Speakers and abstracts

At this page you can find the short bio's of the speakers and abstracts of the talks.

Short bio's 

Nikolaos Grigoriadis

Professor Grigoriadis graduated from the Faculty of Medicine of the Aristotle University of Thessaloniki. He did his PhD thesis and residency in Neurology in the same institution. He has been specialized in clinical and experimental Neuroimmunology and CNS immunopathology in a number of research centers and institutions abroad. He is now Professor of Neurology at the Aristotle University of Thessaloniki and  Head of the of the B’ Dept of Neurology, AHEPA University Hospital, the MS Centre and the Laboratory of Experimental Neurology and Neuroimmunology (www.neuroimmunology.gr). Professor Grigoriadis is member of various international scientific committees such as the European School of Neuroimmunology, ParadigMS, the subcommittee of ENS for Multiple Sclerosis, the ECTRIMS committee (until 2010), Co-founder and Secretary of the Hellenic Academy of Neuroimmunology (www.helani.gr). He is President of the Hellenic Neurological Society. He is Ad Hoc reviewer in more than 40 international scientific journals, co-ordinator in more than 40 multicenter clinical trials for MS and principal investigator in collaborative research projects for experimental cell therapies in CNS autoimmune demyelination. His field of interests are:  Neuroimmunology; Multiple sclerosis; experimental models of autoimmune diseases (EAE etc); neurodegeneration; immunomodulation; cell therapies. He has published more than 180 papers in peer reviewed journals. He has been awarded several times for his scientific work.

Carlo Pozzilli

Professor Pozzilli studied at the University of Rome “La Sapienza”. He then moved to the Hammersmith Hospital in London, UK, to take up a research post in 1980.In 1983, he became a Board Certified Neurologist at the University of Rome. In 1986 obtained a research grant in Neuroimaging at the Tohoku University, Sendai Japan.In 1987, he was awarded a PhD in Clinical Neurosciences by the University of Rome, where he became Full Professor in 2006. In 2002 he funded and become Director of the Multiple Sclerosis (MS) Center of OspedaleS.Andrea, University of Rome which is his actual position. Professor Pozzilli’s fields of interest include the clinical aspects and treatment of MS; he has published more than 350 papers and reviews on these subjects. Professor Pozzilli is a member of several National and International Societies. He has participated as a first investigator in at least 250 multicentre clinical trials on patients with MS. He was also member of the Steering Committee and Advisory Board inseveral multicentre trials.

Vincent van Pesch 

Professor Vincent van Pesch is Clinical Head at the Cliniques Universitaires Saint-Luc and Principal Investigator of the Neurochemistry Unit (Institute of Neuroscience, UClouvain). He is mainly involved in the diagnosis and treatment of neuro-immunological disorders, among which Multiple Sclerosis, with over 1000 patients followed. He is also involved in clinical neurophysiology and responsible for interpreting neurochemistry and neuro-immunological tests. He is involved in the international MSBase registry. His main research interests include biomarkers for MS and other neurological disorders, immunology of MS and more recently the role of microRNAs and extracellular vesicles in MS. He has published over 100 peer-reviewed articles.

Bart Van Wijmeersch

Professor Van Wijmeersch completed his general medical training in 2001 at the University of Leuven, Belgium, after which he started his specialization in Neurology. During this residency he started a PhD in neuroimmunology at the lab of experimental transplantation and neuroimmunology at the Catholic University Leuven. He was promoted in 2008 with a thesis entitled: 'Graft-versus-autoimmunity after induction of mixed bone marrow chimerism in murine models of experimental autoimmune encephalomyelitis'. Since 2008 he is active as neurologist, specialized in Multiple Sclerosis, at the Rehabilitation & MS Center in Overpelt, were he is medical director and leads a multidisciplinary MS-team.  He is a member of the board of the Belgian Study Group for Multiple Sclerosis and the first president of the ParadigMS Foundation, an international organization dedicated to improve the transfer of scientific knowledge on MS to the daily practice of MS care. As associate professor of Neurology at the University Hasselt, he is affiliated with the Biomedical Institute of the University, where he is involved in the clinical and fundamental research in Multiple Sclerosis.


Workshop 1: Progressive forms of Multiple Sclerosis: pathogenesis and treatment options.

