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SATURDAY, MARCH 24, 2018
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Hall C |
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| 07:00-07:50 |
E-Poster Presentations |
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| 08:00-09:50 |
NEUROIMMUNOLOGY: MS, LUPUS, AND NMO
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Chairs: Maciej Jurynczyk, UK & Jan Lycke, Sweden |
| 08:00-08:55 |
Can multiple sclerosis (MS) be reliably differentiated from isolated CNS lupus? |
| Capsule: |
Systemic lupus erythematosus is a name indicater, a systematic disease, the manifestations of which are very heterogeneous. In some cases, the disease appears to be limited to the central nervous system in a presentation similar to that of MS, but requiring different therapies. Can the two be differentiated clinically?
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| 08:00-08:10 |
Host: Iwona Kurkowska-Jastrzebaska, Poland |
| 08:10-08:25 |
Yes: Alicja Kalinowska, Poland |
| 08:25-08:40 |
No: Joab Chapman, Israel |
| 08:40-08:55 |
Discussion and Rebuttals |
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08:55-09:50
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Is the central vein sign (CVS) really helpful in differentiating MS from other white-matter diseases? |
| Capsule: |
MRI is a pivotal tool for the early and accurate diagnosis of MS. Yet, the
current MRI criteria still lack perfect speciality and sensitvity. Recently,
the CVS has been proposed as a new MRI marker which may improve the accuracy of diagnosing MS. However, the predictive value of the CVS for the
development of clinical MS in patients at risk is still not clear.
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| 08:55-09:05 |
Host: Mark Freedman, Canada |
| 09:05-09:20 |
Pro: Robert Zivadinov, USA |
| 09:20-09:35 |
Con: Cris Constaniescu, UK |
09:35-09:50
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Discussion and Rebuttals |
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| 09:50-10:10 |
Coffee Break |
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| 10:10-12:10 |
NEUROMYELITIS OPTICA (NMO) |
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Chair: Andrzej Glabinski, Poland & Vitalie Lisnic, Moldova |
| 10:10-11:10 |
All pathology in NMO is AQP4-IgG and complement dependent |
| Capsule: |
NMO relapses are thought to involve AQP4-IgG binding to its target (AQP4) followed by complement activation. In vitro, elimination of complement markedly abrogates pathology and drugs that reduce complement activity are clinically effective. However, other pathologies are now being described in NMO, some of which do not result in necrosis or are not characterized by evidence of complement activation. The clinical significance of these pathologies is not fully defined.Is complement activation key to NMO pathology and what gains can be expected from complement inhibitors?
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| 10:10-10:20 |
Host: Hans-Peter Hartung, Germany |
| 10:20-10:35 |
Pro: Brian Weinshenker, USA |
| 10:35-10:50 |
Con: Friedemann Paul, Germany |
| 10:50-11:10 |
Discussion and Rebuttals |
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11:10-12:10
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Young Investigator Scholarship Winners
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| 11:10-11:25 |
Targeting key signaling factors as a way to control microglial activation and induction of neuroinflammation: Bogna Badyra, Poland |
| 11:25-11:40 |
Characteristics of multiple sclerosis relapses and factors affecting relapses frequency in patients with immunodulatory therapy: Mrysolav Bozhenko, Ukraine |
| 11:40-11:55 |
Progressive multiple sclerosis patients have a higher burden of autonomic dysfunction compared to relapsing remitting phenotype: Luka Crnosija, Croatia |
11:55-12:10
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Hydronamic hypothesis as an attempt to explain the Uththoff's phenomenon mechanism: Piotr Nogal, Poland |
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| 12:10-13:10 |
Industry Sponsored Symposium (Not for CME) - Hall A |
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| 13:10-13:55 |
Lunch Break & Meet the Expert sessions |
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