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The 4th World Congress on
Controversies in Neurology (CONy)
Barcelona, Spain, Palau de Congressos de Catalunya, October 28-31, 2010 |
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| Scientific Program |
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| Thursday, October 28, 2010 |
| 15:00-17:00 |
Plenary Session I |
| Chairpersons: |
A. Gil Nagel, Spain; A.D. Korczyn, Israel; W.W. Zhang, China |
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| 15:00-15:15 |
Greetings: J. Porta-Etessam, Spain |
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| 15:15-16:00 |
Debate: Neuro-epistemology: Randomized controlled trials are the gold standard in neurorehabilitation |
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Yes: V. Homberg, Germany
Commentator: K. Von Wild, Germany |
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| 16:00-16:45 |
Debate: Can anti-inflammatory drugs benefit neurodegenerative diseases? |
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16:45-17:15 |
Coffee Break |
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| 17:15-19:30 |
Plenary Session II |
| Chairpersons: |
A. Gil Nagel, Spain; A.D. Korczyn, Israel; W.W. Zhang, China |
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| 17:30-18: |
Debate: Free access journals are important and useful |
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Pro: W. Theodore, USA
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| 18:00-18:45 |
Debate: Are there any silent parts in the human brain? |
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| 18:45-19:30 |
Debate: Is Alzheimer's disease a homogeneous nosologic entity? |
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No: A.D. Korczyn, Israel |
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19:30
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Welcome Reception
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| Friday, October 29, 2010 /// Hall A - Epilepsy |
| Session (1) |
Epilepsy: Less Conventional Treatments |
| 08:30-10:30 |
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| Capsule: |
The session addresses less conventional therapeutic approaches to treating epilepsy. It is well known that hormonal cycles influence seizure occurrence and catamenial epilepsy serves as the primary example of this phenomenon. The first debate poses the question whether hornomal therapy is justified. Is there sufficient data to support the use of agents like progesterone to treat seizures? The second debate addresses when physicians should use recently approved drugs, which have a limited number of patient exposures. Should drugs be reserved for patients who have already failed many medications, or is it appropriate to prescribe them as first line agents? |
| Chairpersons: |
V. Donath, Slovakia; J. Kruja, Albania |
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| 08:30-10:30 |
Debate: Should hormonal therapy be used to treat epilepsy? |
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Commentator: M. Carreno Martinez, Spain |
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| 09:30-10:30 |
Debate: Should recently approved antiepileptic drugs be used early in the treatment of epilepsy? |
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Commentator: M. Sperling, USA |
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| 10:30-11:00 |
Coffee Break |
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| Session (2) |
Epilepsy: Psychological Aspects |
| 11:00-13:00 |
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| Capsule: |
Epilepsy is commonly associated with depression and influences may be bidirectional. While it is commonly assumed that stress and sleep deprivation can trigger seizures in people with epilepsy, is this contention supported by objective evidence? Since vagus nerve stimulation can positively affect mood, it is appropriate to prescribe this treatment for depressed patients with epilepsy or are antidepressants always preferred? |
| Chairpersons: |
Z. Afawi, Israel; F. Vajda, Australia |
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| 11:00-12:00 |
Debate: Can stress trigger seizures ? |
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No: W. Theodore, USA
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| 12:00-13:00 |
Debate: Should patients with epilepsy who are depressed be routinly treated with antidepressant medication or vagus nerve stimulation? |
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Commentator: W. Theodore, USA |
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| 13:00-14:00 |
Lunch Break |
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| Session (3) |
Epilepsy: Therapeutic Aspects |
| 14:00-16:00 |
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Capsule:
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Genetic medications have recently become available for many of the newer antiepileptic agents. These have the potential to significantly reduce healthcare expendituers. Is epilepsy a condition like others in which generic substitution is safe or is epilepsy special conditions for which generics pose undue risk? Many studies assert that etiology is the determinant of outcome after status epilepticus. This raises the question as to the extent to which treatment affects outcome |
| Chairpersons: |
K Rejdak, Poland; E. Ben-Menachem, Sweden |
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| 14:00-14:45 |
Debate: Does use of generic medications pose risk with regard to seizure control? |
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Commentator: B. Baykan, Turkey |
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| 14:45-15:30 |
Debate: Does treatment of status epilepticus significantly impact outcome? |
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Commentator: M. Trimble, UK |
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15:30-16:00
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Lecture: Is valproate (VPA) an obligatory teratogen, or is it just a matter of dose?
