17 th state of the art - startseite | schweizerische ... · asure to invite you to the 17th state...

SYMPOSIUM of the Swiss Multiple Sclerosis Society www.multiplesklerose.ch

PROGRAMME | ABSTRACTSSATURDAY, JANUARY 24TH, 2015KKL Lucerne, Culture and Convention Centre

RECENT RESEARCH DEVELOPMENTS: KEY TOOLS TO UNMASK MS

17 STATE OF THE ARTTH

17TH STATE OF THE ART 3 | Lucerne, 24th January 2015

Dear colleagues,

On behalf of the Swiss Multiple Sclerosis Society and its Scienti� c Advisory Board it is our ple-asure to invite you to the 17th State of the Art Symposium.

«Recent research developments: key tools to unmask MS» is the 2015 general theme that proposes a large review of some still unknown key aspects of MS pathophysiology. During the plenary morning session, international experts will present the most recent promising advances in di� erent � elds. Martin Weber and Roland Liblau will respectively explore the role of B and T cells in MS autoimmunity. Britta Engelhardt will discuss the major role of brain barriers in the control of the attack of the central nervous system in MS. Declan Chard and Manuel Comabella will review the best radiological and biological tools susceptible to help to unmask MS burden. Finally, Milo Puhan will present a preview of the National MS Registry, a key project of the Swiss MS-Society.

� e a� ernoon session, with two sets of three parallel interactive workshops, will bring to discus-sion topics relevant to the daily practice. Speakers will present practical situations.

Updated information about the Symposium can be found on the website www.ms-state-of-the-art.ch

In the name of the organisers and speakers, we sincerely hope that the programme meets your interest and that you will be able to attend and actively take part in the discussions.

We wish you an interesting symposium.

PD Dr. Myriam Schluep Patricia MoninPresident of the Director of theScienti� c Advisory Board Swiss MS-Society

WELCOME AND INTRODUCTION


VenueKKL Lucerne, Culture and Convention Centre, Europaplatz 1, CH-6005 Lucernewww.kkl-luzern.ch

Programme committeeBritta Engelhardt, Berne; Claudio Gobbi, Lugano; Patrice Lalive, Geneva; Tobias Derfuss, Basel; Ludwig Kappos, Basel; Michael Linnebank, Zurich and Myriam Schluep, Lausanne (chair)

OrganisationSwiss MS-Society and its Scienti� c Advisory Board

ContactSwiss MS-Society, Josefstrasse 129, CH-8031 ZurichLia Rusterholz, [email protected], www.ms-state-of-the-art.ch

Credits� e Swiss Neurological Society will award 5 credit points.� e Swiss Society of General Internal Medicine (SGIM/SGAM) will award 4.5 credit points.

Kindly supported by

GENERAL INFORMATION


PROGRAMME

PD Dr. Myriam Schluep, LausanneProf. Roland Martin, ZurichProf. Ludwig Kappos, Basel

Welcome with Co� ee and Gipfeli

Patricia Monin, ZurichWelcome from the Swiss MS-Society

Prof. Martin Weber, Göttingen� e underestimated role of B cells in MS

Prof. Roland Liblau, ToulouseT cells that recognise distinct self-antigens drive the progression of CNS autoimmunity

Prof. Britta Engelhardt, Berne How brain barriers control immune cell entry into the CNS

Co� ee Break

Dr. Declan Chard, LondonRecent imaging developments to unmask MS burden

Dr. Manuel Comabella, BarcelonaUse of biomarkers to anticipate MS severity

Prof. Milo Puhan, ZurichNational MS Registry

Lunch

Interactive Workshops A, B, C

Co� ee Break

Interactive Workshops D, E, F

Farewell Apero

Chairpersons

09.30-10.00

10.00-10.10

10.10-10.40

10.40-11.10

11.10-11.40

11.40-12.10

12.10-12.35

12.35-13.00

13.00-13.15

13.15-14.15

14.15-15.00

15.00-15.20

15.20-16.05

16.05


CONTACTS

Programme Committee and Chairpersons

Prof. Tobias Derfuss, BaselUniversity Hospital BaselDepartments of Neurology and Biomedicine

Prof. Britta Engelhardt, BerneUniversity of Berne� eodor Kocher Institute

Dr. Claudio Gobbi, LuganoRegional Hospital of LuganoNeurocenter of Southern Switzerland

Prof. Ludwig Kappos, BaselUniversity Hospital BaselDepartments of Neurology and Biomedicine

Speakers (Lectures)

Dr. Declan Chard, LondonUniversity College LondonInstitute of Neurology

Dr. Manuel Comabella, BarcelonaVall d‘Hebron University HospitalClinical Neuroimmunology Unit

Prof. Britta Engelhardt, BerneUniversity of Berne � eodor Kocher Institute

Prof. Patrice Lalive, GenevaGeneva University HospitalService of Neurology

PD Dr. Michael Linnebank, ZurichUniversity Hospital ZurichDepartment of Neurology

Prof. Roland Martin, ZurichUniversity Hospital ZurichDepartment of Neurology

PD Dr. Myriam Schluep, LausanneLausanne University HospitalService of Neurology

Prof. Roland Liblau, ToulouseToulouse University School of Medicine-PurpanPhysiopathology Center of Toulouse-Purpan

Prof. Milo Puhan, ZurichUniversity of ZurichEpidemiology, Biostatistics & Prevention Institute

Prof. Martin Weber, GöttingenUniversity Medicine GöttingenClinic for Neurology


CONTACTS

Speakers (Workshops)

Prof. Tobias Derfuss, BaselUniversity Hospital BaselDepartments of Neurology and Biomedicine

Prof. Renaud du Pasquier, Lausanne Lausanne University HospitalService of Neurology

Prof. Peter Fuhr, BaselUniversity Hospital BaselDepartment of Neurology

Dr. Claudio Gobbi, LuganoRegional Hospital of LuganoNeurocenter of Southern Switzerland

PD Dr. Cristina Granziera, LausanneLausanne University HospitalDepartment of Clinical Neurosciences

Dr. Christian Kamm, BerneBerne University HospitalDepartment of Neurology

PD Dr. Jens Kuhle, BaselUniversity Hospital BaselDepartment of Neurology

Prof. Patrice Lalive, GenevaGeneva University HospitalService of Neurology

PD Dr. Michael Linnebank, ZurichUniversity Hospital Zurich Department of Neurology

Dr. Sven Schippling, ZurichUniversity Hospital ZurichDepartment of Neurology

Prof. Till Sprenger, BaselUniversity Hospital BaselClinic and Polyclinic for Neurology

Dr. Claude Vaney, Crans MontanaBerner Klinik MontanaNeurological Rehabilitation Unit


Prof. Martin Weber, GöttingenUniversity Medicine Göttingen, Clinic for Neurology

B cells were recently found to play important roles for the development and progression of central nervous system (CNS) autoimmune disease. While earlier investigations focused on the pathogenic contribution of plasma cells producing autoreactive antibodies, and di� erentiated B cells acting as potent antigen-presenting cells (APC) for the activation of pathogenic T cells, our recent data in experimental autoimmune encephalomyelitis (EAE) and MS have emphasized the importance of B cell-derived cytokines as drivers and regulators of disease activity (Lehmann-Horn et al., � er Adv Neurol Disord. 2013).

