Scientific Program - Multiple Sclerosis
Section Heads: Xavier Montalban, Spain & Olaf Stüve, USA |
Please see below the CONy Scientific Program. Please click on the appropriate section to view the relevant program. Please note that the program and timing is subject to change. To view the program timetable / overview, please click here |
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Plenary Lectures Series | Multiple Sclerosis | Epilepsy | Dementia |
Headache | Stroke | Rehabilitation | Neuropsychiatry |
Portuguese Amyloid Neuropathy | OPMD |
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08:30-10:30 |
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Chairs: Maria Edite Rio, Portugal; Lea Pollak, Israel |
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08:30-09:30 |
Debate: Is no evidence of disease activity NEDA a clinically relevant endpoint for therapuetic decisions? |
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Capsule: Currently, numerous clinical and paraclinical biomarkers are utilized to diagnose and monitor MS. There continues to be uncertainty on how specific biomarkers should impact the decision making of neurologists |
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08:30-08:40 |
Host: Uroš Rot, Slovenia |
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08:40-08:55 |
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08:55-09:10 |
No: Friedemann Paul, Germany |
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09:10-09:30 | Discussion and rebuttals | ||
09:30-10:30 |
Debate: My MRI worsened but I didn't. Should I change my disease-modifying treatment? |
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Capsule: New diagnostic tools have made the management of MS patients more complex. What should be the main driver of clinical decision making: Clinical findings? Imaging? A combination of the two? |
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09:30-09:40 |
Host: Xavier Montalban, Spain |
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09:40-09:55 |
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09:55-10:10 |
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10:10-10:30 | Discussion and rebuttals | ||
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Chairs: João Cerqueira, Portugal; Zbigniew Stelmasiak, Poland |
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10:45-11:45 |
Debate: Is vitamin D a substantial disease modifier in patients with MS? |
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Capsule: Why do patients with MS show an accumulation of clinical disability? Is there a biochemical biomarker that explains geographical, gender, and age distribution of the disease? Can this biomarker be modified? Is vitamin D such a marker? |
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10:45-10:55 |
Host: Jera Kruja, Albania |
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10:55-11:10 |
Yes: Friedemann Paul, Germany |
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11:10-11:25 |
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11:25-11:45 | Discussion and rebuttals | ||
11:45-12:45 | Debate: Does the risk of PML associated with certain DMT limit their use and offset their potential efficacy? | ||
Capsule: Opportunistic infections of the central nervous system (CNS) have been associated with MS pharmacotherapies. With natalizumab, progressive multifocal leukoencephalopathy (PML) is a frequent adverse event, which has also been observed less frequently with other DMTs. Does that risk outweight benefits for all of them? | |||
11:45-11:55 | Veronica Popescu, Belgium | ||
11:55-12:10 | Hans-Peter Hartung, Germany | ||
12:10-12:25 | Antonio Uccelli, Italy | ||
12:25-12:45 | Discussion and rebuttals | ||
15:00-17:00 |
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Chairs: Joaquim Pinheiro, Portugal; Luis Cunha, Portugal |
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15:00-16:00 |
Proposition: Patients with radiologically isolated demyelinating syndrome should be considered for MS disease modifying therapy |
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Capsule: The current treatment dogma in patients with relapsing forms of MS is to treat as early as possible to modify the natural course of the disease. Should we treat even earlier? |
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15:00-15:10 |
Host: Xavier Montalban, Spain |
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15:10-15:25 |
Yes: David Leppert, Switzerland |
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15:25-15:40 |
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15:40-16:00 | Discussion and rebuttals | ||
16:00-17:00 |
Debate: Should disease-modifying therapies be stopped in patients who have developed secondary progressive MS? |
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Capsule: All currently approved pharmacotherapies are effective in patients with relapsing forms of MS. Secondary-progressive MS is always a retrospective diagnosis, and it is often challenging to determine the exact time transition. Should patients beyond a certain disease duration and age be exposed to therapies that have potential adverse effects, but may not provide any benefits? |
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16:00-16:10 |
