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Thursday, April 11
Hall A
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15:00-16:30 |
Satellite Symposium of the Society for the Study of Neuroprotection and Neuroplasticity (SSNN)
Chairpersons: N. Bornstein, Israel; D. Muresanu, Romania
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| 15:00-15:20 |
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| 15:20-15:40 |
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| 15:40-16:00 |
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| 16:00-16:20 |
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16:30-16:45 |
Break
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16:45-18:45 |
Opening Session
Chairpersons: M. Emre, Turkey; A.D. Korczyn, Israel
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16:45-17:00 |
Greetings
M. Emre, Turkey; A.D. Korczyn, Israel
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17:00-17:20 |
S. Baloyannis, Greece
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17:20-17:40 |
Hospitals in 13th-15th century Ottoman Empire
A. Demirtas-Tatlidede, Turkey
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Chairpersons: B. Dora, Turkey; L. Kruglov, Russia
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17:40-18:00 |
D. Muresanu, Romania
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18:00-18:45
18:00-18:15
18:15-18:30
18:30-18:45 |
Debate: Is MCI-PD a useful diagnosis?
No: A.D. Korczyn, Israel
Discussion
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Welcome Reception, at the Exhibition Area
18:45
Sponsored by Takeda Pharmaceuticals
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Hall A - STROKE
Section Heads: N. Bornstein, Israel ; N. Uzuner, Turkey
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06:45-08:15 |
E-Poster Presentations - Stroke
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08:30-10:30 |
Acute Ischemic Stroke (AIS)
Chairpersons: Y. Degirmenci, Turkey; J. Wojczal, Poland |
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08:30-09:00 |
Lecture: Are the current outcome parameters in stroke clinical trials clinically relevant? |
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08:30-08:45
08:45-09:00 |
Commentator: N. Bornstein, Israel
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Capsule: |
Intravenous rtPA is the only approved therapy for AIS within 4.5 hours of onset. However, in a sub-group of patients with large artery occlusion, the endovascular approach is preferred by many vascular neurologists. The recent IMS3 trial failed to show that endovascular treatment is better than IV-rtPA. So, does rtPA remain the best and only treatment for AIS? This debate will discuss the consequences of the results of IMS3 and what should be the next step |
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09:00-09:45
09:00-09:15
09:15-09:30
09:30-09:45 |
Debate: Is IV tPA the definite treatment in acute large artery occlusion?
Commentator: M. Bar, Czech Republic
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Capsule: |
All clinical trials used to evaulate tPA were based on CT results. However, with the advanced neuroimaging tools the penumbra can be detected accurately even beyond the approved 4.5 hours and in other uncertain conditions like wake-up stroke this may facilitate the decision regarding the therapeutic approach |
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09:45-10:30
09:45-10:00
10:00-10:15
10:15-10:30 |
Debate: Is AIS evaluation-multimodal CT superior to MRI?
Commentator: D. Heiss, Germany
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10:30-11:00 |
Coffee Break
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11:00-13:00 |
Asymptomatic Carotid Artery Stenosis (ACAS)
Chairpersons: A. Guekht, Russia; K. Kutluk, Turkey |
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Capsule: |
The best management of ACAS is a matter of continuous controversy. To intervene or to adopt a conservative approach with "aggressive" medical therapy for stroke prevention is currently the center of the debate. Intervention vs. best available medical therapy (BAMT) will be discussed |
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11:00-12:00
11:00-11:15
11:15-11:30
11:30-11:45
11:45-12:00
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Debate: Intervention vs. BAMT in ACAS
Discussion
Commentator: J. Norris, UK
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Capsule: |
To intervene or not is a continuous debate for many years, especially nowadays when the natural history of ACAS is more benign. Nevertheless, identifying a high-risk subgroup of patients with ACAS is a challenge. This debate will discuss this important issue - can we identify the high-risk sub-group of ACAS where intervention is justified? |
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12:00-13:00
12:00-12:15
12:15-12:30
12:30-12:45
12:45-13:00
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Debate: Are there any relevant indicators for Intervention in ACAS?