In regard to this dichotomy in B cell function, we were able to demonstrate that primarily the activation status of B cells is crucial for their respective function. While antigen-activated B cells contribute as potent APC, naive tend to down-regulate pro-in� ammatory function of myeloid APC, presumably by provision of regulatory IL-10 (Weber et al., Ann Neurol, 2010). Regarding the relative importance of B cells within other APC, our group could further show that B cell APC function is a prerequisite for development of CNS autoimmune disease, when larger prote-ins need to be recognized and presented (Molnar� et al., J Exp Med, 2013). From this work, two translational projects derived. Firstly, we were able to demonstrate for the � rst time that unselec-tive, anti-CD20 B cell depletion collaterally abolishes pre-existing regulatory B cell function in patients with MS and NMO (Lehmann-Horn et al., J Neuroin� amm, 2011). Secondly, we could demonstrate as a proof of principle that intrathecal application of anti-CD20 could be possibly more selective and e� cient in targeting pathogenic B cell function in CNS autoimmune disease.

THE UNDERESTIMATED ROLE OF B CELLS IN MS


NOTES

Zusammenfassung Fachinformation Betaferon.Zusammensetzung: Eine Durchstechfl asche enthält als WirkstoffZusammensetzung: Eine Durchstechfl asche enthält als WirkstoffZusammensetzung: Eine Durchstechfl : Interferonum beta-1b ADNr (8 Mio. IU/ml nach Rekonstitution) Hilfsstoff asche enthält als Wirkstoff : Interferonum beta-1b ADNr (8 Mio. IU/ml nach Rekonstitution) Hilfsstoff asche enthält als Wirkstoff e: Humanalbumin, Mannitol. : Interferonum beta-1b ADNr (8 Mio. IU/ml nach Rekonstitution) Hilfsstoff e: Humanalbumin, Mannitol. : Interferonum beta-1b ADNr (8 Mio. IU/ml nach Rekonstitution) HilfsstoffIndikationen: Bei Patienten mit schubförmig-remittierender Multipler Sklerose (MS). Bei sekundär chronisch-progredienter MS und bei Patienten mit einem ersten klini-schen, auf MS hinweisenden neurologischen Ereignis. Dosierung/Anwendung: Erwachsene und Kinder und Jugendliche über 12 Jahre: 8 Millionen IU, als Injektion alle zwei Tage subkutan. Kontraindikationen: Überempfi ndlichkeit gegen natürliches oder rekombinantes Interferon beta oder Humanalbumin; Schwangerschaft; schwere zwei Tage subkutan. Kontraindikationen: Überempfi ndlichkeit gegen natürliches oder rekombinantes Interferon beta oder Humanalbumin; Schwangerschaft; schwere zwei Tage subkutan. Kontraindikationen: Überempfidepressive Erkrankungen und/oder Suizidneigung in der Anamnese; Leberinsuffi zienz; nicht adäquat kontrollierte Epilepsie. Vorsichtsmassnahmen: Vorsicht bei Patien-depressive Erkrankungen und/oder Suizidneigung in der Anamnese; Leberinsuffi zienz; nicht adäquat kontrollierte Epilepsie. Vorsichtsmassnahmen: Vorsicht bei Patien-depressive Erkrankungen und/oder Suizidneigung in der Anamnese; Leberinsuffiten mit depressiven Störungen oder Krampfanfällen in Anamnese; Patienten unter Antiepileptika, mit Anämie, Thrombozytopenie, Leukopenie oder gestörter Schild-drüsenfunktion. Vor Behandlungsbeginn und in regelmässigen Abständen folgende Kontrollen: vollständiges Blutbild, Diff erentialblutbild, übliche Laborwerte, GOT, drüsenfunktion. Vor Behandlungsbeginn und in regelmässigen Abständen folgende Kontrollen: vollständiges Blutbild, Diff erentialblutbild, übliche Laborwerte, GOT, drüsenfunktion. Vor Behandlungsbeginn und in regelmässigen Abständen folgende Kontrollen: vollständiges Blutbild, DiffGPT, Gamma-GT. Interaktionen: Vorsicht bei Einnahme von Substanzen, deren Clearance stark vom Zytochrom-P450-System abhängt. Schwangerschaft/Stillzeit: Frauen im gebärfähigen Alter sollten geeignete Kontrazeptionsmassnahmen treff en. Während der Stillzeit entweder das Stillen oder die Behandlung mit Betaferon abbrechen. im gebärfähigen Alter sollten geeignete Kontrazeptionsmassnahmen treff en. Während der Stillzeit entweder das Stillen oder die Behandlung mit Betaferon abbrechen. im gebärfähigen Alter sollten geeignete Kontrazeptionsmassnahmen treffUnerwünschte Wirkungen: Sehr häufi g: Reaktionen an der Injektionsstelle, grippeartige Symptome. HäufiUnerwünschte Wirkungen: Sehr häufi g: Reaktionen an der Injektionsstelle, grippeartige Symptome. HäufiUnerwünschte Wirkungen: Sehr häufi g: Hautnekrosen. Gelegentlich: Anämie, Thrombozytopenien, g: Reaktionen an der Injektionsstelle, grippeartige Symptome. Häufi g: Hautnekrosen. Gelegentlich: Anämie, Thrombozytopenien, g: Reaktionen an der Injektionsstelle, grippeartige Symptome. HäufiLeukopenie, Erhöhungen der SGOT-, SGPT-, Gamma-GT-, Bilirubin-, Triglyceride-Werte; und erhöhter Muskeltonus, Depression, arterielle Hypertonie, Übelkeit, Erbre-chen, Haarausfall, Urtikaria, Pruritus, Exanthem und Myalgie. Sonstige Hinweise: Lagerung unter 25°C, nicht einfrieren. Haltbarkeit des Produkts nach Rekonstitution bis zu 3 Stunden bei 2-8°C. Verkaufskategorie: B. Weiterführende Informationen entnehmen Sie bitte der Fachinformation auf www.swissmedicinfo.ch. L.CH.STH.03.2013.0117-DE/FR/IT

Bayer (Schweiz) AGGrubenstrasse 6, 8045 Zürich

L.CH

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Betaferon® – Mit Familie in die Zukunft.


