Dear Colleagues, We welcome you to join us for the up-coming CONy Congress.
Within the Scientific Program, we have prepared an exciting Multiple Sclerosis Day – including many controversial subjects for debate led by key experts within the Multiple Sclerosis field!
We will appreciate it if you could circulate this mailshot among your colleagues in the MS field.
We are looking forward to seeing you at CONy Berlin!
Mark Freedman, Canada & Friedemann Paul, Germany
CONy Multiple Sclerosis Section Heads
For the selected Multiple Sclerosis Program please see below.
For the full Scientific Program, please click here
Friday, May 9, 2014
Multiple Sclerosis (MS)
MS Section Heads: Mark Freedman, Canada & Friedemann Paul, Germany
Session (1)
Stress and fatigue in Multiple Sclerosis (MS)
Chairpersons: Sámuel Komoly, Hungary; Jera Kruja, Albania
Capsule: It has long been debated whether or not “stress” can exacerbate an underlying autoimmune disease through connections between the CNS and the immune system, but what is the hard evidence that this occurs? Stress means different things to different people.. Would avoiding stress lower attack rates?
Do the current disease modifying agents protect from “stress-induced” exacerbations?
08:30-09:30 Debate: Does "stress" trigger MS attacks?
Debate host: Sven Schippling, Switzerland
Yes: Pasquale Calabrese, Switzerland
No: Hayrettin Tumani, Germany
Capsule: Fatigue is a frequent MS symptom that is perceived by one third of patients as their most burdensome symptom and accounts for premature retirement. Our understanding of pathophysiology, objective measurement and treatment options is sparse. Recently, an association of fatigue with sleep disorders was reported suggesting that treatment of an underlying sleep disturbance may improve fatigue. How strong is the evidence for this? Should every MS patient with fatigue be investigated in a sleep lab?
09:30-10:30 Debate: Does MS related fatigue reflect a sleep disorder?
Debate host: Ludwig Kappos, Switzerland
Yes: Friedemann Paul, Germany
No: Cris Constantinescu, UK
10:30-11:00 Coffee Break
Session (2)
MS Symposium
13:00-14:30 Lunch Break
Session (3)
MS Treatment: What are the limits?
Chairpersons: Nikolaos Grigoriadis, Greece; Eva Havrdova, Czech Republic
Capsule: Natalizumab is a very efficacious drug in active MS. However, although rare, progressive multifocal lencoencephalopathy (PML) is but potentially life-threatening complication. Recent risk stratification algorithms that include duration of treatment, pre-treatment with immunosuppressants and JC virus serostatus have been proposed to improve risk assessment in the individual patient. Can we rely on these parameters to decide on commencing, continuing or discontinuing treatment?
14:30-15:30 Debate: JCV serostatus is a reliable and clinically meaningful biomarker to contain PML risk in natalizumab therapy
Debate host: Olaf Stüve, USA
Yes: Per Soelberg Sørensen, Denmark
No: Hans-Peter Hartung, Germany
Capsule: Despite all efforts to contain inflammatory events in MS we see evidence of irreversible disability along with axonal and neuronal loss. However some of these changes might be amenable to prevention or even reversal. Could there also be endogenous protection and repair mechanisms that can be better understood in order to exploit them for therapeutic purposes?
15:30-16:30 Debate: Regeneration and remyelination are possible in MS lesions
Debate host: Xavier Montalban, Spain
Yes: Wolfgang Brück, Germany
No: Friedeann Paul, Germany
16:30-17:00 Coffee Break
Session (4)
The MRI in MS: Uses and limitations
Chairpersons: Vesna Brinar, Croatia; Florian Deisenhammer, Austria
Capsule: We live in an era heavily relying on technology to tell us the truth, not only in clinical medicine. It is felt that progressive brain atrophy probably represents the accrual of irreversible neurological disability and cognitive dysfunction. But does brain atrophy, as measured by the inverse of brain tissue volumetrics on MRI, truly represent just the loss of CNS tissue? What is pseudo- or pseudo-pseudo atrophy and how does one know the difference? If a treatment does or does not affect MRI measured atrophy, can this be correlated with clinical efficacy? Are we at a stage where MRI measurements of brain atrophy are standardized? If so, how might a clinician utilize such data to assist in making treatment decisions?
17:00-18:00 Debate: Can we judge the efficacy of disease modifying medications based on their effects on MRI brain atrophy?
Debate host: Robert Zivadinov, USA
Yes: David Leppert, Switzerland
No: Xavier Montalban, Spain
Capsule: A good response to therapy might be to be completely “disease activity free” (i.e. no new relapse, progression or MRI lesion) but does this represent all important outcome measures? What if despite being completely free of observable clinical and MRI activity a patient lacks the cognitive power or energy to work? To care for their family or to get any enjoyment out of life? A treatment might be very effective at controlling perceptible disease activity but can induce or aggravate symptoms. How effectively are these other tangibles measured or judged? Is there a way of incorporating them into our treatment decisions?
18:00-19:00 Debate: Can clinical and MRI measures alone be used reliably to make treatment decisions? What about those tangibles like fatigue, cognitive slowing or quality of life?
Debate host: Per Soelberg Sørensen, Denmark
Yes: Sven Schippling, Switzerland
Saturday, May 10, 2014
Multiple Sclerosis (MS)
Session (17)
Future therapies in MS
Chairpersons: Ovidiu Bajenaru, Romania; Jacek Losy, Poland
Capsule: Some newer disease-modifying therapies are promoted by pharmaceutical companies under the promising and tendentious slogan “disease-free status” or “freedom of disease activity”. But are we there yet? To be truly disease-activity free, there would have to be no evidence of relapse, progression or MRI change, but is it conceivable that any of these therapies will completely arrest all perceivable disease activity? If not, then at what point would not being disease-activity free constitute a failure forcing a treatment change? A new MRI lesion? An attack? A change in EDSS? Should clinicians truly be seeking to obtain this “disease-activity free” status to the detriment of all else?
08:00-09:00 Debate: Can we aim for a "disease-free status" with contemporary MS therapies?
Debate host: Hans-Peter Hartung, Germany
Yes: Andrew Chan, Germany
No: Brian Weinshenker, USA
Capsule: From time to time, mass media and patient organizations report miraculous healings of severe and desperate MS by stem cell transplantation. Until recently, cell-based therapies had a dubious reputation in the MS scientific community because of the high treatment related mortality. However, since this has substantially decreased with modified protocols, research on cell-based therapies has experienced a revival. But how convincing is the evidence? If we believe that this approach may be one out of many options how can we identify suitable patients who will have maximal benefit at hopefully lowest risks?
09:00-10:00 Debate: Cell-based therapies hold particular promise for treating MS
Debate host: Mark Freedman, Canada
Yes: Dimitrios Karussis, Israel
No: Olaf Stüve, USA
10:00-10:30 Coffee Break
Session (18)
New Players in MS
Friedemann Paul, Germany; Zbigniew Stelmasiak, Poland
Laquinimod: Krzysztof Selmaj, Poland
Teriflunomide: Andrew Chan, Germany
Fingolimod: Ludwig Kappos, Switzerland
Ocrelizumab: David Leppert, Switzerland
Alemtuzumab: Xavier Montalban, Spain
Daclizumab: Eva Havrdova, Czech Republic

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