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Thursday, March 8
|
| 15:00-17:00 |
Satellite Symposium of the Society for the Study of Neuroprotection and Neuroplasticity (SSNN) |
| Chairpersons: |
N. Bornstein, Israel; D. Muresanu, Romania
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|
15:00-15:30
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The brain, the culture and religion 
J. Schwartz, USA
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15:30-16:00
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Early Cerebrolysin treatment in traumatic brain injury (TBI): A large restrospective multi-centric cohort study 
B.O. Popescu, Romania
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16:00-16:30
16:30-17:00 |
The Prospective Observational COhort Neurotrauma (POCON) study in moderate/severe TBI
P. Vos, The Netherlands
Traumatic brain injury: Long-term clinical consequences
O. Bajenaru, Romania
|
| 17:00-17:15 |
Technical Break
|
| 17:15-19:30 |
Plenary Session |
| Chairpersons: |
M. Brainin, Austria; A.D. Korczyn, Israel
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|
17:15-17:25
17:25-17:45
|
Greetings
W. Grisold, Austria
Hitler's Parkinson's disease and its possible influence on political decisions
A. Lieberman, USA
|
| 17:45-18:05 |
Does the pyschoanalytical theory have neuro-anatomical basis?
I. Steiner, Israel
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| Chairpersons: |
H. Binder, Austria; W.W. Zhang, China
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|
18:05-18:25 |
Are Freud's neuroscience discoveries still valid?
M. Brianin, Austria
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18:25-19:00
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Debate: Can neuroimaging help solve the mind-body problem?
Yes: J. Chapman, Israel
No: A.D. Korczyn, Israel
|
| 19:00 |
Welcome Reception
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Friday, March 9
Hall A - MULTIPLE SCLEROSIS (MS)
Section Heads: M. Freedman, USA & A. Miller, Israel
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| Session 1 |
Multiple Scelrosis (MS) Diagnosis |
| 08:30-10:30 |
|
| Chairpersons: |
A. Miller, Israel; Z. Stelmasiak, Poland
|
| Capsule: |
The newest version of the McDonald diagnostic criteria have virtually removed the diagnostic value of CSF, but many still feel this analysis is complimentary to clinical and MRI criteria while others indicated that CSF adds additional elements. Lumbar punctures are considered by some invasive and the value of the information obtained should outweigh the morbidity of the procedure. Does CSF provide information about diagnosis or prognosis that is not captured by the MRI or the initial clinical picture? Aside from an indication to "rule out other conditions", is there still a role for CSF in the diagnostic work-up of a patient suspected to have MS, regardless of when they present? |
| 08:30-09:30 |
Debate: To tap or not to tap: Is there still a role for lumbar puncture and CSF analysis in MS diagnosis?
Debate host: M. Freedman, Canada
Yes: K. Vass, Austria
No: J. Chapman, Israel |
| Capsule: |
MRI is the best surrogate we have for following disease activity outside of clinical assessment, but some say it is too sensitive picking up changes that are meaningless or that have little functional significance. Much of acquired disability in MS can come from spinal cord involvement and quantitative MRI studies have been difficult to perform due to resolution difficulties in the cord compared to the brain. So once a medication has been chosen, can the MRI be used to assess treatment response? What sorts of changes truly constitute a worrisome change that might warrant a switch in therapy? Is there such a thing as a trivial MRI change? What sort of scan is required? Enhancement or no enhancement? How often would these need to be performed? Given the often cited "disconnect" between what the MRI and the patient show, would MRI be considered a back-up to clinical impression, or could changes in MRI alone warrant treatment decisions? |
| 09:30-10:30 |
Debate: Can MRI be used for therapeutic decision?
Debate host: B. Weinshenker, USA
Yes: U. Baumhackl, Austria
No: F. Deisenhammer, Austria
|
| 10:30-11:00 |
Coffee Break
|
| Session 2 |
MS Therapy |
| 11:00-13:00 |
|
| Chairpersons: |
F. Deisenhammer, Austria; J. Kruja, Albania
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| Capsule: |
MS criteria have changed yet again, with the newest version allowing for diagnostic certainty after a single clinical presentation as long as there is evidence eitehr clinically or by MRI of dissemination in space and the presence of both enhancing (new) and non-enhancing (old) lesions, which now satisfy the dissemination in time criterion. As a result of this newer classification, many of the patients previously called "CIS" are now officially "MS". But waht of the population that is still called "CIS"? Previously there was no agreement to treat CIS patients owing to the possibility that many would either not go on to develop MS or if they did, the disease would be fairly benign and not warrantling medication. What about the "new" CIS? |
| 11:00-12:00 |
Debate: The "new" clinically isolated syndome (CIS): To treat or not to treat?