Discussion |
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| 16:00-16:30 |
Coffee Break |
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| Session (4) |
Autoimmune Processes in Epilepsy |
| 16:30-18:45 |
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| Capsule: |
Epilepsy beginning in midlife is always a cause for concern, and its etiology, diagnosis and treatment are unclear. This session will review the role of neuronal autoantibodies in epilepsy, which are increasingly recognized as a potential etiology of seizure disorders |
| Chairpersons: |
M. Mazurkiewicz-Beldinska, Poland; T. Tomson, Sweden |
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| 16:30-17:00 |
Lecture: Epilepsy and autoimmune disease: Anti-MNDA receptor, LGI1 and other synaptic autoimmune encephaltis:
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| 17:00-17:20 |
Lecture: Glutamate receptor antibodies are found in epilepsy patients, activate glutamate receptors and cause brain damage in animal models:
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| 17:20-17:30 |
Commentator: A. Gil Nagel, Spain |
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17:30-18:45
Capsule: |
New Players in Epilepsy
In response to the lack of adequate response, a new generation of antiepileptic medicaitons is being developed. This final series of talks will review some new agents either recently approved, or in the pharmaceutical pipeline |
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Perampanel: A. Gil Nagel, Spain
Rufinamide: F. Bibbiani, USA
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| Friday, October 29, 2010 /// Hall B - Stroke |
| Session (5) |
Stroke Prevention |
| 08:30-10:30 |
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| Chairpersons: |
A. Halliday, UK; A. Davalos, Spain |
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| 08:30-09:30 |
Debate: What is the future of stroke prevention: Polypill or individualized risk factor modification? |
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Capsule: Stroke prevention is the key factor to fight and to reduce stroke burden around the world. "Mass" Polypill vs. "High risk" approach in stroke prevention is still a matter of debate |
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Individualized risk factor modification: D. Spence, Canada
Commentator: J. Streifler, Israel |
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| 09:30-10:30 |
Debate: Best medical treatment or stenting for intracranial stenosis? |
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Capsule: Intracranial artery stenosis is increasingly recognized as an important cause of stroke. However, management of this disorder is still unclear, with data favoring medical therapy with anticoagulants and antiaggregants being advocated by leaders in the field, while others promote stenting |
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L. Caplan, USA
Commentator: D. Spence, Canada |
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| 10:30-11:00 |
Coffee Break |
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| Session (6) |
Imaging
(Supported by an unrestricted grant from EV3) |
| 11:00-13:00 |
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| Chairpersons: |
M. Bar, Czech Republic; J. Streifler, Israel |
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| 11:00-12:00 |
Debate: What is the best therapy for stroke therapy after thrombolysis fails in acute stroke management? |
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Capsule: Recanalization and perfusion are the main purposes of thrombolysis. However, the recanalization rate with IV rtPA is insufficient and should be improved. Sonothrombolysis is a feasible, applicable and promising techniques to increase the recanalization rate |
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Sonothrombolysis: C. Molina, Spain
Clot retrieval: A. Davalos, Spain
Neither: P. Schellinger, Germany
Commentator: A. Shuaib, Germany |
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| 12:00-13:00 |
Debate: Is current advanced neuroimaging sufficient for treating acute ischemic stroke? |
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Capsule: Currently only small proportions of acute ischemic stroke patients receive thrombolysis mainly due to late arrival and missing the time window of 4.5 hours. Whether the current technology of advanced neuroimaging can identify patients who are suitable for thrombolysis beyond 4.5 hours is still uncertain |
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Yes: A. Davalos, Spain
No: P. Schellinger, Germany
Commentator: L. Caplan, USA |
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| 13:00-14:00 |
Lunch Break |
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| Session (7) |
Management of Acute Stroke |
| 14:00-16:00 |
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| Chairperson: |