Prof. Roland Liblau, ToulouseToulouse University School of Medicine-Purpan, Physiopathology Center of Toulouse-Purpan

� e central nervous system (CNS) is confronted by a double challenge regarding its interactions with the immune system. On the one hand it should allow the immune system to � ght invading pathogens and on the other it should prevent in� ammatory damage given its vital functions and poorly regenerative capacity. A series of mechanisms, collectively referred to as «immune privi-lege», ensure that immune reactions are kept minimal and are rapidly controlled within the CNS.

However, accumulating evidence shows that T cells readily penetrate the brain and spinal cord parenchyma in numerous in� ammatory, infectious or degenerative neurological diseases. � e consequence for CNS resident cells, and more speci� cally for neurons, of their encounter with activated T cells is a question that we have addressed recently using experimental rodent mo-dels. I will present our e� orts to understand how cytotoxic CD8 T cells and helper CD4 T cells can target neuronal antigens and thereby contribute to CNS tissue damage.

Intriguingly, some autoreactive T cells recognise several autoantigens but the functional signi-� cance of such «cross-reactivity» is not fully understood. We have identi� ed, in mice, autore-active CD4 T cells recognising both MOG and NF-M and have investigated their pathogenic contribution using animals de� cient for one or the other self-antigens.

Shedding light on the mechanisms by which T cells promote CNS tissue damage may allow the design of more re� ned therapeutic strategies for immune-mediated neurological diseases, among which multiple sclerosis is the most frequent.

T CELLS THAT RECOGNISE DISTINCT SELF-ANTIGENS DRIVE THE PROGRESSION OF CNS AUTOIMMUNITY


NOTES

* vs. Placebo gemäss DEFINE. Dosierung BID, 2 x 120 mg 1 Woche, dann 2 x 240 mg.1,2

Referenzen: 1. Tecfidera® Fachinformation, Stand Februar 2014, www.swissmedicinfo.ch. 2. Gold R, Kappos L, Arnold DL, et al. Placebo-Controlled Phase 3 Study of Oral DMF for Relapsing Multiple Sclerosis. N Engl J Med. 2012;367(12):1098 – 1107. Die erwähnten Studien können bei Biogen Idec Switzerland AG, Zählerweg 6, 6300 Zug, bestellt werden.

Gekürzte Fachinformation TECFIDERA®. Z: Kapseln mit magensaftresistenten Mikrotabletten zu 120 mg/240 mg Dimethylfumarat. I: Behandlung von Patienten mit schubförmig remittierend verlaufender Multipler Sklerose (RRMS) zur Reduzierung der Schubhäufigkeit. D: Anfangsdosis 120 mg zweimal täglich. Nach 7 Tagen Steigerung auf 240 mg zweimal täglich. Orale Anwendung. Mit Mahlzeiten einneh-men. Die Kapseln oder ihr Inhalt nicht zerkleinern, zerteilen, auflösen, lutschen oder zerkauen. KI: Überempfindlichkeit gegenüber Wirkstoff oder Hilfsstoffen. Eingeschränkte Leberfunktion (Child-Pugh Score) sowie mässig oder schwer eingeschränkte Nierenfunktion. Infektion mit dem HI-Virus (HIV). Schwere aktive sowie aktive chronische Infektionen. Schwere GI Erkrankungen. Leukopenie < 3.0 x 109/l, Lymphopenie < 0.5 x 109/l. Alter < 18 Jahre. Behandlungsbeginn während einer Schwangerschaft (S). VM: Keine gleichzeitige Behandlung mit anderen Fumarsäurederivaten. Labor: Grosses Blutbild (BB) mit Diff-BB: Obligat vor Beginn der Behandlung; empfohlen 3 und 6 Monate nach Therapiebeginn, dann alle 6 – 12 Monate sowie bei entsprechender Klinik; Nieren-/Leberfunktion: Empfohlen vor sowie 6 Monate nach Therapiebeginn, dann alle 6 – 12 Monate sowie bei entsprechender Klinik. Bei Leukopenie < 3.0 x 109/l oder Lymphopenie < 0.5 x 109/l Therapiepause. Bei schweren Infektionen Therapieun-terbrechung erwägen. Anwendung nur mit Vorsicht bei milder Nierenfunktionsstörung sowie nephrotoxischer Co-Medikation. S: Kontrazeptionsmassnahmen im gebärfähigen Alter obligat. Während einer S wird Tecfidera nicht empfohlen; falls doch, nur, wenn klinischer Befund dies zwingend erfordert und Nutzen für Patientin Risiko für Fötus überwiegt. UW: Flushing, Hitzewallungen, Pruritus, Ausschlag, Erythem, Gefühl des Brennens, GI Störungen (Diarrhoe, Übelkeit, Erbrechen, (Ober)Bauchschmerzen, Dyspepsie, Gastritis), Lymphopenie, Leukopenie, Proteinurie, Erhöhung AST und ALT. IA: Erhöhtes Infektionsrisiko bei begleitender Behandlung mit Immunsuppressiva (IS). Bei Vorbehandlung mit IS muss Immunkompetenz vor Therapiebeginn wieder hergestellt sein. Kein Einfluss von 325 mg ASS auf PK Profil. Liste B. Die vollständige Fachinformation ist unter www.swissmedicinfo.ch publiziert. Stand der Information: Februar 2014. TF-CH-0143a_10.2014

Biogen Idec Switzerland AG, Zählerweg 6, 6300 Zug, T +41 41 728 74 44, F +41 41 728 74 40.

Start at the Tecfidera level

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Eine neue Therapie in der 1st line-Behandlung der RRMS1

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Prof. Britta Engelhardt, BerneUniversity of Berne, � eodor Kocher Institute

� e central nervous system (CNS) is an immunologically privileged site to which access of cir-culating immune cells is tightly controlled by the endothelial blood-brain barrier (BBB) loca-lised in CNS microvessels and the epithelial blood-cerebrospinal � uid barrier (BCSFB) within the choroid plexus. Due to the specialised structure of the CNS barriers, immune cell entry into the CNS parenchyma involves two di� erently regulated steps: migration of immune cells across the BBB or BCSFB into the cerebrospinal � uid (CSF) drained spaces of the CNS, followed by progression across the glia limitans into the CNS parenchyma. With a focus on multiple sclerosis and its animal models I will describe the distinct molecular mechanisms required for the migration of di� erent immune cell subsets across the di� erent CNS barriers during immuno-surveillance and MS. I will include discussion of the therapeutic e� cacy and its associated risks by therapeutic targeting of immune cell entry into the CNS in MS.