Carlo Pozzilli and Bart Van Wijmeersch

Multiple Sclerosis (MS) is a chronic disease that damages the myelin of the central nervous system (CNS) and causes neurological impairment and  disability. Progressive MS  (PMS) is characterized by a continuous clinical deterioration without recovery.

Patients who initially present with PMS are termed primary progressive (PPMS), while those who evolve to PMS after initially presenting with RRMS are termed secondary progressive (SPMS).

 Active patients experience superimposed inflammatory episodes  (occurrence of clinical relapses at least once annually and/or enlarged, new or contrast enhancing T2 lesions).

Non-active patients do not have clinical relapses and MRI activity (e.g., gadolinium enhancing MRI lesions, new or enlarging T2 lesions) since 1 year.

Although there are multiple approved drugs for the treatment of RRMS, current treatments have limited therapeutic benefit in PMS patients, especially the non-active population.

In active PPMS patients, Ocrelizumab can be prescribed. Ocrevus is a humanized monoclonal antibody that selectively depletes CD20-expressing B cells.The initial 600 mg dose is administered as two separate intravenous infusions; first as a 300 mg infusion, followed2 weeks later by a second 300 mg infusion. Subsequent infusions are administered as a single 600 mg intravenous infusion every 6 months

Siponimod is indicated for SPMS. Siponimod is a sphingosine 1-phosphate receptor (S1P) modulator which selectively binds the S1P1 and prevents lymphocytes from entering the lymph nodes and the central nervous system (CNS). The approval, was based on results of the EXPAND study, a randomised, double-blind, placebo-controlled trial which compared the safety and efficacy of Siponimod to a placebo.

Considering the lack of other treatment options, PMS patients are prescribed DMT agents off-label as well  as symptomatic treatments (e.g., fampridine) to improve their quality of life.

Workshop 2: NMO spectrum disorders: clinics, diagnosis and treatment options.

Nikolaos Grigoriadis

Diagnostic errors may still common in Multiple Sclerosis (MS). In a number of cases where T2 lesions are identified in MRI may be considered as MS lesions resulting in inappropriate, sometimes harmful therapeutic interventions for the patient. Mono- or multi-focal symptoms consistent with inflammatory demyelinating disease, are subject to differential diagnosis. Neuromyelitis optica spectrum disorders (NMOSD) are autoantibody mediated chronic inflammatory diseases. Serum antibodies (Abs) against the aquaporin-4 water channel lead to recurrent attacks of optic neuritis, myelitis and/or brainstem syndromes. In addition, in some patients with symptoms of NMOSD, Abs against myelin-oligodendrocyte-glycoprotein (MOG) though not AQP4 are detectable. These clinical syndromes are now frequently referred to as “MOG-encephalomyelitis” (MOG-EM). The two groups of disorders may have similar symptoms though distinct clinical courses or lesion distribution throughout central nervous system (CNS) as indicated by the MRI findings.  A central component of diagnostics in NMOSD and MOG-EM is the detection of the correspondent serum Abs. Differential diagnosis from other conditions with similar symptoms such as sarcoidosis or MS and other CNS disorders should be performed on the basis of relevant laboratory test.  In NMOSD as well as in MOG-EM, acute attacks are usually treated with 1,000 up to 2000 (in some cases) mg intravenous methylprednisolone (IVMP) for 3–5 days with complete or almost complete recovery in 50% and 17-35% of IVMP treated MOG-EM and NMOSD attacks, respectively.  In case of poor response, treatment escalation with plasma exchange (PLEX) is indicated. Long term therapy includes immunosuppression to reduce disease activity and to avoid further attacks. However, in the absence of placebo controlled trials, treatment choice is based on case reports, observational studies etc. Thus, Azathaioprine, Rituximab, Mycophenolate Mofetil, low dose Prednisone/Prednisolone may be among the currently used therapeutic options. On the contrary, Treatment with medications indicated for MS such as interferon-beta, glatiramer acetate, fingolimod, alemtuzumab, natalizumab, and dimethyl fumarate is known to have no effects in NMOSD / MOG-EM or may even be proven harmful. Evidently, it is of importance to establish the right diagnosis before any decision making for treatment.

