, a reduction of 20% of patients with benign MS was detected.

M. Amato’s team [University of Florence, Italy]: “Cognitive impairment can help to predict long-term disease course in benign multiple sclerosis patients: a 12 year follow-up study

in 63 PwMS with EDSS ≼3 and disease duration of ≽15y cognitive function was assessed. By the end of follow-up, 20 were noted to be no longer benign with regard to EDSS score. Cognitive impairment was detected in 20. Those who were no longer benign had higher mean T1 lesion volumes. When clinical and MRI parameters were looked at, T1 lesion volumes, number of cognitive tests failed, longer disease duration were related to no longer benign status at follow-up.


T. Olsson’s team [Karolinska Institute, Sweden]: “Concussion in adolescence and multiple sclerosis risk

Trauma has been hypothesised to initiate MS -related autoimmune processes, through proliferation of myelin-antigen-specific T cells (evidence from experimental works).

They used concussion as a marker of traumatic brain injury, and looked to see whether concussion in childhood (birth-adolescence) or adolescence (11-20y) was associated with an elevated risk of MS after the age of 20. Their analysis revealed that it was concussion at adolescence that raised the risk of MS, with evidence that multiple episodes of concussion conferred a greater risk. Moreover, a longer duration of hospital admission, indicating more severe trauma, was associated with a greater risk of MS. Whereas, limb fractures were not associated with MS risk (see Figure).

C. Bernstein’s team [University of Manitoba, Canada]: “Increased incidence of psychiatric disorders five years before diagnosis in multiple sclerosis

Prevalence of psychiatric comorbidities (anxiety, depression, bipolar disorder) is higher than expected in MS, but little is known of their incidence before diagnosis.

Between years of 1989-2012 all PwMS in Manitoba matched to a cohort from the general population.  They found that the incidence of psychiatric disorders was higher in MS than controls pre-diagnosis (depression relative risk [RR] 1.18, anxiety RR 1.09, bipolar RR 1.16). The occurrence of this is found as early as 5y before MS diagnosis (see Figure). They suggest that there may be a prodromal period for MS in which inflammation has developed sufficiently to precipitate psychiatric disorders but not the clinical symptoms of MS.

M. Tintore’s group [Cemcat, Spain]: “Impact of body size on MS risk and prognosis: results from the Barcelona CIS cohort

Obesity in young women has been associated with an increased risk of MS, but little is known about the prognosis.

They studied the possible association between perceived body size at menarche (underweight, normal or overweight) with the age at CIS (first demyelinating event) and the following outcomes: time to second attack (i.e. MS diagnosis) and time to EDSS 3. 518 women completed the survey and 5.6% were overweight at menarche. This was associated with a younger age at CIS, and there was a trend towards higher risk of disability accrual, although this needs to be confirmed in future studies.


Correia’s team [Hospital Egas Moniz – Centro Hospitalar Lisboa Ocidental, Portugal]: “The influence of menopause in multiple sclerosis course

The impact of menopause on the MS disease course is unknown, although it has been noted previously in PwMS after menopause there was faster disability progression and worsening MS symptoms in studies.

They looked at 34 women aged 45-55, post-menopausal, with a diagnosis of MS at least 2y before menopause. Only annualized relapse rate seemed to be influenced by menopause, and the effect was favourable, with a decrease in the number of relapses. After menopause, the disability increase (i.e. the rate of EDSS change) was comparable to the pre-menopausal period. Of course, these findings need to be confirmed in larger prospective studies.

M. Mavi’s team [Karadeniz Technical University & Jasem Laboratory System and Solution, Turkey]: “Methylprednisolone concentrations in breast milk and serum in patients with multiple sclerosis treated with IV pulse methylprednisolone

Women with MS are at an increased risk of relapses in the postpartum period. There is little data available about the concentrations of IV MP in breast milk and exposure to infants as a result. The study looks at this in 21 breastfeeding MS women. They found that the concentration of MP transferred into the breast milk was small and the infant exposure would be very low for a breastfeeding mother an hour after infusion. Mothers can choose to wait 2 to 4h to limit further exposure (see figure).


K. Kotulska’s team [Children’s Memorial Health Institute, Poland]: “Anti-JC virus antibodies in paediatric multiple sclerosis patients“.