E. Diez-Tejedor, Spain; J. Montaner, Spain |
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| 14:00-15:00 |
Debate: Anticoagulants vs. Antipatelets for carotid artery dissection |
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Capsule: Dissection of the carotid and vertebral arteries is the most common cause for stroke in the young. The common practice is to treat with anticoagulants. However, there are only scanty data from randomized controlled trials (RCTs) to support this approach. The debate will shed light on this controversial issue |
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Antiplatelets: O. Bajenaru, Romania
Commentator: L. Caplan, USA |
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| 15:00-16:00 |
Debate: Should treatment of acute stroke be the same for anterior and posterior strokes? |
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Verterbrobisilar and carotid strokes may have different pathogenesis, and of course different presentations. Should this be reflected in therapy for acute events and to prevent recurrences? |
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Commentator: A. Halliday, UK |
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| 16:00-16:30 |
Coffee Break |
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| Session (8) |
Carotid Stenosis |
| 16:30-18:45 |
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| Chairpersons: |
J. Wojczal, Poland; O. Bajenaru, Romania |
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| 16:30-17:30 |
Debate: Are the current tools sufficient to identify the vulnerable plaque? |
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Capsule: Carotid stenosis accounts for 15-20% of all ischemic strokes. The management of asymptomatic carotid stenosis (ACAS) is still controversial. Plaque vulnerability may identify high risk ACAS subjects in whom intervention might be justified |
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Commentator: G. Chrysant, USA |
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17:30-18:45
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New Players in Stroke
Stem cell and neurotrophic factors in acute ischemic stroke therapy: E. Diez Tejedor, Spain
New anticoagulants for atrial fibrillation: D. Spence, Canada
Cerebrolysin: A. Guekht, Russia
Citicoline: C. Molina, Spain
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| Friday, October 29, 2010 /// Hall C - Parkinson's disease (PD)/Movement disorders (MD) |
| Session (9) |
Neuroprotection and Biomarkers |
| 08:30-10:30 |
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| Capsule: |
To halt or modify disease progression is one of the leading clinical research questions in neurodegeneration. The implications for the individual patients are fostered by hope and hype. Yet the insight into cell death and its potential retardation also implies an improved understanding of aging, including genetics and neurotocity. Surogate or biomarkers which accompany different stages of disease or age could greatly facilitate these ongoing research endeavors |
| Chairpersons: |
E. Martignoni, Italy; U. Bonuccelli, Italy |
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| 08:30-09:30 |
Debate: Can neuroprotection be detected in PD? |
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Yes: F. Stocchi, Italy
No: A. Kupsch, Germany
Commentator: J. Kulisevsky, Spain |
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| 09:30-10:30 |
Debate: Is Parkinson's disease primarily a genetic disorder? |
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Commentator: E. Melamed, Israel |
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| 10:30-11:00 |
Coffee Break |
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| Session (10) |
Essential Tremor and Physical Therapy |
| 11:00-13:00 |
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| Capsule: |
Essential tremor (ET), being much more frequent than Parkinson's disease, may be clinically progressive. However it generally is assumed that ET does not belong to neurodegenerative disorders, since cell loss is datable in ET. At the same time, ET and PD may overlap. Thus the present controversy concentrates on the issue of progression in ET and the different subtypes of ET. On the other hand, PD is a clearly progressive disorder. Physical therapy provides pro and contro arguments for the efficacy of physical therapy in PD and discusses the debatable value of specific PD-orientated physical therapy, such as Lee Silverman Voice Training and BIG |
| Chairpersons: |
J. Kulisevsky, Spain; R. Castellani, USA |
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| 11:00-12:00 |
Debate: Is essential tremor a neurodegenerative disease? |
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Yes: U. Bonuccelli, Italy
Commentator: A. Antonini, Italy |
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| 12:00-13:00 |
Debate: |