HOW BRAIN BARRIERS CONTROL IMMUNE CELL ENTRY INTO THE CNS


NOTES

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Dr. Declan Chard, LondonUniversity College London, Institute of Neurology

While white matter lesions are the most obvious pathological manifestation of multiple sclerosis (MS), and white matter lesion load the magnetic resonance imaging (MRI) measure that is most o� en used in clinical practice and trials, they only partly explain clinical outcomes. � is has led to a search for pathology elsewhere that explains this discrepancy, and it has become apparent that white matter lesions actually represent the minority of the overall disease burden in people with MS. For example, white matter that appears to be lesion free when looked at using con-ventional MRI scans is abnormal when it is assessed using techniques such as magnetisation transfer imaging. Grey matter is also not spared the e� ects of MS, and in people with long-standing progressive disease the extent of demyelinating lesions may be signi� cantly greater in grey matter than in white matter. Grey matter lesions are di� cult to see on conventional MRI, but are detectable in much greater numbers using new MRI sequences such as double inversion recovery or phase sensitive inversion recovery. Histopathological studies have also shown that non-lesional grey matter is abnormal, and advanced MRI methods are now being used to assess this.

RECENT IMAGING DEVELOPMENTS TO UNMASK MS BURDEN


NOTES

Referenzen1. De Stefano, et al. Efficacy and safety of subcutaneous interfe-ron β-1a in relapsing-remitting multiple sclerosis: further outco-mes from the IMPROVE study. J Neurol Sci 2012;312(1-2):97-101. 2. Wissenschaftlicher Beirat der Schweizerischen MS Gesell-schaft. Immunmodulierende und immunsuppressive Therapie der MS Zusammenfassung der aktualisierten Empfeh lungen 2012. Schweiz Med Forum 2012;12(39):750-752. 3. Ghezzi A, et al. Current recommendations for multiple sclerosis treatment in pregnancy and puerperium. Expert Rev Clin Immunol 2013;9(7):683–692. 4. Fachinformation Rebif®, www.swissmedicinfo.ch. 5. PSUR No. 26 for Interferon beta-1a/Rebif®, 2012;28.

Gekürzte Fachinformation Rebif®/Rebif®/Rebif® ® multidose/Rebif® RebiDose™

Interferonum beta-1a ADNr. I: Patienten mit einem ersten klinischen, auf Multiple Sklerose (MS) hinweisenden neuro-logischen Ereignis bei Ausschluss anderer Diagnosen und glz. hohem Risiko für das Auftreten einer schubförmigen MS. Schubförmige MS. D: I.Allg. 44 µg, dreimal pro Woche subkutan.KI: Behandlungsbeginn während der Schwanger schaft, Über-empfindlichkeit gegen einen Inhaltsstoff, schwer wiegende Depressionen und/oder Suizidgedanken. V: Depressive Störun-gen, Krampfleiden, nicht adäquat therapierte Epilepsie, Anginapectoris, kongestive Herzinsuffizienz, Arrhythmie, schwere Hypersensitivitätsreaktionen, Hautläsionen an Injektionsstelle, schwere Nieren-/Leberinsuffizienz, schwerwiegende Leber funk-tions störungen, akute Myelosuppression, Alkoholmissbrauch. Regelmässige Kontrolle der Leberenzyme, grosses, resp. Differential blutbild, ggf. Schilddrüsenfunktionstest. IA: Medika-

mente mit enger therapeutischer Breite und/oder Meta-bolisierung über CYP P450 wie Antiepileptika oder Anti-depressiva. Häufigste UAW: Grippeähnliche Symptome, Entzündungen, Hautreaktionen und Schmerzen an der Injektionsstelle, Kopfschmerzen, Myalgie, Arthralgie, Müdig-keit, Rigor, Fieber, Anstieg der Leberfunktionswerte, Pruritus, Ausschläge, Urtikaria, Alopezie, Neutropenie, Lymphopenie, Leukopenie, Thrombozytopenie, Anämie, Durchfall, Erbrechen,Übelkeit, Depression, Schlaflosigkeit, Dyspnoe. P: Rebif® 8.8 µg/0.2 ml und 22 µg/0.5 ml Fertigspritzen: 6+6 (Start-packung*); 22 µg/0.5 ml oder 44 µg/0.5 ml Fertigspritzen: je 12*. Rebif® multidose Patronen zu 66 µg/1.5 ml oder 132 µg/1.5 ml: je 4*. Rebif® RebiDose™ 8.8 µg/0.2 ml und 22 µg/0.5 ml Fertigpens: 6+6 (Startpackung*); 22 µg/0.5 ml oder 44 µg/0.5 ml. Fertigpens: je 12*. [B] (*=kassenzulässig). Für detaillierte Informationen siehe www.swissmedicinfo.ch. AUG14 10/2014 d/f

Merck (Schweiz) AG, Merck Serono, Chamerstrasse 174, CH-6300 Zug, Tel. +41 41 729 22 22, www.merckserono.com

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Dr. Manuel Comabella, BarcelonaVall d‘Hebron University Hospital, Clinical Neuroimmunology Unit

Multiple sclerosis (MS) is a chronic in� ammatory disease of the central nervous system which is characterized by a high degree of heterogeneity in di� erent disease aspects, for instance, clinical manifestations, disease course, radiological � ndings, histopathological characteristics of brain lesions, and response to treatment. In this scenario, there is a necessity in MS of biomarkers that reliably capture these di� erent aspects of disease heterogeneity and may help in the MS diag-nosis and disease strati� cation, prediction of disease course, or identi� cation of new therapies bene� cial for the disease. � is talk will focus on prognostic cerebrospinal � uid molecular bio-markers that may help to predict disease severity in patients presenting with a clinically isolated syndrome or CIS.

USE OF BIOMARKERS TO ANTICIPATE MS SEVERITY


NOTES

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* GILENYA® ist zur Behandlung von Patienten mit schubförmig remittierend verlaufender Multipler Sklerose (MS) zur Reduzierung der Schubhäufigkeit und zur Verzögerung des Fortschreitens der Behinderung indiziert.