Immunosuppressants are becoming very relevant to paediatric MS, and therefore it is important to understand JCV prevalence in this population.

Using the Stratify-JCV test they studied JCV seropositivity in 106 diagnosed with MS/CIS and other neurological conditions (controls) in the paediatric population. They found that the percentage of JCV-seropositive in MS as well as controls was comparable (~ 50.9%) to that seen in adults. Therefore, JCV status may influence the choice of DMTs in this group.

J. Gartner’s team [University Medical Center Gottingen, Georg August University Gottingen, Germany]: “Treatment of highly active multiple sclerosis in paediatric patients

Little is known about the management of highly active paediatric cases of MS.

They studied the response to natalizumab and fingolimod and found that the two treatments resulted in a significant reduction in annualized relapse rate (95% in natalizumab and 75% in fingolimod), new T2 lesions (97% in natalizumab and 81% in fingolimod) and enhancing lesions (97% in natalizumab and 93% in fingolimod) – see figure. This is similar if not better than what’s seen in adult MS.

MSParis2017 Opening Ceremony

About the author

Neuro Doc Gnanapavan


    • Nothing which hasn't been already done before. Outside of the poster sessions the word on the street was that brain atrophy as an outcome measure in trials at least is dead. The biotin study with its pseudoatrophy was the final nail in the coffin.

    • Thanks for moderating this post.

      Can you develop more on on your last point. Why can't BVL be an outcome measure?

    • MEDDAY was improving outcome and and the Brain volume was shrinking.
      Therefore it is not fit for purpose…end of story

    • MD-I am confused. Does this mean that using BVL/atrophy using current MRIs are useless for MS patients as an endpoint for trials for determining progression in all MS patients?

      What does this mean for previous trials that have used MRI as endpoints using brain atrophy/BVL as a measure of progression of the disease-ie. GIlenya? Do not most current anti-inflammatories DMDs equate reduction of disability to BVL/brain atrophy on MRIs?

  • There was a presentation from the University College London Institute of Neurology, “Does ‘benign’ multiple sclerosis exist? A 30-year follow-up study of people presenting with clinically isolated syndrome.” (ther is a video of the presentation online) that contradicts a little the outcomes of the other benign reserches. It was a bit more optimistic.*media=3*speaker=628330

    Another interesting paper from the University College London Institute of Neurology about the spinal cord atrophy was the "New spinal cord and infratentorial lesions in early relapse-onset MS are predictive of secondary progressive disease course after 15 years"

    "A key finding was that people with CIS who had more spinal cord lesions were at 4 1/2 times more likely to develop SPMS 15 years later than people with fewer lesions.

    The research team also said a type of lesion known as a gadolinium-enhancing lesion increased by 1.7 times the chance that a CIS patient would develop SPMS, compared with those who had no such lesions. Gadolinium-enhancing lesions indicate that inflammation is ongoing.

    The bottom line was that an accumulation of lesions in the spinal cord and lower brain regions appears to drive disease progression — a point that physicians should consider when trying to predict whether their patients will develop MS, the team said.

    “Brain atrophy did not appear to differ greatly between the groups, but spinal cord atrophy was more severe,” Brownlee added, emphasizing the need for spinal cord MRIs in CIS patients."

    Another paper that caught my eye was this "Reduced microglial activation through the inhibition of colony-stimulating factor 1 receptor (CSF1R) to promote remyelination and neuroprotection"*ot_id=0*media=3

    • I'd like to add that the benign MS concept is very contentious. Here is how the data as seen on the screen was interpreted- you'll then see how difficult it is to prove or disprove this concept. The retention of cases in natural history studies is poor as people progress they drop out, leaving cases which are truly benign and even in this a proportion passed away!

      The contribution of spinal cord pathology and cord imaging has been investigated by QS for some time. Some of the initial work was done by Gordon Ingle in PPMS in 2002 (Primary progressive multiple sclerosis: a 5-year clinical and MR study. Ingle GT, Stevenson VL, Miller DH, Thompson AJ. Brain. 2003 Nov;126(Pt 11):2528-36) and shows you how slow science takes to enter into clinical practice. The problem is that cord imaging is difficult to standardise and that's why it hasn't entered into clinical practice.
      I used to ask the late C Confavreux repeatedly what he felt was the best predictor of disability and he would tell me it was T1 black holes. He used to laugh and say couldn't I come up with a novel question? I used to always say that I was checking to see if he'd changed his mind!

