Scientific Program - Neuroimmunology

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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: Hans-Peter Hartung, Germany & Jacek Losy, Poland
SATURDAY, MARCH 24, 2018
Hall C
07:00-07:50 E-Poster Presentations
 
08:00-09:50
SESSION 30| NEUROIMMUNOLOGY: MS, LUPUS, AND NMO
  Chairs: Maciej Jurynczyk, UK 
08:00-08:55 Can multiple sclerosis (MS) be reliably differentiated from isolated CNS lupus?
Capsule:
Systematic 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?
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
   
08:55-09:50
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 and speed of diagnosing MS. However, the predictive value of the CVS for the development of clinical MS in patients at risk is still not clear. 
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
Discussion and Rebuttals
   
09:50-10:10  Coffee Break
 
10:10-12:10 SESSION 31| NEUROMYELITIS OPTICA (NMO)
  Chair: Andrzej Glabinski, Poland & Vitalie Lisnic, Moldova
10:10-11:10 All pathology in NMO is AQP4-IgG and complement dependent
Capsule:
Attacks in NMO 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?
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
   
11:10-12:10
MOG-IgG associated conditions represent a distinct neurologic disorder
11:10-11:20 Host: Albert Ludolph, Germany
11:20-11:35 Pro: TBD
11:35-11:50 Con: Dimitrios Karusis, Israel
11:50-12:10
Discussion and Rebuttals
   
12:10-13:10 Industry Sponsored Symposium (Not for CME) - Hall A
 
13:10-13:55 Lunch Break