Referenzen: 1 Cohen JA et al. for TRANSFORMS Study Group. Oral fingolimod or intramuscular interferon for relapsing multiple sclerosis. N Engl J Med. 2010;362(5): 402–415. 2 Kappos L et al. for FREEDOMS Study Group. A placebo-controlled trial of oral fingolimod in relapsing multiple sclerosis. N Engl J Med. 2010;362(5): 387–401. 3 GILENYA® (Fingolimod) Fachinformation (www.swissmedicinfo.ch). 4 Press Release «Novartis Q2 and H1 2014 Condensed Interim Financial Report – Supplementary Data», 17. Juli 2014, www.novartis.com/downloads/investors/financial-results/quarterly-results/2014-07-interim-financial-report-en.pdf

Z: Kapseln zu 0.5 mg Fingolimod. I: Behandlung von Patienten mit schubförmig remittierend verlaufender multipler Sklerose (MS) zur Reduzierung der Schubhäufigkeit und zur Verzögerung des Fortschreitens der Behinderung. D: 0.5 mg 1x täglich oral. Spezielle Dosierungsempfehlungen: Keine Dosisanpassung erforderlich bei Niereninsuffizienz, bei leichter Leberinsuffizienz ist Vorsicht geboten. Einzelheiten s. www.swissmedicinfo.ch. KI: Myokardinfarkt, instabile Angina pectoris, Schlaganfall/TIA, dekompensierte Herzinsuffizienz (stationär behandlungspflichtig), oder Herzinsuffizienz NYHA-Klasse III/IV in den vorangehenden 6 Monaten. • Schwere Herzrhythmusstörungen, die eine Behandlung mit Klasse Ia und III Antiarrhythmika bedürfen. • AV-Block 2. Grades vom Typ Mobitz II oder ein AV-Block 3. Grades oder Sick-Sinus-Syndrom, sofern der Patient nicht mit einem Schrittmacher versorgt ist. • QTc-Intervall ≥ 500 ms bei Baseline. • Mittlere und schwere Leberinsuffizienz/Leberzirrhose (entsprechend Child-Pugh-Klasse B und C). • Akute oder chronisch aktive Hepatitis B Infektion • Bestehendes Makulaödem. • Kinder und Jugendliche. • Schwangerschaft und Stillzeit. VM: Überwachung nach Erstgabe von Gilenya: Bei allen Patienten 6-stündige Überwachung auf Symptome einer Bradykardie sowie auf atrioventrikuläre Überleitungsstörungen: stündliche Messungen von Puls und Blutdruck, 12-Kanal-EKG vor Behandlungsbeginn und nach der 6-stündigen Überwachung, Möglichkeit einer kardiologischen Notfallbehandlung, kontinuierliche (Echtzeit-) EKG-Überwachung während der ersten 6 Stunden wird empfohlen. • Während der ersten beiden Behandlungswochen werden nach einer Therapieunterbrechung von einem Tag oder mehr dieselben Vorsichtsmassnahmen wie bei der Erstgabe empfohlen; nach einer Therapieunterbrechung von mehr als 7 Tagen während der dritten und vierten Behandlungswoche werden dieselben Vorsichtsmassnahmen wie bei der Erstgabe empfohlen; nach einer Therapieunterbrechung von mehr als zwei Wochen nach dem ersten Behand-lungsmonat gelten dieselben Vorsichtsmassnahmen. • Bei Auftreten von symptomatischen Bradyarrhythmien in den ersten 6 Stunden: Überwachung bis zum vollständigen Abklingen der Symptome. • Wenn Herzfrequenz 6 Stunden nach Ersteinnahme den niedrigsten Wert erreicht: kardiales Monitoring bis zur Erholung der Herzfrequenz mindestens jedoch um 2 Stunden verlängern. • Wenn im EKG 6 Stunden nach der ersten Dosis: Herzfrequenz <45 Schläge/Min, persistierender neuer AV-Block 2. Grades oder höhergradiger AV-Block, QTc-Intervall ≥ 500 ms oder wenn ein AV-Block 3. Grades zu jedwedem Zeitpunkt auftritt: Verlängerung des kardialen Monitorings mindestens über Nacht. • Falls nach der ersten Dosisgabe medikamentöse Behandlung aufgrund von Bradyarrhythmien notwendig ist: Beobachtung über Nacht in einer medizinischen Einrichtung und bei der zweiten Dosis gleiche Überwachungsstrategie wie nach der ersten Dosis. • Für bestimmte Patientengruppen Gilenya nur dann in Betracht ziehen, wenn der erwartete Nutzen die potentiellen Risiken überwiegt: prädisponierte Patienten mit bekannter ischämischer Herzkrankheit (inkl. Angina pectoris), Stauungsinsuffizienz, zerebrovaskulärer Krankheit, unkontrolliertem Bluthochdruck, schwerer unbehandelter Schlafapnoe, sowie Patienten mit Erkrankungen in der Vorgeschichte: Myokardinfarkt, Herzstillstand, rezidivierende Synkopen, symptomatische Bradykardie: vor Behandlungsbeginn eine/n Kardiologen/in konsultieren und geeignetes kardiales Monitoring (mindestens über Nacht) festlegen. • Patienten unter Betablockern, Calciumkanalblockern (mit verlangsamender Wirkung auf die Herzfrequenz wie Verapamil, Dilitiazem, Ivabradin), anderen Substanzen, die die Herzfrequenz reduzieren (z.B. Digoxin, Azetylcholinesterasehemmer, Pilocarpin): vor Behandlungsbeginn eine/n Kardiologen/in konsultieren, um eine Umstellung des Arzneimittels auf eine Substanz ohne Herzfrequenz verlangsamende Wirkung bzw. verzögernde Wirkung auf die AV-Überleitung zu prüfen oder falls die Umstellung der Medikation nicht möglich, geeignetes kardiales Monitoring (inkl. kontinuierlichem EKG) mindestens über Nacht durchführen. • Bei Patienten mit signifikanter QTc-Verlängerung (QTc >470 ms bei Frauen, QTc >450 ms bei Männern) vor Behand-lungsbeginn oder zusätzlichen Risikofaktoren für das Auftreten einer QT-Verlängerung (wie z.B. Hypokaliämie, Hypomagnesiämie oder angeborenes Long-QT-Syndrom): vor Behandlungsbeginn eine/n Kardiologen/in konsultieren und geeignetes kardiales Monitoring (mindestens über Nacht inkl. kontinuierliches EKG-Monitoring in einer medizinischen Einrichtung) festlegen. • Akute oder chronische Infekte, insbesondere bei Verdacht auf Vorliegen einer Infektion mit Viren der Herpesgruppe. • Gleichzeitige Anwendung einer antineoplastischen, immunsupprimierenden oder immunmodulierenden Therapie. • Varizella-Zoster-Virus (VZV) Antikörperbestimmung bei Patienten, die weder Windpocken hatten noch gegen das VZ Virus geimpft wurden und Erwägung einer Impfung. • Augenärztliche Untersuchung mit Beurteilung des Augenhintergrunds, einschliesslich der Makula, vor Beginn und nach 3- bis 4-monatiger Therapie. • Visusuntersuchungen alle 6 Monate durch den Neurologen. • Regelmässige ophthalmologische Untersuchungen bei Patienten mit Diabetes mellitus, Uveitis und Makulaödem in der Krankengeschichte. • Bestimmung der Leberwerte vor Beginn und 1, 3 und 6 Monate nach Beginn der Therapie, im weiteren Verlauf periodisch. • Pulmonologische Untersuchung bei symptomatischen Patienten. • Dermatologische Untersuchungen bei Risikopatienten für maligne kutane Neoplasien. • Regemässige Blutbildkontrollen. • Bei der Umstellung von Natalizumab und von anderen Immunsuppressiva auf Gilenya ist Vorsicht geboten. • Weitere Einzelheiten s. www.swissmedicinfo.ch. IA: Antineoplastika, Immunsuppressiva, immunmodulierende Therapie bis 2 Monate nach Absetzen von Fingolimod. • Umstellung von lang wirkenden Immuntherapeutika wie Natalizumab oder Mitoxantron mit entsprechenden zeitlichen Abständen. • Attenuierte Lebendimpfstoffe, reduzierte Wirkung anderer Impfstoffe bis 2 Monate nach Absetzen der Therapie. • Betablocker, Calciumkanalblocker mit verlangsamender Wirkung auf die Herzfrequenz oder andere Substanzen, die die Herzfrequenz verlangsamen können bei Therapiebeginn. UW: Sehr häufig: Grippale Virusinfektionen, Kopfschmerzen, Husten, Durchfall, Rückenschmerzen, erhöhte Alanintransaminase. • Häufig: Bronchitis, Sinusitis, Gastroenteritis, Herpesvirus-Infektionen, Tinea-Infektionen, Leukopenie, Lymphopenie, Depression, Schwindel, Parästhesie, Migräne, Augenschmerzen, Verschwommensehen, Bradykardie, atrioventrikuläre Blocks, Hypertonie, Atemnot, Ekzem, Alopezie, Pruritus, Asthenie, erhöhte Gammaglutamyltransferase (GGT), erhöhte Leberenzymwerte, Gewichtsabnahme, erhöhte Bluttriglyzeride, anormaler Leberfunktionstest. • Gelegentlich: Pneumonie, Makulaödem. • Selten und sehr selten s. www.swissmedicinfo.ch. P: Kapseln zu 0.5 mg: 28* und 98*. Verkaufskategorie: B. *Kassenzulässig. Weitere Informationen entnehmen Sie bitte www.swissmedicinfo.ch. Novartis Pharma Schweiz AG, Risch; Domizil: Suurstoffi 14, 6343 Rotkreuz, Tel. 041 763 71 11.