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Is physical therapy beneficial in PD?: M. Munneke, The Netherlands
Is the clinimetric analysis sufficiently sensitive to functional assessment in PD or should it be supported by kinematic analysis?: S. Katayama, Japan
Commentator: L. Battistin, Italy |
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| 13:00-14:00 |
Lunch Break |
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| Session (11) |
Camptocormia and Gambling |
| 14:00-16:00 |
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| Capsule: |
PD may be associated with motor and non-motor copmlications such as camptocormia or gambling. Recently, biopsy-proven evidence has accumulated showing that camptocormia may be a myopathy in PD, contrasting the most traditional view of dystonic disorder which will be discussed in the first part of the session. Gambling on the other hand is a non-motor complication of PD. Is it related to drug intake or disease progression? What are the risk factors? Do genetics play a role and can we predict and influence the evolution of gambling in PD? |
| Chairpersons: |
L. Battistin, Italy; P. Martinez Martin, Spain |
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| 14:00-15:00 |
Debate: Camptocormia in PD: Is this a dystonia or a myopathy? |
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Dystonia: E. Melamed, Israel
Myopathy: A. Kupsch, Germany
Commentator: A. Antonini, Italy |
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| 15:00-16:00 |
Debate: Pathological gambling in PD: Disease related or drug related? |
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Drug related: A. Antonini, Italy
Commentator: F. Stocchi, Italy |
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| 16:00-16:30 |
Coffee Break |
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| Session (12) |
New Players in Neurodegenerative Diseases |
| 16:30-18:45 |
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| Chairpersons: |
D. Truong, USA; L. Varona, Spain |
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| 16:30-17:30 |
Debate: Their cognitive capacity and judgement allows most ALS patients to make valid life and death decisions that should be respected |
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Commentator: A. Ludolph, Germany |
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18:00-18:45
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New Players
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| Saturday, October 30, 2010 /// Hall A - Multiple Sclerosis |
| Session (13) |
MS: Therapeutic Dilemmas |
| 08:30-10:30 |
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| Capsule: |
In order to establish unequivocally the benefit of new drugs, they should be compared to placebos in double-blinded, placebo-controlled studies. However, there is a problem when using placebo when an effective drug exists in the market. Another issue is whether sometimes imprecise clinical data are absolutely essential for clinical decisions in MS, or whether at times MRI can be used - for example to declare a therapy not useful and to switch to an alternative, even when the clinical situation is unchanged |
| Chairpersons: |
J. Losy, Poland; L. Vecsei, Hungary |
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| 08:30-09:30 |
Debate: Are placebo-controlled clinical trials still ethical/necessary in RRMS? |
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Commentator: P. Vermersch, France |
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| 09:30-10:30 |
Debate: Should any treatment decisions be made based on MRI, such as change from IFN to other DMD, even if there is no clinical evidence of disease activity? |
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Commentator: D. Leppert, Switzerland |
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| 10:30-11:00 |
Coffee Break |
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| Session (14) |
Etiology and Pathogenesis of MS |
| 11:00-13:00 |
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| Capsule: |
The search for the cause of MS has been going on for over a century, yet it is unclear whether the disease is due to an infective agent, immune attack, or perhaps a vascular disorder |
| Chairpersons: |
J. Kruja, Albania; V. Brinar, Croatia |
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| 11:00-12:00 |
Debate: Does chronic venous insufficiency paly a role in MS pathogenesis? |
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Commentator: A. Miller, Israel |
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| 12:00-13:00 |
Debate: Are infections key environmental factors in MS? |
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Commentator: P. Kennedy, UK |
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| 13:00-14:00 |
Lunch Break |
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| Session (15) |
MS Treatments |
| 14:00-16:00 |