Debate host: L. Airas, Finland
To treat: H.-P. Hartung, Germany
Not to treat: K. Vass, Austria
|
| Capsule: |
The treatment of MS is becoming highly complex with a wrath of new agents set to enter the marketplace. Some are oral agents with novel mechanisms of action while others are parenteral monoclonal antibodies. T cell vaccination, stem cell transplantation and even small molecules are currently in active trials. Given the overall safety of the two commonest treatments IFNß and GA for the past two decades, how can we assess the benefit of the newest agents over the previous in the absence of "head-to-head" trials? Even if benefit is small or superior, how does one weigh such benefit in view of the potential and unforeseen hazards of the newer medicines, especially in the long term? |
| 12:00-13:00 |
Debate: It is still impossible to adequately assess risk management of new disease modifying therapies
Debate host: M. Sandberg-Wollheim, Sweden
Yes: J. Losy, Poland
No: E. Havrdova, Czech Republic
|
| 13:00-14:00 |
Lunch Break
|
| Session 3 |
Neuromyelitis Optica (NMO) |
| 14:00-16:00 |
|
| Chairpersons: |
E. Buenz, USA; H. Leitner, Austria
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| Capsule: |
NMO or neuromyelltis optica is an evolving disease it seems. With the discovery of serum test for antibodies to aquaporin-4 (the NMO antibody test) the thought was that it would be possible to completely distinguish NMO from MS or other demyelinating diseases. However, it would appear that patients diagnosed with MS have antibodies to aquaporin-4 and there are other patients with mixed autoimmune disease and CNS demyelination often ascribed to those diseases (e.g. Siogren's) that also have detectable NMO antibodies. Do these patients have two diseases? |
| 14:00-15:00 |
Debate: Are MS and aquaporin-4 positivity mutually exclusive?
Debate host: P. Sorensen, Denmark
Yes: B. Weinshenker, USA
No: J. Chapman, Israel
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|
15:00-16:00
15:00-15:10
15:10-15:20
15:20-15:30
15:30-15:40
15:40-15:50
15:50-16:00
|
NEW PLAYERS IN MS
Alemtuzumab: E. Havrdova, Czech Republic
Fingolimod: H.-P. Hartung, Germany
Laquinimod: A. Miller, Israel
Ocrelizumab: D. Leppert, Switzerland
Teriflunomide: M. Freedman, Canada
Neudexta: A. Miller, Israel
|
| 16:00-16:30 |
Coffee Break
|
| Session 4 |
Therapy in Pregnancy and in the Future |
| 16:30-18:30 |
|
| Chairpersons: |
C. Constantinescu, UK; H. Tumani, Germany
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| Capsule: |
The predominant population of MS patients are women who are fertile, therefore before considerating a therapy for their MS, they have concerns about the effects of agents on fertility, potential fertility, effects should they inadvertently get pregnantand whether or not they can be treated and breastfeed. As no study can be formally done in pregnant or breastfeeding women, any data regarding safety has come from post-marketing studies and pregnancy registries, but how good are these data and can they be relied upon to make treatment recommendations? |
| 16:30-17:30 |
Debate: Some disease modifying therapies are safe during pregnancy and breastfeeding
Debate host: J. Losy, Poland
Yes: M. Sandberg-Wollheim, Sweden
No: L. Airas, Finland
|
| Capsule: |
Clearly the most un-met need in the treatment of MS is to stop progression and repair the damage that has collected. But is that even possible or realistic? Some have argued that even though axons are present and seen together with oligodendrocyte progenitor cells, repair is minimal. Others have seen evidence of remyellination in most patients, though clinically this was hard to realize. Imaging has shown that some "repair" may indeed occur but the functional significance is unknown. Is some damage more repairable that others? Current medications for the most part do "damage control", but few have actually shown to stimulate repair. Is this the hope of stem cells or newer therapies in development? |
| 17:30-18:00 |
Debate: Can the damage in MS be repaired?
Debate host: H.-P. Hartung, Germany
Yes: T. Kuhlmann, Germany
No: E. Buenz, USA
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Friday, March 9
Hall B - DEMENTIA
Section Heads: R.Bullock, UK & L. Grinberg, USA
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| Session 5 |
Is How We Live Rather Than How Long We Live More Important in Managing Dementia? |
| 08:30-10:30 |
|
| Chairpersons: |
L. Kruglov, Russia; R. Schmidt, Austria
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| Capsule: |
Some researchers suggest that music therpy is particularly beneficial for older adults with various types of dementia. According to them, music activates unconscious emotions and memories. Although some studies conclude that music therapy is effective for improving cognitive symptoms, only limited evidence supports its usefulness in the treatment. Apparently, the benefit depends on the type of dementia and symptom tacked. The present debate will shed light on this topic |
| 08:30-09:30 |
Debate: Is music beneficial for dementia patients towards recovery?
Yes: V. Brandes, Austria
No: T. Stegemann, Austria
Commentator: R. Bullock, UK
|
| Capsule: |
Can nutrient mixtures counteract synaptic deficiencies e.g. in Alzheimer's Disease and thereby improve cognitive functions? Might this strategy also work in other neurologic diseases with synaptic deficiencies? |
| 09:30-10:30 |
Debate: Can nutrients modify the synapse loss and cognitive impairments of neurodegenerative diseases?
Yes: R. Wurtman, USA
No: E. Ott, Austria
Commentator: M. Schmitz, Austria
|
| 10:30-11:00 |
Coffee Break
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| Session 6 |
Are We Looking in the Right Place for Biomarkers in Alzhiemer's Disease (AD)? |
| 11:00-13:00 |
|
| Capsule: |
Inflammation has long been proposed as having a role in AD, although it remains unclear whether inflammation represents a cause or consequence of AD. Indeed, neuropathological studies show increased expression of inflammatory mediators and microglial activation in AD. On the other hand, clinical trials using anti-inflammatory drugs failed |
| Chairpersons: |
G. Chakhava, Georgia; E. Ott, Austria
|
| 11:00-12:00 |
Debate: Will there ever be a valid biomarker for AD?