Wirksamkeit 52% zusätzliche Schub-

reduktion gegenüber Interferon Beta-1a (i.m.)1

Verträglichkeit 1x täglich oral,

gut verträglich1–3

ErfahrungÜber 100’000 MS-Patienten

behandelt4

Wirksamkeit, der Sie vertrauen – Erfahrung, auf die Sie bauen.1–4*

Gewinner Prix Galien

2014


Prof. Milo Puhan, ZurichUniversity of Zurich, Epidemiology, Biostatistics & Prevention Institute

� e Swiss MS-Society has committed itself to funding a Swiss Multiple Sclerosis Registry (SMSR). � e main goal of the SMSR is to conduct surveillance of MS, and to promote MS research that re� ects the perspective of patients in Switzerland. More speci� cally, the goals are to estimate the number of patients with MS in Switzerland and the burden of disease for a� ected persons, their relatives, and society as a whole. � e registry should also aid Swiss MS research by establishing a large database of well-documented MS patients and by enabling international collaborations.

In order to achieve these very di� erent goals we will implement a � exible, layer-based design. � e di� erent layers are distinguished by the level of commitment by participants and the type and amount of data collected (i.e. from basic information about interested stakeholders in layer 1 to detailed phenotyping in layer 4). We will, in collaboration with social media and IT specia-lists, implement an IT infrastructure that will include a web platform through where interested stakeholders (patients, relatives, health care professionals, researchers, etc.) can get information about the registry and MS in general and interact.

� e SMSR shall be operated in a spirit of cooperation and mutual trust. Regional, national and international collaborations will be central to the SMSR. As a large-scale project the SMSR will have a clearly de� ned governance structure for making transparent and agreed decisions. A steering committee will oversee the activities and make strategic decisions. To avoid compe-ting interests, the core (data collection) of the SMSR will be � nanced by the Swiss MS-Society. Additional funding for speci� c sub-studies can and will be sought from other parties under the condition that those funds are unrestricted.

� e expected bene� ts of the SMSR are manyfold. � rough their active participation, patients and their proxies will experience better networks, more and better information on disease-related topics and advice regarding physical and mental health. � rough translational research from the lab to the patients we expect that health care services and access to existing therapies and, as a consequence, prognosis and quality of life of patients will improve.

NATIONAL MS REGISTRY


NOTES

AKTIV LEBEN. GESTERN. HEUTE. MORGEN.

COPAXONE® Z: Glatirameracetat. I: Behandlung von Patienten mit CIS sowie zur Reduktion der Schubfrequenz und zur Verlangsamung des Fortschreitens von Behinderungsgrad, Intensität und Schwere der Krankheit bei remittierenden Formen der MS mit einem Score von ≤5 auf der EDSS. D: Injektion s.c. an wechselnden Injektionsstellen, 20 mg täglich. KI: Hypersensibilität gegenüber Inhaltsstoffen, Schwangerschaft. IA: Überempfi ndlichkeitsreaktionen, Nierenfunktion niereninsuffi zienter Patienten regelmässig überprüfen. UAW: Schwindel, Depression, Angst, erhöhter Muskeltonus, Palpitationen, Vasodilatation, Dyspnoe, Nausea, Obstipation, Diarrhoe, Rash, Schwitzen, Arthralgien, Reaktionen an der Injektionsstelle, Kopfschmerzen, Asthenie, Schmerzen, Thoraxschmerzen, grippeähnliche Symptome, Rückenschmerzen. ATC: L03AX13 P: COPAXONE® 28 Fertigspritzen (20mg/ml) [B], Kassenzulässig. Weiterführende Informationen siehe Arzneimittelinformation www.swissmedicinfo.ch. Teva Pharma AG, Kirschgartenstrasse 14, 4010 Basel, www.tevapharma.ch.

Referenzen: 1. Johnson KP. Glatiramer acetate for treatment of relapsing-remitting multiple sclerosis. Expert Rev Neurother. 2012;12(4):371-384. 2. Ziemssen T et al. Poster presented at CONY, Berlin, 2014.

11/

2014

ÜBER 2 MILLIONENPATIENTENJAHRE ERFAHRUNG1 – 2

INTERACTIVE WORKSHOPS


14.15-15.00

15.00-15.20

15.20-16.05

16.05

Clinical case management� ese six interactive workshops are focused on the discussion of practical cases, with emphasis on aspects relevant to the daily management of MS patients.

Interactive Workshops A, B, C

Workshop AProf. Renaud Du Pasquier, Lausanne and Prof. Tobias Derfuss, Basel Complications of current and emerging MS therapies

Workshop BProf. Till Sprenger, Basel and PD Dr. Cristina Granziera, Lausanne MRI to monitor patients with brain and spinal cord white matter changes

Workshop CProf. Patrice Lalive, Geneva and PD Dr. Jens Kuhle, Basel Can cerebrospinal � uid and blood biomarkers add to the management of MS?