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13:00-14:00 |
Lunch Break
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14:00-16:00 |
Stroke Prevention
Chairpersons: D. Bartko, Slovakia; R. Nitrini, Brazil |
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Capsule: |
Atrial fibrillation (AF) is a major risk factor for cardio-embolic strokes.Warfarin was proven to reduce the risk of stroke by about 62%. However, only 1/3 patients with AF are actually taking coumadin and of them, only 50% achieve therapeutic INR. New anticoagulants are at least equally effective with no need for monitoring blood levels. Will coumadin disappear to be replaced by these new, more expensive drugs? |
| 14:00-15:00 |
Debate: AF-related stroke should be treated only with new anticoagulants |
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14:00-14:15
14:15-14:30
14:30-14:45
14:45-15:00 |
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Capsule: |
Patient foramen ovale (PFO) is associated with AIS in the young. However, association does not mean causation and the fact that PFO is present in young patients with cryptogenic strokes does not necessarily mean that we should close it |
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15:00-16:00
15:00-15:15
15:15-15:30
15:30-15:45
15:45-16:00
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Debate: PFO - to close or not to close?
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16:00-16:30 |
Coffee Break
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16:30-18:00 |
Stroke Management
Supported by an unrestricted grant from Takeda Pharmaceuticals
Chairpersons: M. Bar, Czech Republic; J. Streifler, Israel |
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| Capsule: |
Neuroprotection is one of the major strategies of the management of AIS. However, for decades the stroke scientific community has been looking for the "magic neuroprotective drug" - but the saga of neuroprotection in AIS is very sad. Until recently, many compounds which were proven promising in animal models failed in human trials.. Whether neuroprotection is still a valid concept for the treatment of AIS is the topic of this interesting debate |
| 16:30-17:30 |
Debate: Are neuroprotedtion agents still an option for acute ischemic stroke (AIS)? |
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16:30-16:45
16:45-17:00
17:00-17:15
17:15-17:30 |
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17:30-18:00
17:30-17:45
17:45-18:00 |
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Hall B - HEADACHE
Section Heads: Hayrunnisa Bolay, Turkey ; Alan Rapoport, USA
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07:00-08:15 |
E-Poster Presentations - Headache & Pain
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08:30-10:30 |
Clinical Trial Endpoints; Migraine and the Cortex
Chairpersons: H. Bolay, Turkey; A. Rapoport, USA
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Capsule: |
New medications come to market on the basis of double-blind, placebo-controlled clinical trials with very specific endpoints. Are the endpoints used in these trials clinically relevant? |
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08:30-09:30
08:30-08:45
08:45-09:00
09:00-09:15
09:15-09:30 |
Debate: The endpoints used in headache drug trials are clinically relevant
Yes: S. Baskin, USA
Discussion
Commentator: A. Siva, Turkey
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Does a migraine attack begin in the cortex and is the cortex critical in the migraine process? |
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09:30-10:30
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Debate: The cortex is critical in the pathophysiology of migraine
Discussion
Commentator: L. Edvinsson, Sweden
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10:30-11:00 |
Coffee Break
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11:00-13:00 |
Migraine Therapy
Supported by an unrestricted grant from Allergan
Chairpersos: M. Ashina, Denmark; A. Siva, Turkey
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Capsule: |
OnabotulinumtoxinA is becoming the accepted treatment for chronic migraine in many countries and is gaining approval from the authorities all over the world. Is it the best treatment for chronic migraine? |
| 11:00-12:00 |
Debate: The best treatment for chronic migraine is onabotulinumtoxin A (Botox) |
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11:00-11:15
11:15-11:30
11:30-11:45
11:45-12:00 |
Discussion
Commentator: H. Hamburger, The Netherlands
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| Capsule: |
CGRP is a vital molecule in the body and blocking its effect in the brain seems to be helpful in migraine. Is it the key molecule in headache and if not, why not? |
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12:00-13:00
12:00-12:15
12:15-12:30
12:30-12:45
12:45-13:00 |
Debate: CGRP is the key molecule in migraine
Discussion
Commentator: L. Vecsei, Hungary
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13:00-14:00 |
Lunch Break
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14:00-16:00 |
Stimulating the Spenopalatine Ganglion (SPG) in Cluster Headache; Role of Imaging in Headache Management
Chairpersons: A. Özge, Turkey; J. Schim, USA
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Capsule: |