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| Capsule: |
The mainstay of treatment of MS particularly today is with injectable drugs, either glatiramer acetate or β-interferons. However, these drugs have limited efficacy and new drugs are being developed, in the hope that their advantages will lead them to replace existing DMDs |
| Chairpersons: |
J.A. Garcia Merino, Spain; D. Karussis, Israel |
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| 14:00-15:00 |
Debate: Are we close to patient population oriented treatment algorithm in MS? |
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(Partially supported by an unresticted grant from Teva Pharma and Sanofi-Aventis)
No: X. Montalban, Spain
Commentator: G. Ebers, UK |
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| 15:00-16:00 |
Debate: How to treat a highly active RRMS patient after one disease modifying drug (DMD) has failed? |
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(Partially supported by an unrestricted grant from Cardian BCT Europe)
Switch to another DMD: M. Freedman, Canada
Monoclonal antibody therapies: P. Vermersch, France
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| 16:00-16:30 |
Coffee Break |
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| Session (16) |
New Players in MS |
| 16:30-19:00 |
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| Chairpersons: |
Z. Stelmasiak, Poland; T. Derfuss, Switzerland |
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| 16:30-17:15 |
Debate: Should all MS patients be treated with statins? |
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Commentator: P. Kennedy, UK |
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17:15-19:00
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New Players
Ocrelizumab: D. Leppert, Switzerland
Prolonged-release fampridine tablets: X. Montalban, Spain
Teriflunomide: M. Freedman, Canada
Emerging treatments for pseudobulbar affect: D. Wynn, USA
Fingolimod: H.-P. Hartung, Germany
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| Saturday, October 30, 2010 /// Hall B - Headache / Pain |
| Session (17) |
Headache: Tension-type headache vs. migraine - Effectiveness of botulinum toxin |
| 08:30-10:30 |
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| Capsule: |
An old debate in the headache field is whether the two most common types of chronic headache, tension-type headache and migraine are two separate entities or whether tension-type headaches are actually mild forms of migraine. Post traumatic headache often presents with normal neurological examination and no abnormal studies, just headache. However, there is usually a post head trauma, with many symptoms and some psychological problems. So, is the pathophysiology neurological or psychological? |
| Chairpersons: |
H. Hamburger, The Netherlands; R. Weeks, USA |
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| 08:30-09:30 |
Debate: Is tension-type headache a separate and not a type of migraine? |
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Yes: C. Lampl, Austria
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| 09:30-10:30 |
Debate: Is post traumatic headache is neurological as opposed to a psycho-social- societal disorder? |
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Yes: M. Kapisyzi, Albania
No: R. Weeks, USA
Commentator: L. Vecsei, Hungary |
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| 10:30-11:00 |
Coffee Break |
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| Session (18) |
Headache: Where Migraine Starts - When to Give Triptans?
(Partially supported by an unrestricted grant from MSD) |
| 11:00-13:00 |
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| Capsule: |
A heavily debated topic in migraine today is where in the brain the first phase of the attack begins, some saying the cerebral cortex, and others saying that it originates in the brain stem. There is much scientific evidence for both. Triptans are widely thought of as the most effective medicine to give in a moderate to servere attack of migraine; but must they be given early, when the headache is mild, or can they be given later in the attack? |
| Chairpersons: |
M. Kapisyzi, Albania; C. Lampl, Austria |
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| 11:00-12:00 |
Debate: Does the first phase of a migraine attack originate in the cerebral cortex as opposed to the brain stem? |
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Commentator: N. Mathew, USA |
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| 12:00-13:00 |
Debate: Do triptans have to be given early in the attack when the headache is mild? |
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Commentator: A. Rapoport, USA |
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| 13:00-14:00 |
Lunch Break |
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| Session (19) |
Headache: What causes post traumatic headache - Will CRGP antagonists be effective?