Yes: P. Giannakopoulos, Switzerland
No: P. Riederer, Germany
Commentator: M. Windisch, Austria
|
| 12:00-13:00 |
Debate: Is there a casual link between dementia and inflammation?
Yes: L. Liss, USA
No: B.O. Popescu, Romania
Commentator: M. Windisch, Austria
|
| 13:00-14:00 |
Lunch Break
|
| Session 7 |
Running Before We Can Walk - Is Prodromal AD a Valid Research Target? |
| 14:00-16:00 |
|
| Chairpersons: |
P. Feldschreiber, UK; A. Guekht, Russia
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| Capsule: |
The great effort for developing preclinical biomarkers for AD raises the question of whether this information will be beneficial to patients and families. In a situation in which no treatment is available, such diagnosis may potentially cause severe anxiety and depression. On the other hand, it might help the patient plan his or her present and future steps according to their wishes when they are still cogntively intact |
| 14:00-15:00 |
Debate: Does early diagnosis add real value for the patients with neurodegenerative diseases?
Yes: L. Spiru, Romania
No: R. Bullock, UK
Commentator: E. Giacobini, Switzerland
|
| Capsule: |
Lately, new diagnostic criteria have been proposed for AD. The goal is to deter AD in earlier stages than before. THis has been made possible due to enhancement of clinical and neuropsychological testing, as well as the introduction of imaging. However, it is clear by clinicopathological studies that the AD neuropathological process starts years before it can be detected by currently available imaging and clinical examination. How early are we able to detect AD using the available tools? |
| 15:00-16:00 |
Debate: Can we identify incipient AD-dementia?
Yes: O. Bajenaru, Romania
No: B.O. Popescu, Romania
Commentator: P. Giannakopoulos, Switzerland
|
| 16:00-16:30 |
Coffee Break
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| Session 8 |
Holding Farith - Is Manipulation of Amyloid Metabolism Central to the Search of AD Treatment? |
| 16:30-18:30 |
|
| Chairpersons: |
J. Leszek, Poland; M. Novak, Austria
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| Capsule: |
Amyloid imaging is emerging as a potential powerful biomarker in AD diagnosis and treatment follow-up. Despite the promising use of the imaging modality, several limitations regarding sensibility, specificity and costs should be overcome before its implementation for clinical use. Recent imaging/neuropathological studies have been instrumental in helping us to understand and tackle its limitations |
| 16:30-17:30 |
Debate: Is amyloid imaging clinically helpful?
Yes: R. Bullock, UK
No: M. Schmitz, Austria
Commentator: L. Liss, USA |
| Capsule: |
The amyloid hypothesis has dominated the Alzheimer field for over 20 years. However, all the research addressing this hypothesis resulted in meager therapeutic advances to date. Are we ready to refute the amyloid hypothesis and focus on other alternatives? This debate will address the current knowledge about the role of amyloid in AD pathogenesis, the novel amyloid-targeted drug trials and past failures |
| 17:30-18:30 |
Debate: Amyloid is a false target in AD therapy
Yes: E. Giacobini, Switzerland
No: J. Thome, Germany
Commentator: P. Giannakopoulos, Greece
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|
Friday, March 9
Hall C - REHABILITATION / NEURPSYCHIATRY
Rehablitation Section Heads: V. Homberg, Germany & D. Muresanu, Romania
Traumatic Brain Injury Section Heads: H. Binder, Austria & P. Vos, The Netherlands
|
| Session 9 |
|
| 08:30-10:30 |
|
| Capsule: |
Currently it is difficult to find the correct approach for brain protection and recovery, especially because we do not fully understand all endogenous neurobiological processes, the complete nature of the pathophysiological mechanisms, and the links between these two categories. Moreover, we continue to use a simplistic and reductionist approach in this respect. Nowadays, there are two strategies in brain protection and recovery – monomodal and multimodal. The first debate will highlight the historical evolution of this concept. The second debate will address post-stroke depression with a major impact on functional recovery, cognition and even survival. The close relation between appropriate early treatment and good outcome has not emerged in all clinical studies. Prophylactic treatment for depression in all patients with first-ever stroke may also positively influence the outcome |
| Chairpersons: |
D. Muresanu, Romania; L. Saltuari, Austria
|
| 08:30-09:30 |
Debate: Pharmcogenic influence on brain recovery: Which principle to use?
The monomodal strategy: V. Homberg, Germany
The multimodal strategy: D. Muresanu, Romania
Commentator: P. Vos, The Netherlands
|
| 09:30-10:30 |
Debate: Should antidepressants be used regularly in poststroke rehabilitation?