Chronic cluster headache may be one of the toughest types of head pain syndromes to treat. Should we be looking to sphenopalatine ganglion stimulation or continue to treat with medications and other techniques? |
| 14:00-15:00 |
Debate: Chronic cluster headache is best treated with SPG stimulation |
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14:00-14:15
14:15-14:30
14:30-14:45
14:45-15:00
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Discussion
Commentator: A. Rapoport, USA
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| Capsule: |
Neuroimaging has become very sophisticated and acurate. But is it helpful in diagnosing various headache disorders? |
| 15:00-16:00 |
Debate: Neuroimaging is an essential tool for diagnosis of headache disorders |
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15:00-15:15
15:15-15:30
15:30-15:45
15:45-16:00 |
Discussion
Commentator: M. Lainez, Spain
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16:00-16:30 |
Coffee Break
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16:30-18:30 |
Sleep and Migraine
Chairpersons: H. Hamburger, The Netherlands; V. Romanenko, Ukraine
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Capsule: |
Sleep disorders are prevalent in many headache syndromes. Can treating the sleep problems help the patient enough so other therapies are not needed? |
| 16:30-17:30 |
Debate: Treating sleep disorders is often an effective way to combat headache syndromes |
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16:30-16:45
16:45-17:00
17:00-17:15
17:15-17:30 |
Discussion
Commentator: A. Özge, Turkey
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| Capsule: |
Behavioral medicine techniques can be helping on their own or in combination with lifestyle changes and medication. The question is - can they work on their own as effetive treatment for headache? What are clock genes and how can they effect sleep and headache in humans? |
| 17:30-18:00 |
Debate: Most headache patients can be treated with behavioral medicine techniques alone |
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17:30-17:45
17:45-18:00 |
Yes: S. Baskin, USA
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18:00-18:30 |
Closing lecture
Chairpersons: M. Kapisyzi, Albania; W. Kozubski, Poland
Update: Clock genes and migraine
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Hall C - PARKINSON'S DISEASE
Section Heads: B. Elibol, Turkey; D. Truong, USA
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07:00-08:15 |
E-Poster Presentations – Movement disorders & Motor neuron disease
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08:30-10:30 |
Outcome Parameters and Treatment of Parkinson's Disease (PD)
Supported by an unrestricted grant from UCB
Chairpersons: O. Dogu, Turkey; D. Truong, USA |
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| Capsule: |
Randomized clinical trials are the cornerstone of decisions about drug efficacy. However, the endpoints of these studies are arbitrary and not always relevant or comparable. Therefore, discussions about which is a better drug in a given situation are not always straightforward |
| 08:30-09:00 |
Lecture: Are the current outcome parameters in PD clinical trials clinically relevant? |
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08:30-08:45
08:45-09:00 |
Commentator; M. Emre, Turkey
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The clnical phenotype of PD overlaps with that of other neurodegenerative diseases. It has been suggested that brain scanning with radio-isotope markers can help, but this is debated |
| 09:00-09:45 |
Debate: Is molecular imaging really helpful in diagnosing PD? |
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09:00-09:15
09:15-09:30
09:30-09:45
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Commentator: L. Battistin, Italy
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| Capsule: |
While dopaminergic drugs are the mainstay therapy in PD, there are various preparations using different modes of delivery. Are they really so different? |
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09:45-10:30
09:45-10:00
10:00-10:15
10:15-10:30 |
Debate: Which is the better dopaminomimetic therapy in PD?
Commentator: M. Onofrj, Italy
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10:30-11:00 |
Coffee Break
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11:00-13:00 |
Pathogenesis and Imaging in PD
Chairpersons: S. Katayama, Japan; M. Onofrj, Italy |
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| Capsule: |
Levodopa has revolutionized the treatment of PD and is still the most efficacious oral drug. Does this mean that it should be the first-line option in treating newly diagnosed patients? |
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11:00-12:00
11:00-11:15
11:15-11:30
11:30-11:45
11:45-12:00
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Debate: All PD patients should start treatment with levodopa and go slow
Supported by an unrestricted grant from Novartis
Discussion
Commentator: M. Emre, Turkey
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| Capsule: |
Vascular parkinsonism is a recognized clinical entity. But do vascular factors contribute to idopathic PD? |
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12:00-13:00
12:00-12:15
12:15-12:30
12:30-12:45
12:45-13:00
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Debate: Do vascular factors influence the course of PD?