(Partialy supported by an unrestricted grant from MSD) |
| 14:00-16:00 |
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| Capsule: |
There is allot of discussion about off-label use of botulinum toxin type-A for chronic migraine and until recently there has been little scientific evidence that it is effective, although it is widely considered to be an effective treatment by many headache specialists. For 20 years CGRP has been studied scientifically and considered a possible cause of pain in migraine. Soon we may have a CGRP antagonist to treat an acute migriane attack. Will it be a valuable new agent? |
| Chairpersons: |
H. Hamburger, The Netherlands; D. Truong, USA |
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| 14:00-15:00 |
Debate: Is botulinum toxin type-A an effective and safe treatment for chronic migraine? |
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Yes: A. Mauskop, USA
No: C. Lampl, Austria
Commentator: M.-C. Wilson, USA |
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| 15:00-16:00 |
Debate: Will the first marketed CGRP antagonist be an important addition to the migraine treatment armamentarium? |
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No: M. Levin, USA
Commentator: N. Mathew, USA |
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| 16:00-16:30 |
Coffee Break |
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| Session (20) |
Headache Treatment: Magnesium and Electrical Nerve Stimulation for Everyone? |
| 16:30-18:30 |
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| Chairperson: |
H. Bolay, Turkey; R. Weeks, USA |
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| 16:30-17:15 |
Debate: Should magnesium be given to every migraineur? |
| Capsule: |
Many studies show that magnesium intravenously or by mouth can help a migraineur. Should every migraineur receive magnesium? |
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Commentator: M. Kapisyzi, Albania |
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| 17:15-18:00 |
Debate: Occipital nerve stimulation is a valuable and effective form of headache treatment |
| Capsule: |
There have been many patients treated successfully with occipital nerve stimulation for chronic headache, but is there any scientific proof of effectiveness and is this a safe and effective treatment for chronic headache? |
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Con: M. Levin, USA
Commentator: H. Bolay, Turkey |
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| Chairpersons: |
A. de Ru, The Netherlands; A. Rapoport, USA |
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18:00-18:30
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Lecture: The importance of sleep to the headache patient
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| Saturday, October 30, 2010 /// Dementia - Hall C |
| Session (21) |
Dementia: Diagnostic and Pathogenetic Concepts |
| 08:30-10:30 |
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| Capsule: |
Mild cognitive impairment is one of the most disputed concepts in the field: Is it really useful as a diagnostic entity, or should it be dropped altogether, replaced by more specific diagnosis wherever this is possible? Another long-standing controversy in the field of Alzheimer's disease is the relative role of tau as opposed to amyloid pathology in the disease pathogenesis. This is not without a reason - all available genetic evidence points towards amyloid whereas pathological correlations rather favor tau |
| Chairpersons: |
R. Castellani, USA; M. Emre, Turkey |
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| 08:30-09:30 |
Debate: Is MCI a useful diagnostic concept? |
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No: R. Bullock, UK
Commentator: T. del Ser, Spain |
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| 09:30-10:30 |
Debate: Is tau more important than amyloid in the pathophysiology of AD? |
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Commenator: M. Windisch, Austria |
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| 10:30-11:00 |
Coffee Break |
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| Session (22) |
Dementia: Treatment of Alzheimer's disease - When to Start and When to Continue
(Partially supported by an unrestricted grant from Ana Aslan) |
| 11:00-13:00 |
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| Capsule: |
There are two treatment modalities with proven efficacy in the treatment of patients with AD. Cholinesterase inhibitors have been primarily investigated in mild to moderate stages of the disease whereas NMDA antagonist memantine is indicated in patients with moderate to severe disease. In the backdrop of clinical trials, which are traditionally conducted in selected patient populations the question is when to start treatment of ChE-I. The second question is when to combine the two treatment strategies, in particular in the light of recent trials suggesting that combination treatment may be more beneficial |
| Chairpersons: |
L. Battistin, Italy; P. Modrego, Spain |
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11:00-12:00 |
Debate: Should cholinesterase inhibitors (ChE-I) be initiated as early as possible in the treatment of AD? |
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Yes: M. Davidson, Israel
No: R. Bullock, UK
Commentator: L. Frolich, Germany |
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| 12:00-13:00 |