Co� ee Break

Interactive Workshops D, E, F

Workshop DDr. Claudio Gobbi, Lugano and Dr. Christian Kamm, Berne New treatment options: pro and contra

Workshop EDr. Sven Schippling, Zurich and Prof. Peter Fuhr, Basel OCT and electrophysiological techniques as tools to monitor MS: update

Workshop FPD Dr. Michael Linnebank, Zurich and Dr. Claude Vaney, Montana Increasing MS patients’ mobility: update

Farewell Apero


Prof. Renaud du Pasquier, LausanneLausanne University Hospital, Service of Neurology

Prof. Tobias Derfuss, BaselUniversity Hospital Basel, Departments of Neurology and Biomedicine

Recently, a number of new treatments have been registered for the treatment of relapsing-remitting MS and some more are in the late stage of clinical development. � ese treatments obviously open new possibilities but also present novel challenges.

� is workshop will focus on the side e� ect pro� le of the new oral therapies Gilenya®, Aubagio®, and Tec� dera® and also discuss the emerging treatments with alemtuzumab and daclizumab that have completed phase III clinical development. � e most prominent problem of all these therapies, to varying degrees - are infectious complications.

However, every drug has its own risk pro� le and therefore requires speci� c precautions. We will provide information on screening exams before start of treatment and safety monitoring during treatment. We will also touch the topic of switching and sequencing treatments that may also have an in� uence on the treatment emerging side e� ects.

WORKSHOP A

COMPLICATIONS OF CURRENT AND EMERGING MS THERAPIES


NOTES


Prof. Till Sprenger, BaselUniversity Hospital Basel, Clinic and Polyclinic for Neurology

PD Dr. Cristina Granziera, LausanneLausanne University Hospital, Department of Clinical Neurosciences

MRI is a key paraclinical tool for the diagnosis and di� erential diagnosis of demyelinating dis-orders. It is also becoming more and more important for monitoring the disease course of MS and related disorders as MRI is very sensitive to subclinical disease activity.

However, there is no general agreement on how and when to follow up MS patients with MRI. Several MRI metrics such as lesional Gadolinium enhancement, new or enhancing T2 lesions, lesion volume, black holes, brain atrophy, or subtle tissue changes as detected with MTR or DTI could potentially inform treatment decisions. As of yet, however, a consensus remains to be for-med as to what levels of MRI activity should lead to treatment change or at least a consideration of change. Furthermore, some of the MRI metrics are di� cult to standardise and implement in clinical practice.

In this workshop, we will discuss conventional and advanced neuroimaging metrics that could guide treatment decisions.

WORKSHOP B

MRI TO MONITOR PATIENTS WITH BRAIN AND SPINAL CORD WHITE MATTER CHANGES


NOTES


Prof. Patrice Lalive, GenevaGeneva University Hospital, Service of Neurology

PD Dr. Jens Kuhle, BaselUniversity Hospital Basel, Department of Neurology

Despite the fact that diagnosis of multiple sclerosis (MS) is based on clinical suspicion and typi-cal magnetic resonance imaging � ndings, cerebrospinal � uid (CSF) analysis remains important in order to support the diagnosis and exclude alternative diseases. � is is especially important since our understanding of the de� ning disease pathogenesis remains incomplete and no spe-ci� c markers are currently available to con� rm the disease. According to the recent diagnostic criteria, MS requires establishing that «there is no better explanation for the clinical picture».

Using optimised, standardised methodology, preferentially protein separation by isoelectric fo-cusing followed by immunoblotting, more than 95% of patients with MS have CSF oligoclonal bands (OCB) of IgG class not detectable in serum, thereby providing powerful evidence for the diagnosis of MS. Although the clinical picture as well as � ndings from MRI are essential for an MS diagnosis, this should be re-evaluated in CSF OCB-negative patients, keeping in mind the many disease entities imitating MS.

We will review the stepwise approach to CSF analysis and present some patient cases illustrating the relevance of CSF analysis. � e assessment classically includes blood tests to exclude infec-tions and systemic autoimmune diseases. Here, we propose to make a short, non-exhaustive review of viral and immunological tests that can be performed in the assessment of a patient with suspicion of MS. In addition we will discuss the utility of new biological tests, including vitamin D, EBV serology, oligoclonal IgM bands, new antibodies like KIR 4.1, chitinase 3 like 1 and neuro� laments that may help to monitor therapeutic decision in MS in future.

WORKSHOP C

CAN CEREBROSPINAL FLUID AND BLOOD BIOMARKERS ADD TO THE MANAGEMENT OF MS?


NOTES


Dr. Claudio Gobbi, LuganoRegional Hospital of Lugano, Neurocenter of Southern Switzerland

Dr. Christian Kamm, BerneBerne University Hospital, Department of Neurology

Considering the growing number of therapeutic agents in multiple sclerosis with di� erent mo-des of action, application, e� cacy, tolerability and safety pro� les, the future challenge will be to choosing the most e� cacious, safe and tolerable drug for the individual patient.

� is workshop aims at discussing the current treatment options focusing on the «pros» and «cons» of «old» vs. «new» drugs and at proposing a treatment algorithm. � is will � nally be illustrated and discussed with the aid of practical case reports.

WORKSHOP D

NEW TREATMENT OPTIONS: PRO AND CONTRA


NOTES


Dr. Sven Schippling, ZurichUniversity Hospital Zurich, Department of Neurology

Prof. Peter Fuhr, BaselUniversity Hospital Basel, Department of Neurology

Until about 20 years ago, the main role of electrophysiology in the assessment of MS was diag-nostic. With the broad accessibility of MRI, evoked potentials have largely lost their diagnostic importance. However, research into and clinical application of disease modifying treatment have led to an increased interest in prognosis and long term monitoring, and in this domain functional assessment including characterization of neurophysiological capacity is important. A reliable and valid way to characterize some important aspects of neurophysiological capacity consists in the recording of evoked potentials (EP). Since MS may a� ict any central nervous connection, the sensitivity of EP recording increases with the number of modalities and the length of the tested tracts. � erefore, multimodal (visual, somato-sensory, motor, and possibly other) EP are used to assess electrophysiologically a patient. Multimodal EP yield numerical data and have been demonstrated to correlate with clinical � ndings in cross-sectional and lon-gitudinal comparison. Moreover, probably in part due to the sensitivity of EP to subclinical lesions, they also correlate with prognosis over two and up to 20 years.

While validity of multimodal EP to characterize groups of patients has been shown repeatedly, their applicability for counselling individual patients is still a goal of current research. Never-theless, they can be helpful to de� ne prognostic groups of patients in MS and measure their course, and therefore, may contribute to acceleration of clinical trials.