Discussion
Commentator: K. Jellinger, Austria
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13:00-14:00 |
Lunch Break
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14:00-16:00 |
The Complex Space of PD
Supported by an unrestricted grant from Britannia Pharmaceuticals
Chairpersons: B.Elibol, Turkey; I. Rektor, Czech Republic
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Capsule: |
The definition of the advanced stage in Parkinson Disease is still under debate. This presents the clinician with difficult decisions such as when to start advanced therapies in PD and which combination of drugs should be given at this stage, in order to optimize quality of life and clinical function |
| 14:00-15:00 |
Debate: How large is the advanced space of PD, when does it really start in PD? |
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14:00-14:15
14:15-14:30
14:30-14:45
14:45-15:00 |
Discussion
Commentator: M. Emre, Turkey
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Deep brain stimulation (DBS) management is an effective treatment for advanced PD, but at which stage? |
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15:00-16:00
15:00-15:15
15:15-15:30
15:30-15:45
15:45-16:00
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Debate: NMDA antagonists are useful in PD
Discussion
Commentator: R. Inzelberg, Israel
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16:00-16:30 |
Coffee Break
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16:30-18:30 |
Treatment Complications in PD
Chairpersons: N. Bharucha, India; R. Horowski, Germany |
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| Capsule: |
Treatment of PD with levodopa is complicated by the appearance of motor fluctuations. How should these be managed? |
| 16:30-17:30 |
Debate: Adjunctive therapy should be initiated as soon as wearing-off is detected
Supported by an unrestricted grant from H. Lundbeck and Teva Pharmaceutical Industries |
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16:30-16:45
16:45-17:00
17:00-17:15
17:15-17:30
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Discussion
Commentator: R. Inzelberg, Israel
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| Capsule: |
Recent interest has focused on the use of antagonists in the N-methyl D-aspartate (NMDA) subtype of glutamate receptor in PD as a long-term treatment – what is the evidence? |
| 17:30-18:30 |
Debate: When should DBS for PD be initiated |
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17:30-17:45
17:45-18:00
18:00-18:15
18:15-18:30 |
Discussion
Commentator: V. Srinivasan, India
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Hall D - Rehabilitation / MS / Dystonia
Rehabilitation Section Heads: V. Homberg, Germany; D. Muresanu, Romania
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07:00-08:15 |
E-Poster Presentations – Multiple Sclerosis |
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08:30-10:30 |
Chairpersons: O. Bajenaru, Romania; M. Brainin, Austria
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| Capsule: |
Randomized controlled trials (RCTs) are generally accepted as being the gold standard for the epistemology of evidence based medicine. The biometric rationales for this approach are primarily used for highly powered pharmacological studies with high numbers of enrolled patients. It is doubtful if a similar approach can and should be used for the assessment of efficacy of training or neuromodulatory attempts in rehabilitation. Here usually we are dealing with much smaller sample sizes and a much higher inhomogeneity of populations. The question to be solved is which alternative strategies are available to come to a scientifically equally acceptable level of certainty about treatment efficacy |
| 08:30-09:30 |
Debate: RCTs for post-stroke neurorehabilitation: Are we on the right path? |
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08:30-08:45
08:45-09:00
09:00-09:15
09:15-09:30 |
Yes: D. Muresanu, Romania
No: H. Binder, Austria
Discussion
Commentator: V. Homberg, Germany
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| Capsule: |
The various forms of cerebral palsy (CP) are the worldwide most frequent source of outlasting impairment and handicap starting in early infancy. Over the last decade treatment options for this disorder have significantly increased. This is however contrasted by a notorious ignorance of "adult age” neurologists to become interested in these patients when they grow into adulthood resulting in a care gap. Efforts have to be made to get the neurological community more interested into the long term treatment of CP patients. In this respect CP care and treatment options are a prominent example of "transition” problems in clinical neurology |
| 09:30-10:30 |
Burning point: Transitional neurology - How to deal with CP problems across the lifespan |
| 09:30-09:45 |
The neuropediatrician's view: Better treatment than ever of CP in childhood: K. Müller, Germany |
| 09:45-10:00 |
The neurologist's view: What to do with the grown up CP kid? V. Homberg, Germany |
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10:00-10:15
10:15-10:30 |
Discussion
Commentator: B.O. Popescu, Romania
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10:30-11:00 |
Coffee Break
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11:00-13:00 |
Traumatic Brain Injury (TBI)
Chairpersons: M. Chopp, USA; B.O. Popescu, Romania
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| 11:00-12:00 |
Debate: Acute spinal cord injury: Conservative or surgical treatment? |
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11:00-11:15
11:15-11:30
11:30-11:45
11:45-12:00 |
Surgical: K. von Wild, Germany
Conservative: W. El Masry, UK
Discussion
Commentator: V. Homberg, Germany
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| 12:00-13:00 |
Debate: Biological molecules: Progesterone vs. trophic factors treatment? |
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12:00-12:15
12:15-12:30
12:30-12:45
12:45-13:00 |
Trophic factors: D. Muresanu, Romania
Progesterone: H. Binder, Austria
Discussion
Commentator: K. von Wild, Germany
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| 13:00-14:00 |
Lunch Break
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14:00-16:00 |
Can the Natural History of MS be Modified?