Debate: Should combination treatment with ChE-I and memantine be started as early as possible? |
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No: L. Frolich, Germany
Commentator: R. Bullock, UK |
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| 13:00-14:00 |
Lunch Break |
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| Session (23) |
Dementia: Prospects on Diagnosis and Treatment of AD |
| 14:00-16:00 |
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| Capsule: |
Amyloid cascade hypothesis was the first integrative mechanistic attempt to explain the pathgenesis of AD. Since its inception, additional data has been gathered, which has been interpreted both as supportive of, as well as against it; an expert discussion on where we stand today is timely. As potential therapeutic interventions to modify the disease process are being investigated early diagnosis which will enable interventions at the earliest stages of the disease, are becoming more important. Can surrogate markers help us in this regard and improve (or even beat) the accuracy of clinical diagnosis? |
| Chairpersons: |
J. Cedarbaum, Spain; M. Emre, Turkey |
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| 14:00-15:00 |
Debate: Is the amyloid hypothesis still valid? |
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(Partially supported by an unrestricted grant from IOS Press)
Commentator: P. Giannakopoulos, Switzerland |
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| 15:00-16:00 |
Debate: Should statins be used as neuroprotective agents in MCI? |
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(Partially supported by an unrestricted grant from Ferrer)
Yes: M. Davidson, Israel
No: A. Cedazo-Miguez, Sweden
Commentator: F. Cruz Sanchez, Spain |
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| 16:00-16:30 |
Coffee Break |
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| Session (24) |
Present and Future in "Neuroprotection" Related Concepts and Clinical Consequences
(Partially supported by an unrestricted frant from the Society for the Study of Neuroprotection and Neuroplasticity) |
| 16:30-18:30 |
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| Capsule: |
The more we deepen our understanding about brain biology and brain-mind interface, the better we realize that we have to readapt all our paradigms to reality. The old concept, that neuroprotection means suppressing pathophysiological processes and the idea that a signle mechanism molecule might be effective in clinical practice are obsolete today. This represents the root cause of failure |
| Chairperson: |
L. Caplan, USA; M. Seijo, Spain |
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16:30-17:30
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Quantum mechanics and the brain
Quantum brain and self directed neuroplasticity: J.M. Schwartz, USA
Quantum conception of the mind-brain connection: H. Stapp, USA |
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17:30-18:30
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Present and future neuroprotection
Clinical neuroprotection is presently disappointing: L. Caplan, USA
Future approaches are very promising: D. Muresanu, Romania
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| Sunday, October 31, 2010 /// Hall A - Neuroimmunology |
| Session (25) |
Therapy of Immune-mediated Peripheral Neuropathies |
| 08:30-10:30 |
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| Capsule: |
Chronic immune-mediated neuropathies pose serious therapeutic challenges. Failure to treat or failure of therapy is associated with severe neruological disability, but certain therapeutic modalities carry the risk of major side effects. What are the best approaches? Are there gold standards? |
| Chairperson: |
M. Dalakas, Greece & UK; A. Chaudhuri, UK |
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| 08:30-09:30 |
Debate: Long term treatment of CIDP: IVIg vs. Immunosuppression |
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Pro IVIg: H.-P. Hartung, Germany
Commentator: A. Chaudhuri, UK |
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| 09:30-10:30 |
Debate: Can rituximab effectively treat myelin-associated glycoprotein (MAG) neuropathies? |
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Yes: M. Dalakas, Greece & UK
Commentator: I. Wirguin, Israel |
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| 10:30-11:00 |
Coffee Break |
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| Session (26) |
Pathogenesis, Diagnosis and Therapy of Peripheral Neuropathies and Neuroimmunology |
| 11:00-13:30 |
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| Capsule: |
The session focuses on several important issues in clinical neurology, the major one being the role of oligonclonal bands (OCB). These have been considered (one of) the holy grail(s) of multiple sclerosis. The search at the epitopes that these IgG are directed against have attracted much scientific interest, so far with no success. Is the effort justified? |
| Chairperson: |
H.-P. Hartung, Germany; G. Ebers, UK |
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| 11:00-11:50 |
Debate: Guillain Barre Syndrome: Re-treat with a second IVIg infusion vs. No evidence for a second course |
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Re-treat with a second IVIg infusion: I. Wirguin, Israel
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| 11:50-12:40 |
Discussion Lecture: Are the oligoclonal bands in the CSF a red herring?