Yes: V. Homberg, Germany
No: A. Erfurth, Austria
Commentator: H. Binder, Austria
|
| 10:30-11:00 |
Coffee Break
|
| Session 10 |
|
| 11:00-13:00 |
|
| Capsule: |
TBI is a field with one of the greatest un-met needs in medicine. Studies using therapeutic strategies as an investigational modality reported better treatment effects but, considering lesions from the past, a successful pharmacological approach in brain protection and recovery may require a change of concept. Drugs that have multimodal and pleiotropic actions should be considered because of their capacity to protect the brain against the immediate consequences of injury and at the same time stimulate recovery. Biomarkers can serve as an indicator of cerebral damage with the advantage of providing dynamic information about the cellular and molecular changes. Recent published data show the idea that a realistic approach can be made only by combining multiple types of biomarkers and maybe using different investigative tools. There is also an increasing interest in using biomarkers as a treatment monitoring tool |
| Chairpersons: |
H. Binder, Austria; P. Vos, The Netherlands
|
| 11:00-12:00 |
Debate: Supporting brain protection and recovery after traumatic brain injury (TBI): Surgical procedures vs. Pharmacological interventions
Surgical procedures: C. Matula, Austria
Pharmacological interventions: D. Muresanu, Romania
Commentator: K. von Wild, Germany
|
| 12:00-13:00 |
Debate: Biomarkers of TBI are useful adjuncts in clinical practice
Yes: P. Vos, The Netherlands
No: L. Battistin, Italy
Commentator: D. Muresanu, Romania
|
| 13:00-14:00 |
Lunch Break
|
| Session 11 |
Neuropyschiatry |
| 14:00-16:00 |
|
| Chairpersons: |
H. Binder, Austria; W. Struhal, Austria
|
| Capsule: |
Results of experimental research allow us to suppose that emotional and social reaction, including aggression and violence, are regulated and modulated by numerous transmitters and neuromodulators, inherent for instance HPA axis hormones, neuropeptide AVP, 5-HT and GABA among others. At the same time it is indisputable, that childhood maltreatment predispose to impulsive aggression and antisocial symptoms in the later life |
| 14:00-15:00 |
Debate: Change of aggression / violence during life is explained by neurological factors
Yes: M. Willeit, Austria
No: A. Pritz, Austria
Commentator: S. Kasper, Austria
|
| Capsule: |
It has been suggested that somatisation represents an innate coping mechanism learned from early parent-child interactions. Though the neurobiological substrate of functional symptoms remains ambiguous, we know, that brain can functional as well as morphological adapt to environmental challenges and stress |
| 15:00-16:00 |
Debate: Functional symptoms have a neurobiological substrate based on adaptation to environmental challenges and stress
Yes: A. Staniloiu, Germany
Somatisation is a coping mechanism learned form early parent-child interactions: J. Fiegl, Austria
Commentator: V. Homberg, Germany
|
| 16:00-16:30 |
Coffee Break
|
| Session 12 |
Neuropyschiatry Syndromes and New Interventions |
| 16:30-18:30 |
|
| Capsule: |
Cognitive impairment is common in Parkinson's disease but it is still unclear when it starts and whether it can be reliably diagnosed prior to the appearance of motor symptoms. Also, the therapeutic possibilities with TMS are expanding |
| Chairpersons: |
B. Elibol, Turkey; V. Kostic, Serbia
|
| 16:30-17:30 |
Debate: Transcranial magnetic stimulation is an effective treatment for neuropsychiatric disorders
Yes: J. Thome, Germany
No: I. Rektorova, Czech Republic
Commentator: G. Ransmayr, Austria
|
| 17:30-18:30 |
Debate: Is there a cognitive dysfunction in early PD?
Yes: P. Martinez-Martin, Spain
No: F. Stocchi, Italy
Commentator: C. Falup-Pecurariu, Romania |
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Friday, March 9
Hall D
Infectious Diseases Section Head: I. Steiner, Israel
|
| Session 13 |
Neuro-oncology |
| 08:30-10:30 |
|
| Chairpersons: |
W. Grisold, Austria; P. Stambrook, USA
|
| 08:30-09:10 |
Debate: Leptomeningeal carcinomatosis
Intrathecal treatment: S. Oberndorfer, Austria
Systemic treatment: W. Grisold, Austria
Discussion
|
| 09:10-09:50 |
Debate: Steroids in neuro-oncology
Pro: S. Oberndorfer, Austria
Con: W. Grisold, Austria
Discussion
|
| 09:50-10:30 |
Debate: Glioma in the elderly
Treatment yes: J.-J. Zhu, USA
Treatment no: S. Oberndorfer, Austria
Discussion
|
| 10:30-11:00 |
Coffee Break
|
| Session 14 |
Obstacles to Drug Development in Neurology |
| 11:00-13:00 |
|
| Chairpersons: |
H. Budka, Austria; J.-J. Zhu, USA
|
|
11:00-12:00 |
Debate: The regulator's approach to the safety and efficacy of new medicines hinders the development and supply of new agents
Yes: P. Feldschreiber, UK
No: P. Vermersch, France
Commentator: M. Krams, USA
|
|
12:00-12:30 |
Glioblastoma: NextGen sequencing reveals multiple routes leading to EGF receptor disruption
P. Stambrook, USA
|
| 12:30-13:00 |
Discussion
S. Oberndorfer, Austria
J.-J. Zhu, USA
|
| 13:00-14:00 |
Lunch Break
|
| Session 15 |
Are Antidepressant Drugs Exerting Their Therapeutic Actions via Moduation of Adult Neurogenesis? |
| 14:00-16:00 |
|
| Capsule: |
Historically, adult neurogenesis is among recent discoveries in neuroscience and, despite great excitement, time will be required to clearly understand its contribution to brain physiology. In particular hippocampal neurogenesis is proposed to represent a common point of convergence for stimuli that activate neuronal circuits relevant for setting mood, emotion and cognition. Experimental evidence also suggests that modulation of hippocampal neurogenesis may represent a crucial component in the mechanism of action of drugs showing antidepressant effects. Clarifying this issue is fundamental for future drug discovery as well as for understanding brain structure and functional plasticity |
| Debate hosts: |
M. Grilli, Italy; M. Memo, Italy
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|
14:00-14:10
14:10-14:35
14:35-15:00
15:00-15:25
15:25-16:00
|
Introduction
Definitely
M. Grilli, Italy
Perhaps
S. Couillard-Despres, Austria
Perhaps
P. Lucassen, The Netherlands
Discussion
Moderator: J. Thome, Germany
|
| 16:00-16:30 |
Coffee Break
|
| Session 16 |
Infectious Issues on Neurological Conditions |
| 16:30-17:30 |
|
| Capsule: |
The session focuses on several important issues in clinical neurology: The impact (or lack of it) of adjunct steroid therapy in bacterial and viral neurological infections, and the possible etiology of chlamydophyla in neuro-psychiatric conditions |
| Chairpersons: |
A. Bowirrat, Israel; B. Pfausler, Austria
|
| 16:30-17:10 |
Debate: Are chlamydophila infections a major factor in neurologic and psychiatric diseases?