Chairpersons: G. Akman Demir, Turkey; J. Kruja, Albania
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| Capsule: |
Assuming that environmental stimuli are responsible for the expression and severity of MS, can manipulating exposure or taking precautions (e.g. smoking cessation, treatment of EBV infections, Vitamin D supplementation) alter disease susceptibility or severity? |
| 14:00-15:00 |
Debate: Will environmental and behavioral changes alter susceptibility or the course of MS? |
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14:00-14:15
14:15-14:30
14:30-14:45
14:45-15:00 |
Debate host: G. Ebers, UK
Discussion
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Highlighting the role of interferons and the question on whether any DMD treatment prevents the development of secondary progresive disease |
| 15:00-16:00 |
Debate: Does interferon therapy delay or prevent the development of secondary progressive disease? |
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15:00-15:15
15:15-15:30
15:30-15:45
15:45-16:00 |
Debate host: M. Freedman, Canada
Discussion
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| 16:00-16:30 |
Coffee Break
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16:30-18:30 |
Treatment of Dystonia
Chairpersons: E. Broussolle, France; Z. Pirtošek, Slovenia
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| Capsule: |
In treating drug-resistant dystonia, should botulinum toxin give way to deep brain stimulation (DBS)? |
| 16:30-17:30 |
Debate: Is DBS better than botulinum toxin in primary dystonia? |
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16:30-16:45
16:45-17:00
17:00-17:15
17:15-17:30 |
Discussion
Commentator: U. Walter, Germany
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17:30-18:30 |
Supported by an unrestricted grant from Winston and Strawn
Debate: Is the currently proposed European and US guidance on data required for biosimilars/follow on biologics appropriate both scientifically and regulatorily for the evaluation of risk:benefit of such products?
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Hall A - MULTIPLE SCLEROSIS
Section Heads: M. Freedman, Canada; A. Siva, Turkey
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06:45-08:15 |
Meet the Experts
Breakfast Session
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07:00-08:15 |
E-Poster Presentations – Miscellaneous
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08:30-10:30 |
Outcome Measures in multiple sclerosis (MS) clinical studies; Origin of MS: Inflammatory or degenerative? Genetic or environmental?
Chairpersons: M. Freedman, Canada; A. Siva, Turkey |
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| Capsule: |
There are a number of reasons for trying to find better outcome measures in clinical studies for MS today, not the least of which is the pressure to prove efficacy as quickly and as meaningfully as possible. There are now a slew of new agents that are effective for relapsing forms of MS such that use a placebo comparative group is almost deemed unethical, forcing any new agent to be compared against an active comparator. Using the traditional outcome measures (e.g. relapse rate or EDSS progression), it is clear that new studies would have to recruit prohibitively high numbers of patients to show even a minor superiority of a newer agent. But is this possible? |
| 08:30-09:00 |
Debate: Are the present outcome measures for assessing efficacy of disease modifying therapies in MS clinically relevant?
