Scientific Program - Multiple Sclerosis

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Please see below the CONy Scientific Program. Please click on the appropriate section (ordered by ABC) to view the relevant program. Please note that the program and timing is subject to change. To view the program timetable, please click here
 

Section Heads: Nikolaos Grigoriadis, Greece & Olaf Stuve, USA
FRIDAY, MARCH 24, 2017
Hall A
09:00-11:00
MULTIPLE SCLEROSIS (MS): MEASUREMENT OF PROGRESSION
Chair: Rana Shiraliyeva, Azerbaijan
Proposition: Biomarkers in the CSF are helpful in measurement of the effectiveness of MS
Capsule:
Currently, neurologist rely on clinical relapses, accumulation of neurological disability, and the number and activity of lesions on MRI to measure disease activity in MS patients. There is a quest for biological markers to predict and characterize this disorder, as well as to monitor pharmacotherapies. Are CSF studies ready for prime time?
Host: Mark Freedman, Canada

Yes: Uros Rot, Slovenia
No: Robert Zivadinov, USA
Discussion and rebuttals
Proposition: Optical coherence tomography (OCT) is an essential tool in following up MS patients
Capsule:
Neurologists follow MS patients by assessing them clinically, and by obtaining magnetic
resonance images of the brain and spinal cord in regular intervals. Neither method is very good at quantifying the progression of the disease. There is an unmet need for a reliable and inexpensive method to monitor patients with multiple sclerosis. Has OCT fulfilled its promise to be that method?
Host: TBA
Yes: Friedemann Paul, Germany
Not yet: Jacek Losy, Poland

Discussion and rebuttals
10:45-12:45 MS PATHOGENESIS
Chair: Zbigniew Stelmasiak, Poland
Debate: Is MS primarily due to genetic or modifiable risk factors?
Capsule:
The etiology of MS remains an enigma. Currently, 205 risk alleles have been 
associated with MS susceptibility, but each one has a very minor effect size. There are also observations that associate environmental factors and infectious agents with MS. What is the magnitude of genetic and environmental contributors to the pathogenesis of this disorder? Which ones are more important?
Host: Uros Rot, Slovenia
Genetic: Abhijit Chaudhuri, UK
Risk Factors: Ron Milo, Israel
Discussion and rebuttals


Debate: Is neurodegeneration in MS always the consequence of inflammation or it is a
separate pathogenetic mechanism?
Capsule:
Neurologists and sceintists are divided with regard to the pathogenesis of MS. Is it "outside in", meaning that an aberrant adaptive immune response drives an organ-specific inflammatory disease that leads to neurodegeneration, or is it "inside out", meaning that a neurodegenerative process releases autoantigens into immune compartments and triggers a secondary autoimmune process.
Host: Olaf Stuve, USA
Inflammation: Jacek Losy, Poland
Separate Process: Nikolaos Grigoriadis, Greece
Discussion and rebuttals

15:00-17:00
MULTIPLE SCLEROSIS (MS)
Debate: Brain atrophy measurements should be used to guide therapy in MS
Capsule:
The brain of MS patients shrinks over the disease course. How can this knowledge be utilized to understand this disease? Do pharmacological interventions alter the rate of brain atrophy? Should we measure this effect in following up patients?
Host: Jens Wuerfel, Germany
Pro: Robert Zivadinov, USA
Con: Ludwig Kappos, Switzlerand
Discussion and rebuttals


Debate: Relapses do not matter in relation to long term disability
Capsule: All approved pharmacotherapies for patients with multiple sclerosis are effective in reducing the frequency of clinical relapses. The ultimate goal is to diminish the accumulation of neurological disability over time. Do current therapies accomplish that goal?
Host: Jera Kruja, Albania
Pro: TBA
Con: Abhijit Chaudhuri, UK
Discussion and rebuttals
17:00-19:00
MULTIPLE SCLEROSIS (MS)
Debate: MS treatment algorithms: Induction approaches vs. escalating procedures vs. de-escalation strategies
Capsule: There are currently 14 approved agents for the treatment of relapsing forms of MS. All these agents are effective in reducing the frequency of clinical relapses. However, these medications have very distinct safety-to efficacy ratios. It is currently not possible to predict with certainty whether a patient will have a benign or aggressive disease course. Should neurologist be cautious and start therapy with a moderately effective but safe agent, or should they start with a very potent agent that may alter the disease course?
Host: Ludwig Kappos, Switzerland

Induction: Wolfgang Bruck, Germany
Escalation: Olaf Stuve, USA
Discussion and rebuttals
Lecture: What we can learn from failed drug studies in MS
Mark Freedman, Canada