Vincent van Pesch

The diagnostic criteria of Neuromyelitis Optica Spectrum Disorders (NMOSD) have considerably evolved during the past 20 years, allowing for more precise and earlier diagnosis. Along with increasing knowledge regarding the pathology of this broadening disease entity, there have been significant advances in therapeutic strategies. This workshop will review current diagnostic criteria of NMOSD, highlight key clinical and radiological features distinguishing MS from anti-aquaporin-4 and anti-MOG-mediated disease and discuss NMOSD diagnostic pitfalls. An update on existing and future treatments as well as treatment algorithms will be provided. The workshop will be illustrated by clinical cases.

Plenary session

Biomarkers in MS - Nikolaos Grigoriadis

Multiple Sclerosis is an autoimmune, multifactorial disorder with its main hallmarks the persistent neuroinflammation and chronic neurodegeneration. Despite its extensive study, the lack of reliable and specific biomarkers for the disease makes it difficult to achieve differential diagnosis and delays early treatment. The disease is also characterized by high heterogeneity, a factor that complicates the process of finding suitable biomarkers. A number of biomarkers such as the anti-Aquaporine 4, the anti-MOG Abs are among those currently being used for the differential diagnosis of CNS demyelinating processes, the anti-JCV Abs for the safe administration of DMTs, particularly natalizumab (NTZ) treatment together with the anti-NTZ neutralizing Abs in case of treatment failure are well established for the daily clinical practice.  Interestingly enough, there is increasing evidence indicating that the plasma neurofilament light chain (pNfL) concentrations in relapsing remitting multiple sclerosis (RRMS) may be a valuable biomarker reflecting the neurodegenerative process which underlies the corresponding disability progression. Moreover, recent reports provide evidence that  the choice of disease modified treatment in RRMS is significantly associated with degree of reduction in pNfL, which supports a role for pNfL as a drug response marker. In addition, all “omics” approaches are high throughput, data-driven, and holistic methodologies and metabolomics in particular may be used for the discovery of biomarkers. Metabolomics use the means of cutting-edge technologies, like NMR and MS, in the analysis of high throughput data and following the requirements of personalized medicine aims to a patient-tailored healthcare. Also, seeks to capture the complexity of metabolic networks, create a personalized metabolomic profile for the disease and the final goal is to identify metabolites that can be used as candidate biomarkers in daily clinical practice. Those biomarkers will contribute not only in prognostic evaluation but also as a mean of monitoring the disease or treatment efficacy.

The implementation of soluble as well as novel imaging biomarkers may complement current clinical and imaging monitoring. However, the road map to establish a molecule as potential biomarker in a complex disease such as MS is a long one. On the other hand, it may be the only way to develop a precision medicine approach in the overall management of the disease.

Epidemiology of MS - Carlo Pozzilli

Multiple sclerosis (MS) is a major cause of neurological disability with a considerable socioeconomic burden. This presentation provides an overview of recent estimates of the worldwide prevalence and incidence rates, of changes in the distribution MS by age and sex, as well as looking at some recent advances in understanding of environmental epidemiology and the natural history of MS.

Although MS is present in all regions of the world, the incidence and prevalence is higher in some countries than in others. This is occurring in populations at high risk (such as Sardinia) and in those at low risk (such as Norway), suggesting that, whatever the causative factors of MS may be, their influence appears to increase.

In addition, an increase in the female/male ratio has been demonstrated over time in many countries around the world.

One of the most striking indicators of a potential environmental role has always been considered to be the gradient of MS prevalence with latitude.

Susceptibility to MS is complex, with evidence supporting both genetic and environmental factors, with genetic effects shaping the population risk for MS. A major supporting factor for a genetic effect is the positive family history of MS observed in 20% of all patients of European descent and estimates of MS heritability (the proportion of phenotypic variance attributable to heritable factors)range from 25 to 76%.Although epidemiological studies provide evidence of a genetic basis, the specific gene or genes remain elusive.

A large number of environmental or lifestyle factors have been identified to play a role in MS including smoking, pre-pubertal diet, childhood obesity, pollution, exposure to the Epstein-Barr virus and low exposure to sunlight (mediated through vitamin D insufficiency). A number of studies support a significant role for hypovitaminosis D as a risk factor for multiple sclerosis. Additional research is needed to conclusively prove which factors are important in increasing the risk of MS.