Yes: R. Wank, Germany
No T. Derfuss, Switzerland
|
| 17:10-17:50 |
Debate: Steroids in herpes simplex encephalitis
Yes: U. Meyding-Lamade, Germany
No: T. Derfuss, Switzerland
|
| 17:50-18:30 |
Debate: Steroids in bacterial meningitis
Yes: I. Steiner, Israel
No: E. Schmutzhard, Austria |
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Saturday, March 10
Hall A - STROKE
Section Heads: N. Bornstein, Israel & M. Brainin, Austria
|
| Session 17 |
|
| 08:30-10:30 |
|
| Chairpersons: |
D. Krieger, Denmark; A. Shuaib, Canada
|
| Capsule: |
Aspirin is the most widely used antithrombotic drug for secondary stroke prevention. Many RCTs have shown that aspirin reduced the risk of recurrent stroke by approximately 15-20%. Currently statins are prescribed routinely for secondary stroke prevention based on many RCTs conducted mainly in cardiology. Only one study-SPARCL was specifically designed for secondary stroke prevention. The issue of this debate - are statins more effective that the good old aspirin? |
| 08:30-09:30 |
Debate: Statins are more effective than aspirin in secondary stroke prevention
Yes: D. Spence, Canada
No: J. Streifler, Israel
Commentator: N. Bornstein, Israel
|
| Capsule: |
Post-stroke fatigue (PSF) is a well-known phenomenon after stroke that affects a significant number of patients and may have an impact on outcome. The main problem is that fatigue is not very well defined, hence may be influenced by many subjective factors. Therefore, the question whether the time is ripe o perform a clinical trial on treatment of post-stroke fatigue is very relevant. The debate will deal with the issue of interventional clinical trials in PSF |
| 09:30-10:30 |
Debate: Do we know enough about post-stroke fatigue to perform treatment trials?
Yes: A. Lerdal, Norway
No: M. Brainin, Austria
Commentator: J. Kesselring, Switzerland
|
| 10:30-11:00 |
Coffee Break
|
| Session 18 |
Treatment of Post-Stroke Complications |
| 11:00-13:00 |
|
| Chairpersons: |
D. Spence, Canada; J. Streifler, Israel
|
| Capsule: |
Transcranial magnetic stimulation (TMS) has become a main focus of research in the treatment of various neurological/psychiatric conditions. Aphasia may affect 15-20% of stroke patients; however no specific therapy has proved effective for this devastating condition. The usefulness of TMS in the treatment of aphasia is still debatable and will be discussed |
| 11:00-12:00 |
Debate: TMS is an effective therapy of aphasia
Yes: J. Mally, Hungary
No: J. Rothwell, UK
Commentator: W.-D. Heiss, Germany
|
| Capsule: |
Limb spasticity is a major problem of patients following moderate and severe strokes and may cause major disability to patients. The best therapeutic approach is still not well established. Botolinum toxin was suggested as a potential therapeutic solution, but its routine use in post-stroke spasticity is debatable |
| 12:00-13:00 |
Debate: Spasticity in stroke: Should Botulinum toxin be routinely used?
Yes: L. Csiba, Hungary
No: D. Truong, USA
Commentator: P. Kanovsky, Czech Republic
|
| 13:00-14:00 |
Lunch Break
|
| Session 19 |
Acute Stroke Management |
| |
Partially supported by eV3 |
| 14:00-16:00 |
|
| Chairpersons: |
N. Bornstein, Israel; W.-D. Heiss, Germany
|
| Capsule: |
High blood pressure (BP) is common after acute ischemic stroke (AIS) and may be observed in up to 70%-80% of AIS patients. However, the best management of BP is still a major issue of debate since lowering BP may cause hypoperfusion and aggravate the ischemic situation of the brain. So far, the best management of high BP in the acute phase of ischemic stroke is unknown and is still debatable |
| 14:00-15:00 |
Debate: Should blood pressure be lowered immediately after stroke?