      The last one I didn't see – may be mouse doc knows about it?

    • Thank you very much for your response. Imagine if it is hard to prove or dispove benign MS what happens to real questions :/

      To my eyes benign is an obsolete term that needs to be replaced by "mild" MS. Then the questions will change towards a more clear image of the disease. By grading the intensity of ones MS could lead to better pharmacological approaches (mild, medium, aggressive and even the middles of those). Of course MS is unpredictable and unstaible but…

      "Benign" is at least misleading when it is referring to an EDSS 3.
      Too many years of arguing about something that many researchers renounce.

      A patient with not patience -speaking of terminology 🙂

    • I don't believe in Benign MS.

      I see pwMS with the name "Benign MS" in their charts but clearly they mostly have psychiatric disorders associated with MS or cognitive problems (recent memory loss, difficulty in processing information, etc.), and suffer from too much fatigue.

      It seems that MS is a motor related illness, and if you don't have motor impairment you have nothing, "you have Benign MS."

      A real fallacy.

  • With the indefensible and inexcusable omission of HSCT. The most significant development in treating MS in decades.

    • HSCT was discussed in the European Charcot Foundation section on induction treatments and was glossed over as it was overall felt that the current induction treatments with better side effect profiles will supersede this in the future.
      The aim of the summary was to draw the readers attention to what they might not heard of. Probably the biggest area for development in the next few years is going to be in paediatric MS, which sadly has been an orphan to adult MS as far as treatments are concerned but this is about to change…

    • "induction treatments… with better side effect profiles will supersede this in the future"

      Did you read that back? Is that a joke? Are you being sarcastic?

      I simply can't fathom how on earth you believe that, given all the evidence strongly suggests the complete opposite.

    • The HSCT story may be analogous to the rirux-/ocrelizumab debacle – a sad chapter in medicine. Pharma is the 800 lb gorilla in the room when it comes to HSCT. If the data for current induction therapies supersedes HSCT then why perform it? Northwestern University in Chicago has been performing HSCT for years. They need to explain to the MS community why.

    • No sarcasm intended. I work at St Bartholomews Hospital which is a centre for Cancer Research and deal with complications of HSCT on a weekly basis. These range from graft vs host disease, PML, leukoencephalopathy, development of other new autoimmune disorders, idiosyncratic SE- blindness, pulmonary emboli, guillain barre syndrome…
      HSCT appeals to me as a clinician. But clinicians who use it should also know how to manage its complications.
      Luis – high dose chemo followed by autologous haematopoietic SCT is treatment for PCNSL. HSCT should provide good outcomes on atrophy, but is it better than say natalizumab? The Sheffield group should be completing their study of HSCT versus Tecfidera, Gilenya, and Tysabri in Nov 2017 – maybe they'll report at the next AAN. I'd be interested to see their results.

    • Sweden shows some guts! After running the RTX trial that should have been conducted 10 years ago and not under mafia-like threats, now I read that last year they recognised HSCT as a second and even first line treatment.
      Kudos Sweden for reminding us what caring for patients first looks like.
      Part of this success I believe is that Sweden has a health system that not only is public and well funded but that this allows different specialities to collaborate in harmony (speaking for neurologists and heamatologists – I believe that this conflict is evident at the limited participation of HSCT at ECTRIMS).

      Thanks Luis for your research.

      PS. Patients will be be more than happy to hear that something less cruel than chemotherapy is as good. No one wants to go through this if it is not necessary. But for many patients it is nothing less than life saving.

    • Yes Sweden are a leading light in the alternative treatments, but I think it is because Swedish Neurologists are in charge of their budgets.

    • More patients per capita undergo
      transplantation in Sweden than anywhere
      else in the world; why is this?
      We had some very positive early
      experiences with this procedure that
      prompted us to move on to the development
      of a clinical programme. In Sweden, all
      physicians can prescribe and use any
      approved drug with hardly any constraints.
      Since we use existing drugs that have been
      around for decades, we do not have to file
      a lot of paperwork and navigate through
      bureaucracy in order to use this treatment.
      In addition, healthcare in Sweden is
      publicly funded and not primarily based
      on individual performance. That means
      that I have nothing to lose by referring ‘my’
      patients to the haematologists who perform
      the actual transplant. Therefore, I can have
      the patient’s best interest at heart at all
      times. Over the years, we have been very
      lucky to collaborate with enthusiastic and
      open-minded haematologists, radiologists
      and laboratory personnel.