WORKSHOP E

OCT AND ELECTROPHYSIOLOGICAL TECHNIQUES AS TOOLS TO MONITOR MS: UPDATE


NOTES


PD Dr. Michael Linnebank, ZurichUniversity Hospital Zurich, Department of Neurology

Update: Detailed e� ects of prolonged-release fampridine on disability of patients with mul-tiple sclerosis (FAMPKIN and FAMPKIN-EXT)

Background and Objective: Recent Phase III clinical trials demonstrated the bene� cial e� ects of fampridine (4-aminopyridine) on gait velocity in a subset of patients with MS. Fampridine blocks voltage-gated potassium channels leading to enhanced signal conduction in demyelina-ted nerve � bers. � e FAMPKIN core study (http://clinicaltrials.gov) aimed to characterise the e� ects of prolonged-release (PR) fampridine on di� erent modalities of ambulatory function including muscle strength, stability and coordination. � e extension study (Fampkin-EXT) fol-lowed the core study and aimed to assess the long-term e� ects and tolerability of fampridine in some of the patients who completed the core study (n=53 patients).

Methods: FAMPKIN designed as a phase II, double-blind, randomized and placebo-controlled cross-over study assessed gait function during two double-blind fampridine or placebo treatment phases (each 6 weeks). Walking was investigated using di� erent clinical tests, questionnaires and detailed kinematic-kinetic gait analysis. 55 patients with relapsing-remitting, primary- and secondary-progressive MS completed the study (34 women, 21 men; age 48.4 +/- 9.7 years; median EDSS = 4.5). 53 patients previously enrolled in the FAMPKIN study were included in the extension study (33 women, 20 men; age: 49.7 +/- 9.2 years; EDSS 5.3 +/- 1.2) and treated with prolonged-release fampridine (10mg twice daily; open-label).

Results: In the FAMPKIN core study, patients were classi� ed into responder and non-responder according to the criteria used by Goodman et al. (Lancet, 2009). 31% (n=17) of all participants were fampridine-responder, 5% (n=3) were placebo-responder, and 9% (n=5) met the respon-der criteria in both phases. During fampridine treatment, gait velocity (timed-25-foot walk) was increased by 5.8% in the total population (n=55), 12.3% in the pure fampridine-responder subgroup (n=17), and by 3.3% in non-responders (n=29) compared to the placebo treatment. Walking endurance (6-minute walk test) was improved by 8.5% in the total population, 13.5% in responders, and 6.1% in non-responders. Stationary and dynamic measures of stability did not reveal signi� cant changes induced by fampridine. A portable accelerometer device (actime-ter) measured physical activity during 14 days in each double-blind treatment period. Physi-cal activity during daily life was signi� cantly increased during the fampridine treatment phase compared to the placebo phase in the pure fampridine-responder subgroup, but not the other subgroups.

WORKSHOP F

INCREASING MS PATIENTS’ MOBILITY: UPDATE


Gait pro� les consisting of multiple kinematic and kinetic parameters demonstrated heterogene-ous, fampridine-induced gait modi� cations. � e di� erential changes in the gait pattern among patients most probably re� ect individual improvements of the gait pattern depending on the speci� c de� cits of each patient.

� e results of the � rst extension year con� rm the data of the core study: patients got slower (timed-25-foot walk: -15%) when fampridine was stopped for 14 days a� er continuous treat-ment for 11.5 months. Walking endurance (6-minute walk test) was reduced by 9% a� er the 14 days washout phase. � ese changes in walking function were self-perceived by the patients, as demonstrated by the 12-item MS walking scale (12MSWS).

Conclusion: � e present studies demonstrate bene� cial e� ects of fampridine on di� erent as-pects of locomotion and indicates the clinical relevance of this treatment for a proportion of patients with MS. Fampridine is a well tolerated symptomatic treatment for MS patients and can exert its bene� cial e� ects over long periods of application.

WORKSHOP F


Dr. Claude Vaney, Crans MontanaBerner Klinik Montana, Neurological Rehabilitation Unit

Assessing quickly and graphically the Mobility in MS and other neurological Disease with the new Iphone App Sagas 10

Objectives: Assuming that this tool could also be used for other neurological diseases where walking and hand function is impaired, we set out to examine the validity and the responsive-ness of SaGAS 10 in neurological patients attending a rehabilitation facility. Furthermore, we evaluated whether the 25 feet walking has a high correlation with the 2-minute walking test in patients with slow walking speed.

Methods: 646 consecutive patients with di� erent neurological diseases (MS 296, stroke 152, Par-kinson 21, neuromuscular disorders 42, trauma 42, others 93) were assessed at the beginning and at the end of their rehabilitation stay using the FIM (Functional Independence Measure), the RMI (Rivermead Mobility Index, the 2-minute timed walking distance at maximum speed (2MWD) and the 3 measures composing SaGAS 10 (the 25 feet timed walk at fast speed with a � ying start (T25FW) and the nine-hole peg test (9-HPT) for each hand separately). Construct validity was assessed with correlations between FIM, RMI and the SaGAS 10, where correlations above 0.7 were hypothesized. Responsiveness was assessed by a receiver operating characteristic curves (ROCs) analyses comparing changes in SaGAS 10 with minimal clinically important changes in the RMI. An area under the curve value (AUC) of at least 0.7 was considered as appropriate.

Results: � e correlation of the SaGAS 10 with the Rivermead Mobility Index is above 0.7 in all of the neurological diagnostic groups; the highest correlation coe� cient was found in patients with stroke: 0.76. � e correlation of the SaGAS 10 with the FIM was over 0.7 for stroke and MS. � e responsiveness was acceptable with AUCs of 0.72 for stroke and values over 0.7 for all groups, with the exception of MS. � e e� ect-sizes were moderate to high, especially for stroke with Cohen’s d values of 0.48. � e correlation between the 25 feet test and the 2 minutes wal-king test was 0.63 for those walking slower than 0.96 m/s; and 0.64 for those walking faster than 0.96 m/s.

Conclusions: � ese results indicate that SaGAS 10 is valid and sensitive to changes over time and that it could be a useful measure not only for patients with MS, but also for patients with other neurological diseases. Our results indicate that for slow walkers the 25 feet walking test might be a good alternative for the 2-minutes walking test.

WORKSHOP F

INCREASING MS PATIENTS’ MOBILITY: UPDATE


NOTES

WE THANK YOU FOR YOUR PARTICIPATION AND WISH YOU A SAFE JOURNEY HOME.

SEE YOU NEXT YEAR AT THE 18TH STATE OF THE ART SYMPOSIUM.

BEST REGARDSSWISS MULTIPLE SCLEROSIS SOCIETY

GOODBYE

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