Yes: D. Spence, Canada
No: M. Fisher, USA
Commentator: J. Wojczal, Poland
|
|
15:00-15:10
|
Treatment of acute ischemic stroke: The Bern Experience
M. Arnold, Switzerland
|
|
15:10-16:00 |
Debate: In patients with a large vessel occlusion, is IV thombolysis beneficial to patient outcomes prior to thrombectomy?
Yes: M. Arnold, Sweden
No: A. Shuaib, Canada
|
| 16:00-16:30 |
Coffee Break
|
| Session 20 |
Acute Stroke Therapy |
| 16:30-18:30 |
|
| Chairpersons: |
D. Bartko, Slovakia; M. Brainin, Austria
|
| Capsule: |
Hypoperfusion is the hallmark of AIS. In addition to thrombolysis, several methods and devices were developed to augment cerebral blood flow (CBF) to the brain in AIS. The concept of CBF augmentation is AIS is still a debatable question and will be discussed |
| 16:30-17:30 |
Debate: Augmentation of blood flow in acute stroke improves outcome
Yes: A. Shuaib, Canada
No: M. Fisher, USA
Commentator: W.-D. Heiss, Germany
|
| Capsule: |
Hypothermia is currently used as a routine established treatment after cardiac arrest, and was shown to be an effective treatment following stroke in animal models. However, its usefulness in the treatment of AIS in humans is still debated |
| 17:30-18:30 |
Debate: Is hypothermia effective as add-on therapy in acute stroke?
Yes: D. Krieger, Denmark
No: E. Schmutzhard, Austria
Commentator: J. Petersson, Sweden
|
|
Saturday March 10
Hall B - HEADACHE / PAIN
Section Heads: C. Lampl, Austria & A. Rapoport, USA
|
| Session 21 |
Familial Hemiplegic Migraine (FHM) and the Importance of Blood Vessels in Migraine |
| 08:30-10:30 |
|
| Capsule: |
FHM is associated with 3 definite abnormalities and possibly others. Will this help us to understand the genetic abnormalities associated with the more common types of migraine? Fifty years ago, migraine was claimed a vascular headache. More recently, research has shown that migraine is based in the cortex and brain stem and their connections. But some still argue that migraine is primarily a vascular disorder |
| Chairpersons: |
C. Lampl, Austria; A. Rapoport, USA
|
| 08:30-09:30 |
Debate: FHM is a useful genetic model for common migraine
Yes: M. Ferrari, The Netherlands
No: M. Ashina, Denmark
Commentator: J.M. Lainez, Spain
|
| 09;30-10:30 |
Debate: Migraine is primarily a vascular disorder
Yes: E. Shevel, South Afrcia
No: J. Olesen, Denmark
Commentator: M. Ferrari, The Netherlands
|
| 10:30-11:00 |
Coffee Break
|
| Session 22 |
Botulinum Toxin is a Treatment and the Usefulness of ICHD-II Criteria |
| 11:00-13:00 |
|
| Capsule: |
Onab otulinumtoxinA (Botox) is now approved in some countries as safe and effective treatment of chronic migraine; but the evidence and clinical data are not accepted by all. The ICHD-II is the latestversion of diagnostic criteria for all types of headache, produced by a committee of the International Headache Society and used by headache specialists all over the world, but its usefulness and necessity are still questioned |
| Chairpersons: |
A. Siva, Turkey P. Martelletti, Italy
|
| 11:00-12:00 |
Debate: Botulinum toxin is a necessary, safe and effective treatment of chronic migriane
Yes: J. Schim, USA
No: C. Lampl, Austria
Commentator: J.M. Lainez, Spain
|
| 12:00-13:00 |
Debate: The ICHD-II diagnostic criteria are useful and necessary for clinicians and researchers
Yes: J. Olesen, Denmark
No: E. Shevel, South Africa
Commentator: P. Martelletti, Italy
|
| 13:00-14:00 |
Lunch Break
|
| Session 23 |
Antidepressants in Migraine Therapy and Mild Headaches in a Migraineur |
| 14:00-16:00 |
|
| Capsule: |
Many neurologists use tricyclic antidepressants as their first choice for migraine prevention. Others prefer other preventives. Mild, frequent headaches appear to have different characteristics from migraine. Are they tension-type headaches or actually mild forms of migraine? |
| Chairpersons: |
M. Ashina, Denmark; M. Kapisyzi, Albania
|
| 14:00-15:00 |
Debate: Antidepressants are the best drugs to treat frequent migraine
Yes: J.M. Lainez, Spain
No: H.L. Hamburger, The Netherlands
Commentator: D. Mitsikostas, USA
|
| 15:00-16:00 |
Debate: Mild, frequent headaches in a migraineur or in a non-migraineur are tension-type headaches, not mild migraines
Yes: M. Levin, USA
No: A. Siva, Turkey
Commentator: E. Gross, USA
|
| 16:00-16:30 |
Coffee Break
|
| Session 24 |
All About Placebo and CGRP Blockade |
| 16:30-18:30 |
|
| Capsule: |
Placebo is used in registration trials for acute care and preventive migraine medications. Is this arm necessary and useful? CGRP has been studied for 25 years or more and 3 CGRP antagonists have been carefully tested in the clinic. Is CGRP blockade an effective treatment for migraine and will we see a medication come to market? |
| Chairpersons: |
E. Gross, USA; D. Mitsikostas, Greece
|
| 16:30-17:30 |
Debate: Placebo is useful and important in headache treatment and research
Yes: R. Weeks, USA
No: F. Andrasik, USA
Commentator: H.L. Hamburger, The Netherlands
|
| 17:30-18:30 |
Debate: CGRP receptor blockade is the most effective treatment for migraine
Yes: L. Edvinsson, Sweden
No: H. Bolay, Turkey
Commentator: A. Siva, Turkey
|
|
Saturday, March 10
Hall C - PARKINSON'S DISEASE & MOVEMENT DISORDERS (PD/MD)
Section Heads: F. Stocchi, Italy & D. Truong, USA
|
| Session 25 |
Parkinson's Disease |
| 08:30-10:30 |
|
| Capsule: |
Cumulating evidences suggest that non-motor symptoms are a big component of Parkinson's disease (PD) symptomatology. Where should we address our attention more: Motor or non-motor symptoms? |
| Chairpersons: |
B. Dagens, UK; G. Wenning, Austria
|
| 08:30-09:30 |
Debate: Do motor symptoms remain the major component of PD?