Yes: A. Vincent, UK
Commentators: M. Dalakas, Greece & UK; H.-P. Hartung, Germany |
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| 12:40-13:30 |
Debate: Skin biopsy – Is this a useful diagnostic tool for painful neuropathies? |
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| Sunday, October 31, 2010 /// Hall B - Neurodegenerative Diseases |
| Session (27) |
Rehabilitation |
| 08:30-09:30 |
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| Capsule: |
The challenge of clinical neurorehabilitation is that the strategies and techniques should manage high heterogeneity of patients |
| Chairpersons: |
V. Homberg, Germany; D. Muresanu, Romania |
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|
| 08:30-09:30 |
Debate: Spasticity must be treated |
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Commentator: O. Bajenaru, Romania |
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| Session (28) |
Biomarkers in Diagnositcs of Neurological Disorders |
| 09:30-10:30 |
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| Capsule: |
Early diagnosis of neurological disorders can be improved by specific biomarkers. This session presents the currently known biomarkers and will discuss the controversy – the pro's and con's of the various biomarkers. Data will also be presented on clinically applied biomarkers which can be used as screening tools and for accelerating drug discovery. The session will present how these biomarkers can be incorporated into clinical drug trials, translational medicine and be used to elucidate proposed novel mechanisms of disease and drug action |
| Chairpersons: |
B.O. Popescu, Romania; K. Wesnes, UK |
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|
| 09:30-10:00 |
Lecture: EVP-6124, a potent nicotinic alpha7 co-agonist in cognition models:
G. Koenig, USA |
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| 10:00-10:30 |
Lecture: The place of surrogate endpoints in the development of new neurological medicines:
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|
| 10:30-11:00 |
Coffee Break |
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| Session (29) |
Controversial Biomarkers in Diagnostics of Neurological Disorders |
| 11:00-12:45 |
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| Capsule: |
Early diagnosis of neurological disorders can be improved by specific biomarkers. This session presents the currently known biomarkers and will discuss the controversy – the pro's and con's of the various biomarkers. Data will also be presented on clinically applied biomarkers which can be used as screening tools and for accelerating drug discovery. The session will present how these biomarkers can be incorporated into clinical drug trials, translational medicine and be used to elucidate proposed novel mechanisms of disease and drug action |
| Chairperson: |
R. Ravid, The Netherlands; I. Turcu, Romania |
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| 11:00-11:30 |
Lecture: Are neuro-psychological tests the best biomarkers for preclinical dementia?:
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| 11:30-11:50 |
Lecture: The role of Bio markers in Drug development and discovery
E. Vaudano, Belgium |
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| 11:50-12:10 |
Lecture: Plasma based biomarkers as screening tools for AD:
H. Soares, USA |
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12:10-12:30
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Lecture: Magnetic Resonance Spectroscopy (MRS) in mid cognitive impairment as a marker of early Alzheimer's diease:
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|
| 12:30-12:45 |
Discussion
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| 13:30-14:00 |
Poster Awards & Closing Ceremony |
| Chairpersons: |
A. Gil Nagel, Spain; A.D. Korczyn, Israel; W.W. Zhang, China |
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