Host: Zsolt Illes, Denmark |
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16:10-16:25 |
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16:25-16:40 |
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16:40-17:00 | Discussion and rebuttals | ||
17:15-19:00 |
Chairs: Maria Jose Sa, Portugal; Xavier Montalban, Spain |
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17:15-18:10 |
Debate: Anti B cell or non specific anti B+T therapy |
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Capsule: Clinical trials with ocrelizumab in patients with relapsing-remitting MS demonstrated that B cell depletion with anti-CD20 therapy is effective. Are therapies that target non-B cells obsolete? Does the targeting of numerous cellular targets provide additional benefits? |
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17:15-17:25 |
Host: Mark Freedman, Canada |
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17:25-17:40 |
Pro Anti B: Hans-Peter Hartung, Germany |
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17:40-17:55 |
Pro Anti B+T: Bruno Gran, UK |
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17:55-18:10 | Discussion and rebuttals | ||
18:10-19:00 |
Debate: Can we expect long-term clinical improvement through remyelination? |
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Capsule: The histopathological substrate of clinical disability has not been fully elucidated. Is it demyelination? Is it neurodegernation? Is it a combination of the two? |
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18:10-18:20 |
Host: David Leppert, Switzerland |
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18:20-18:35 |
Yes: Olaf Stüve, USA |
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18:35-18:50 |
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18:50-19:00 | Discussion and rebuttals |
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Chair: TBA |
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09:40-10:00 | Effect of glatiramer acetate on peripheral blood brain-derived neurotrophic factor and phosphorylated TrkB levels in relapsing-remitting MS Anca Dana Buzoianu, Romania |
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15:00-17:00 |
Chair: Eduardo Freitas, Portugal; Hans-Peter Hartung, Germany |
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15:00-16:00 |
Debate: Placebo controlled treatment in neuromyelitis optica (NMO) are unethical and not needed |
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Capsule: Most patients with NMO have a relapsing disease course and may accumulate neurological disability with each relapse. There are fewer paraclinical datapoints on MRO than in patients with MS. There are substantially fewer patients. How should pharmacotherapies be testied? |
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15:00-15:10 |
Host: Zslot Illes, Denmark |
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15:10-15:25 |
Yes: Ron Milo, Israel |
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15:25-15:40 |
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15:40-16:00 | Discussion and rebuttals | ||
16:00-17:00 |
Debate: NMO-IgG is sufficient to cause the pathology of an NMO lesion without participation of T cells |
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Capsule: Anti-aquaporin4 IgG is one biomarker for neuromyelitis optica. In animal models, these antibodies have been show to be pathogenic. Can we ignore the role of T cells. Is it sufficient to focus therapeutic efforts on B cells? | |||
16:00-16:10 |
Host: Antonio Uccelli, Italy |
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16:10-16:25 |
Yes: Brian Weinshenker, USA |
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16:25-16:40 |
No: Olaf Stuve, USA |
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16:40-17:00 | Discussion and rebuttals | ||
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NEUROIMMUNOLOGY: TREATMENT
Chair: Sergiu Blumen, Israel; Anca Dana Buzoianu, Romania |
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17:15-18:10 |
Debate: Which should be the first-line therapy for CIDP? Steroids vs. IVIg |
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Capsule: Evidence-based first-line therapies for CIDP consist of corticosteroids, IVIg and plasma exchange. The choice of the first-line treatment is based frequently on personal perception of the balance between short-term efficacy, safety and cost of the treatment in the specific patient, but other factors such as later treatment dependence and ability to withdraw treatment are usually not considered sufficiently | |||
17:15-17:25 |
Host: Vivian Drory, Israel |
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17:25-17:40 |
Steroids: Eduardo Nobile-Orazio, Italy |
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17:40-17:55 |
IVIg: Marinos Dalakas, Greece |
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17:55-18:10 | Discussion and rebuttals | ||
18:10-18:50 | Re-evaluation of modern and older treatments in MS | ||
18:10-18:20 | Gylenya: Mark Freedman, Canada | ||
18:20-18:30 | Laquinimod: Hans-Peter Hartung, Germany | ||
18:30-18:40 | Tecfiedera: Ron Milo, Israel | ||
18:40-18:50 | Teriflunomide: Ovidiu Bajenaru, Romania |