Yes: P. Odin, Germany
No: P. Martinez-Martin, Spain
Commentator: C. Falup-Pecurariu, Romania
|
| 09:30-10:30 |
Debate: Can we modify disease progression?
Yes: J. Duda, USA
No: A. Antonini, Italy
Commentator: L. Battistin, Italy
|
| 10:30-11:00 |
Coffee Break
|
| Session 26 |
Treatment of PD: New Insight |
| 11:00-13:00 |
|
| Capsule: |
Dopamine agonists remain big players in the treatment of PD. Is the balance between benefit and side effects still in favor of these drugs? Is there space for a new approach in the traetment of PD? |
| Chairpersons: |
R. Katzenschlager, Austria; P. Taba, Estonia
|
| 11:00-12:00 |
Debate: Dopamine agonists are still fundamental in the treatment of PD
Yes: H. Reichmann, Germany
No: U. Meenakshisundaram, India
Commentator: U. Bonuccelli, Italy
|
| 12:00-13:00 |
Debate: Is there room for a new non-dopaminergic treatments in PD?
Yes: A. Lieberman, USA
No: A. Antonini, Italy
Commentator: I. Rektorova, Czech Repbulic
|
| 13:00-14:00 |
Lunch Break
|
| Session 27 |
Levodopa and Motor Complications in PD |
| 14:00-16:00 |
|
| Capsule: |
Dyskinesia remains a big challenge in the long-term effect of PD. Is there a way to avoid dyskinesia? Being the short half-life of levodopa one of the factors leading to motor complications, is there a way to improve levodopa delivery? |
| Chairpersons: |
K. Jellinger, Austria; G. Ransmayr, Austria
|
| 14:00-15:00 |
Debate: Are dyskinesias an inevitable side effect of levodopa?
Yes: F. Stocchi, Italy
No: A. Lieberman, USA
Commentator: H. Reichmann, Germany
|
| 15:00-16:00 |
Debate: Can levodopa delivery be improved?
Yes: V. Srinivasan, India
No: P. Odin, Germany
Commentator: F. Stocchi, Italy
|
| 16:00-16:30 |
Coffee Break
|
| Session 28 |
Multiple System Atrophy |
| 16:30-18:30 |
|
| Capsule: |
What is Multiple system atrophy (MSA): Is it a disease per se or a clinical variant of the same disease? |
| Chairpersons: |
C. Falup-Pecurariu, Romania; V. Srinivasan, India
|
| 16:30-17:30 |
Debate: Are MSA and PD distinct clinical entities?
Yes: G. Ransmayr, Austria
No: G. Wenning, Austria
Commentator: K. Jellinger, Austria
|
| 17:30-18:30 |
Debate: Are multi-system atrophy (MSA)-parkinsonism and MSA-cerebellar the same disease?