Supported by an unrestricted grant from Merck Serono |
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08:30-08:40
08:40-08:50
08:50-09:00 |
Debate host: C. Hawkes, UK
Yes: O. Aktas, Germany
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| Capsule: |
An ongoing quandary in MS is what causes the ultimate loss of axons and neurons that underlies disability progression - is there an evolving profile of inflammation or is there a second independent process of neurodegeneration? |
| 09:00-09:45 |
Debate: Is disability progression in MS due to an inflammatory or neurodegenerative process? |
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09:00-09:15
09:15-09:30
09:30-09:45
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Debate host: A. Bar-Or, Canada
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| Capsule: |
Some diseases are driven primarily from genetics whereas others are reactionary - a result of predominantly environmental stimuli. How strong is the evidence for genetics playing a role beyond minor susceptibility? How compelling are the epidemiological studies pointing to specific environmental factors? |
| 09:45-10:30 |
Debate: MS - Environmental or genetic? |
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09:45-10:00
10:00-10:15
10:15-10:30 |
Debate host: O. Stuve, USA
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10:30-11:00 |
Coffee Break
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11:00-13:00 |
Clinical Issues in MS
Chairpersons: M. Keegan, USA; Z. Stelmasiak, Poland |
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| Capsule: |
Many believe that MS is a single entity with variable expression rather than distinct conditions that belie the variable phenotypic expression. Medications for MS address relapsing forms, but have proven ineffective for either progressive form (primary or secondary). Natural history studies suggest that patients with a progressive course behave similarly regardless of whether primary or secondary. Are pathologies or pathoimmunology that different? |
| 11:00-12:00 |
Debate: Primary progressive MS and secondary progressive MS are different manifestations of a single disease
Partially supported by an unrestricted grant from Bayer Israel |
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11:00-11:15
11:15-11:30
11:30-11:45
11:45-12:00
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Debate host: R. Milo, Israel
Discussion
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| Capsule: |
Distinguishing neuromyelitis optica (NMO) from MS is important for selecting the correct treatment approach, but what about those patients with predominantly "optico-spinal" presentation? What if such patients also were positive for NMO antibodies, but fulfilled all MS diagnostic criteria? How much overlap, if any, is there between NMO and MS? |
| 12:00-13:00 |
Debate: Are MS and NMO two polarized diseases? Does this have treatment implications? |
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12:00-12:15
12:15-12:30
12:30-12:45
12:45-13:00
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Debate host: M. Keegan, USA
Discussion
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| 13:00-13:45 |
Biogen Idec Symposium
Changing perspectives in MS: Pursuing efficacy; managing risk
P. Vermersch, France
Shedding light on a gray area: MRI monitoring and diagnosis of PML
M.P. Wattjes, The Netherlands
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13:30-14:30 |
Lunch Break
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14:30-16:30 |
Isolated Syndromes and Therapy
Chairpersons: A. Altintas, Turkey ; C. Hawkes, UK |
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| Capsule: |
Most current treatments are predominantly "T" cell therapies, yet there are still many patients who do not respond well or even poorly to such therapies. Could it be that the target is not the "T" cell? Would treating a "T" cell sub-optimal responder with a "B" cell directed therapy lead to a better treatment response? Is there a way of knowing whether a certain patient has mostly a "T" or "B" cell dominated disease? |
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14:30-15:30
14:30-14:45
14:45-15:00
15:00-15:15
15:15-15:30
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Debate: Targeted therapy in MS: Should we aim at B or T lymphocytes?
Supported by an unrestricted grant from Novartis
Debate host: M. Sandberg-Wollheim, Sweden
Discussion
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| Capsule: |
How much can we really rely on the MRI to predict that someone has MS - a condition that will lead to relapses and progression? Medications work best given as early as possible in the course of the disease, so if one could start even before it expresses itself clinically, then perhaps treatment outcomes would be even better. Is this similar to treating symptomatic carotid stenosis? |
| 15:30-16:30 |
Debate: Radiologically isolated syndrome (RIS) patients are at high risk of developing MS and warrant treatment with disease modifying drugs (DMD) |
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15:30-15:45
15:45-16:00
16:00-16:15
16:15-16:30
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Debate host: P. Vermersch, France
Discussion
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16:30-17:00 |
Coffee Break
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17:00-18:45 |
New Players in MS
Chairpersons: A. Bar-Or, Canada; N.Grigoriadis, Greece
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17:00-17:15
17:15-17:30
17:30-17:45
17:45-18:00
18:00-18:15
18:15-18:30
18:30-18:45 |
Gilenya: G. Akman Demir, Turkey
Teriflunomide: M. Freedman, Canada
BG12: O. Bajenaru, Romania
Alemtuzumab: E. Havrdova, Czech Republic
Laquinimod: H.-P. Hartung, Germany
Ocrelizumab: D. Leppert, Switzerland
Daclizumab: R. Milo, Israel
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18:45-19:00 |
Poster Awards & Closing Ceremony |
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Hall B - DEMENTIA
Section Heads:R. Bullock, UK; L. Grinberg, USA; H. Gurvit, Turkey
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06:45-08:15 |
Meet the Experts
Breakfast Session
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07:00-08:15 |
E-Poster Presentations – Dementia & Alzheimer's disease
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08:30-10:30 |
Treatment Options in Dementia
Chairpersons: R. Bullock, UK; O. Tanridag, Turkey |
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| Capsule: |
Randomized clinical studies are the cornerstone of decisions about drug efficacy. Hwever the endpoints of these studies are arbitrary and not always relevant or comparable. Therefore, decisions about which is a better drug in a given sitatuion are not alrways straightforward |
| 08:30-09:00 |
M. Ropacki, USA
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| Capsule: |
Agitation and aggression are major problems in the management of patients with dementia. Do we know how these should be treated? |
| 09:00-09:45 |
Debate: Agitation and aggression in Alzheimer's disease (AD) as a diagnostic entity for drug development |
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09:00-09:15
09:15-09:30
09:30-09:45 |
Supported by an unrestricted grant from Elan Pharmaceuticals
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| Capsule: |
Cholinesterase drugs are the main agents approved for the treatment of AD. However, they only have a minor effect |
| 09:45-10:30 |
Debate: With 25 years' hindsight, were the cholinergic drugs worth developing? |
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09:45-10:00
10:00-10:15
10:15-10:30 |
Commentator: O. Tanridag, Turkey
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10:30-11:00 |
Coffee Break
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11:00-13:30 |
Can the Natural History of Dementia be Modified?