    • "Patients will be be more than happy to hear that something less cruel than chemotherapy is as good." Chemotherapy is at the centre of the conditioning and ablative therapy.

  • Simply put. Research is stagnant since all pharma and pharma sponsored research is actively looking for only maintenance therapies as opposed to a cure. There are only so many immune mediated targets you can target. Pardon the punn. Medicine is no more about curing but more about alleviating symptoms. Name me one medical condition that has been cured in the last 10 years where pharma is taking in money from treatments!

  • Hsct chemo strength is nowhere near that used for cancer. Not even close. Which is why side effects of hsct are minimal for the vast majority of patients.

    • There are two regimens myeloablative (not different from that offered for cancer) and lymphoablative but nonmyeloablative HSCT conditioning regimen (or partial regimen). Check which one you're being offered; the latter has less side effects.

  • Another thing that surprised me at the conference (from your speciality) was that lumbar puncture…came back! I didn't know it had gone away!
    A procedure that from what you have told us can give a 95% accuracy if done the right way. There is too much unecessary fuss about l.p. that does not reflect reality. Sure it is an unpleasant procedure but nothing really harsh and what it offers really outweights the trouble.
    How many years will pass discussing if benign MS exists and if l.p. should be done… The marmot day or just old habits?

    • My thought was that this was mainly to cover the US and their insurance practices. LPs are hardly performed there but having a change in a guideline that's widely accepted may pave the way…

  • Dear Anon
    You said….
    "There were 10,000 delegates. Let's assume conservatively that the cost of each delegate was £1,000"….."That equates to £10 million for the delegates to attend".

    This is why cities write to me to ask me to organize a meeting in their cities. It is good business for the local economies. Meetings are expensive to put on and attend.

    The meetings are about education and information and as part of their careers have to attend meetings to get CME (continuing medical education) points, which they have to do each year. So yes ECTRIMS is a trade show and this is why you have PACTRIMS, ACTRIMS, LACTRIMS, etc local doctors are being educated as you don't want people practicing what they learned thirty years a go in medical school…when the message there were no treatments for MS.
    In the digital age you know about these because we are a more open socieity

    As to the costs I agree ,it is a lot and the people who pay are society as we bear the costs of the treatments on offer at these trade shows. ECTRIMS is tiny compared to some meetings such as some cardiac meeting have 25,000 delegates, there are only a few places in US that can accommodate so many people at once.

    "The costs were paid by the public sector (academic bodies, hosptal boads etc.)". Probably at all. A large part of the costs are borne by the pharmaceutical industry either directly or indirectly as they pay huge sums to ECTRIMS and this pays to get the speakers to the meeting ETC….

    My trip was paid for by ECTRIMS, I went their to do a Job for them,…so pharma indirectly paid as did you by buying their products.

    "I didn't see any stories from the conference in the UK national press which suggests there were no major breakthroughs".

    There were a number of new products that I saw, more choice, more on the way.

    "It leaves a bad taste in my mouth given that we are a long way from having neuro-protective or neuro-restorative treatments"

    There were a number neuroprotective and restorative studies reported.

    "I'm glad to see that Prof Mouse was alloweed a foreign jolly for a change".

    One of the few….but it was hard work, with meeting after meeting and as for

    Not sure appreciate comments about MD2.

    • MD I'm glad you made the effort to answer this one. I do find it strange that anon believes that the UK press are the way to communicate science in the current times…the fact anon was on this site proves my point without further ado.

  • This is a good one

    Trial to See if Disease-modifying Therapies Not Necessary in Older MS Patients

    " The relative futility of presently available DMTs in aging MS patients, especially those with progressing symptoms, argues strongly for development of approaches that diminish neurodegeneration and enhance CNS recovery and/or regeneration"


    • We know that the immune system ages like everything as we get older, which questions the approach of blanket immunomodulation at an older age, not withstanding the poor tolerance to side effects when we're older.

      But in those already on immunomodulatory treatment the rebound phenomenon, I believe would still apply for some time. So I would not advocate withdrawal of pre-existing treatment on this supposition.



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