Chairpersons: H. Gurvit, Turkey; L. Grinberg, USA |
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| Capsule: |
Stress is one of the environmental factors insinuated in causing neurodegeneration. Is this correct, and will stress reduction be helpful in preventing or slowing cognitive decline in AD? |
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11:00-12:00
11:00-11:15
11:15-11:30
11:30-11:45
11:45-12:00
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Debate: Stress has a causative role in AD and mild cognitive impairment (MCI)
Partially supported by an unrestricted grant from Ana Aslan
Discussion
Commentator: L. Middleton, UK
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| Capsule: |
The widespread use of statins, with their pluripotent effects, should be viewed in the context of neurodegeneration. Can statins protect against dementia, or can they exacerbate it? |
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12:00-13:00
12:00-12:15
12:15-12:30
12:30-12:45
12:45-13:00
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Debate: The statin dilemna
Discussion
Commentator: Y. Berner, Israel
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13:00-13:30
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Lecture: Searching for AD-related biological vulnerability in cognitively intact people: From therapeutic hopes to ethical issues
P. Giannakopoulos, Switzerland
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13:30-14:30 |
Lunch Break
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Prevention of AD: What does it take?
Supported by an unrestricted grant from Janssen Pharmaceutical Companies
Chairpersons: L. Middelton, UK; M. Ropacki, USA
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Facing the failure of studies aimed to cure AD, the focus is shifting towards disease prevention. Can this be achieved, and how can interventions be studied?
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Pharmacological and non-pharmacological studies for the prevention of AD
L. Middleton, UK
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Imaging and other biomarkers of pre-clinical and pre-dementia AD
R. Perneczky, Germay
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Diet and risk of AD
N. Scarmeas, USA
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What is needed to develop and validate clinical endpoints for a preclinical population?
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16:30-17:00 |
Coffee Break
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Neuropathology of Dementia
Chairpersons: K. Jellinger, Austria; K. Wesnes, UK
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| Capsule: |
Once the first clniical signs of neurodegeneration dieases are suspected, efforts are split between symptomatic relief and slowing the downard course |
| 17:00-18:00 |
Debate: Disease modification in neurodegenerative disorders - is it a valid concept and can it be studied? |
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17:00-17:15
17:15-17:30
17:30-17:45
17:45-18:00
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Discussion
Commentator: K. Jellinger, Austria
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18:00-18:30
18:45-19:00 |
State-of-the-art lecture: Dementia pathology 2013 - Any new insights?
Poster Awards & Closing Ceremony, Hall A
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Hall C - Epilepsy
Section Heads: B. Baykan, Turkey; M. Sperling, USA
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| 06:45-08:15 |
Meet the Experts
Breakfast Session
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| 07:00-08:15 |
E-Poster Presentations – Epilepsy
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08:30-10:30 |
Genetic Generalized Epilepsies
Chairpersons: Z. Afawi, Israel; M. Sperling, USA
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| Capsule: |
Juvenille myoclonic epilespy (JME), the prototype of genetic generalized epilepsies is a well-known and world-wide recognized epilepsy syndrome. Many recent clnical and neuro-imaging aspects were investigated and the results created some confusion about its nature, like focal findings, therapy-resistant cases and frontal lobe predominance. Thus there is a need for well-defined clinical and EEG criteria |
| 08:30-09:30 |
Debate: Is JME a well-definted epileptic syndrome? |
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08:30-08:45
08:45-09:00
09:00-09:15
09:15-09:30
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No: I. Blatt, Israel
Discussion
Commentator: P. Striano, Italy
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| Capsule: |
Epilepsy is a complex genetic disorder and there have been huge efforts to discover its genetic etiology worldwide. Despite many genes discovered so far, the full picture is far from understood. So, neurologists want to know if there is a role for genetic investigations in the management of epilepsy patients in current practice |
| 09:30-10:30 |
Debate: Does genetic testing have a role in epilepsy management? |
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09:30-09:45
09:45-10:00
10:00-10:15
10:15-10:30 |
Discussion
Commentator: I. Blatt, Israel
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| 10:30-11:00 |
Coffee Break
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11:00-13:30 |
Classical Questions of Epilepsy Management in the Modern Era
Chairpersons: B. Baykan, Turkey; J. Kruja, Albania
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| Capsule: |
Stroke is one of the frequent underlying causes of symptomatic focal epilepsies but there is still no consensus about the usefulness of prophylactic treatment in patients having had a stroke, both in acute setting in which there may be significant edema and increased intracranial pressure and in the chronic settling. Are there situations in which prophylactic treatment has value? |
| 11:00-12:00 |
Debate: Should patients with cortical strokes be treated prophylactically against seizures? |
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11:00-11:15
11:15-11:30
11:30-11:45
11:45-12:00 |
Discussion
Commentator: K. Agan, Turkey
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| Capsule: |
Since the work of Gibbs and Lennox in the 1930's, the EEG has been used in the management of epilepsy patients worldwide. However, epilepsy is primarily a clinical diagnosis and EEG can be misleading in some cases. Does it still have an essential role in the era of modern neurimaging and genetics? |
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12:00-13:00
12:00-12:15
12:15-12:30
12:30-12:45
12:45-13:00
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Debate: EEG is usually necessary when diagnosing epilepsy
Discussion
Commentator: V. Kimiskidis, Greece
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13:00-13:30
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Speaker: C. Ozkara, Turkey
Commentator: E. Ben-Menachem, Sweden
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| 13:30-14:30 |
Lunch Break
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14:30-16:30 |
Management of Special Patients with Epilepsy
Chairpersons: V. Donath, Slovakia; K. Rejdak, Poland
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| Capsule: |
The number of treatment options for epilepsy has continued to expand. Electrical stimulation of either peripheral or central nervous system has been demonstrated to afford benefit in randomized controlled trials. When these stimulation devices should be employed remains controversial, especially stimulation of the anterior nucleus of the thalamus. When should physicians recommend that it be utilized? Should it be reserved for vagus nerve stimulation (VNS) failures, or substitute for VNS? The following debate will address these issues |
| 14:30-15:30 |
Debate: Proposition: DBS should only be used after VNS has failed
Partially supported by an unrestricted grant from Medtronic |
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14:30-14:45
14:45-15:00
15:00-15:15
15:15-15:30 |
Yes: M. Sperling, USA
No: P. Boon, Belgium
Discussion
Commentator: M. Holtkamp, Germany
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| Capsule: |
Antiepileptic drugs can pose risk to a developing fetus. As more is learned about these agents, should some be preferred during pregnancy or is our level of knowledge insufficient to offer preferences? |
| 15:30-16:30 |
Debate: Are some antiepileptic drugs preferred during pregnancy? |
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15:30-15:45
15:45-16:00
16:00-16:15
16:15-16:30
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Discussion
Commentator; E. Ben-Menachem, Sweden
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| 16:30-17:00 |
Coffee Break
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| Session 28
17:00-18:30
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Problems of Anti-Epileptic Drug Treatment
Chairpersons: M. Holtkamp, Germany; C. Ozkara, Turkey
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| Capsule: |
Many antiepileptic drugs have effects far beyond the brain. Some induce hepatic microsomal enzymes with the potential to alter the metabolism of other drugs and endogenous hormones and vitamin levels. Is this a significant problem so that such drugs should be avoided, or is this an easily managed minor issue? |
| 17:00-18:00 |
Debate: Should enzyme-inducing antiepileptic drugs be avoided? |
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17:00-17:15
17:15-17:30
17:30-17:45
17:45-18:00
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Discussion
Commentator: E. Beghi, Italy
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| Capsule: |
Status epilepticus is considered a medical emergency. There is evidence that prolonged or repetitve seizures can cause neuronal injury and that some types of status epilepticus cause systemic metabolic derangements. Yet there are many different types of status epilepticus. Whether aggressive therapy is warranted for all status epilepticus is subject for debate |
| 18:00-18:30 |
Debate: Is aggressive therapy justified for all types of status epilepticus? |
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18:00-18:15
18:15-18:30
18:45-19:00 |
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