Yes: J. Duda, USA
No: D. Truong, USA
Commentator: U. Meenakshisundaram, India
|
|
Saturday, March 10
Hall D - EPILEPSY
Section Heads: C. Baumgartner, Austria & M. Sperling, USA
|
| Session 29 |
Epilepsy Classification and Novel Imaging Techniques: Useful in Clinical Practice or Simply l’art pour l’lart? |
| 08:30-10:30 |
|
| Chairpersons: |
V. Donath, Slovakia; A. Guekht, Russia
|
| Capsule: |
The International League against Epilepsy recently proposed a new classification of seizures and epileptic syndromes. Most importantly, the concept of generalized and focal epilepsies was dropped. Etiology is now classified as genetic, structural-metabolic, and unknown. This new classification raised intense discussions in the epilepsy community and it remains to be awaited how the classification will translate into clinical practice |
| 08:30-09:30 |
Debate: The new seizure and epilepsy classifications are useful in clinical practice
Yes: A. Schulze-Bonhage, Germany
No: C. Baumgartner, Austria
Commentator: M. Sperling, USA
|
| Capsule: |
Novel imaging techniques have revolutionized our understanding of the epileptic brain and the approach to medically refractory epilepsies during pre-surgical evaluation. However, it remains to be seen whether these techniques should be part of the routine evaluation of all epilepsy patients and whether this will change epilepsy management in general |
| 09:30-10:30 |
Debate: Imaging technical such as DTI and fMRI should be employed in the routine diagnosis of patients with epilepsy
Yes: W. Theodore, USA
No: I. Rektor, Czech Republic
Commentator: S. Bonelli, Austria
|
| 10:30-11:00 |
Coffee Break
|
| Session 30 |
Disease Modification: Reality or Wishful Thinking? |
| 11:00-13:00 |
|
| Chairpersons: |
J. Kruja, Albania; K. Rejdak, Poland
|
| Capsule: |
Although numerous very effective antiepileptic drugs have been introduced during the last 20 years, all these drugs have failed in the prevention of epilepsy and in modifying its natural course. These drugs therefore need to be considered as anticonvulsant rather than as antiepileptic drugs. Possible approaches for prevention and disease modification which are of utmost importance in epilepsy management will be the focus of this debate |
| 11:00-12:00 |
Debate: Can epilepsy be prevented and its natural course modified?
Yes: M. Sperling, USA
No: M. Holtkamp, Germany
Commentator: W. Theodore, USA
|
| Capsule: |
Several studies suggest that vagus nerve stimulation (VNS) is more efficacious in seizure control when applied early in the course of epilepsy. Nevertheless, in most patients VNS is applied only later after an average disease during of 20 years or more when multiple antiepileptic drugs have failed. In this debate, the advantages and disadvantages of early VNS will be discussed |
| 12:00-13:00 |
Debate: Vagus nerve stimulation should be routinely offered after failure of 2-3 AEDs in patients who are not candidates for resective surgery
Yes: P. Boon, Belgium
No: A. Schulze-Bonhage, Germany
Commentator: C. Baumgartner, Austria
|
| 13:00-14:00 |
Lunch Break
|
| Session 31 |
Special Treatment Situations: Anything New? |
| 14:00-16:00 |
|
| Chairpersons: |
C. Baumgartner, Austria; W. Theodore, USA
|
| Capsule: |
Several intravenous formulations of new antiepileptic drugs recently showed promising results in the treatment of various forms of status epilepticus. However, no randomized controlled trials exist systematically comparing the strengths and weaknesses of these drugs. Such trials will probably not be available in the near future for methodological reasons. The practical approach to modern management of status epilepticus will therefore be highlighted in this debate |
| 14:00-15:00 |
Debate: New AEDs should be used as first-line options in the treatment of status epilepticus
Yes: W. Theodore, USA
No: P. Boon, Belgium
Commentator: I. Rektor, Czech Republic,
|
| Capsule: |
High does valproate treatment during pregnancy is associated with an increased incidence of major congenital malformations and reduced cognitive functions in exposed children with a clear dose relationship. On the other hand, some patients can only be controlled with valproate and uncontrolled seizures are harmful to the fetus as well. Therefore the decision to prescribe valproate to a woman of childbearing age can be a challenging issue |
| 15:00-16:00 |
Debate: Should valproate be prescribed to women of childbearing age?
Yes: A. Guekht, Russia
No: G. Luef, Austria
Commentator: M. Sperling, USA
|
| 16:00-16:30 |
Coffee Break
|
| Session 32 |
Hands-on or Hands-off AED Serum Levels? |
| 16:30-18:30 |
|
| Chairpersons: |
H. Goldberg-Stern, Israel; M. Sperling, USA
|
| Capsule: |
Monitoring antiepileptic drug (AED) serum concentrations is widely practiced in clinical epilepsy management and can be quite useful in certain treatment decisions. On the other hand, dosing accordingly to AED serum concentrations without clinical considerations can be disadvantageous to the patients. The pros and cons as well as the indications for AED serum concentration monitoring will be highlighted in this debate |
| 16:30-17:30 |
Debate: Antiepileptic drugs (AED) serum concentrations are very useful in epilepsy treatment monitoring
Yes: G. Luef, Austria
No: C. Baumgartner, Austria
Commentator: M. Sperling, USA
|
| 17:30-18:30 |
CASE PRESENTATIONS AND DISCUSSION
A series of challenging cases will be presented to course faculty for discussion of diagnosis and management
Moderator: M. Sperling, USA
Panel: All Epilepsy Faculty
|
|
Sunday, March 11
Hall A - PROBLEMS & SOLUTIONS
|
| Session 33 |
Mindfulness and the Clinical Relevance of Human Neuroplasticity |
| 08:30-10:30 |
|
| Capsule: |
A moderator and four experts debating a hot topic. The ambition: To walk away with one or two positions on very concrete proposals on how to fix a particular problem |
| Moderator: |
J. Schwartz, USA |
| Speakers: |
E. Antonova, UK; S. Greenfield, UK; I. Ivanov, USA
|
|
Neurobiological research in our era has generally assumed that brain mechanisms alone will ultimately suffice to explain all psychologically described phenomena. This assumption stems from the idea that all causal mechanisms relevant to neuroscience can be formulated solely in terms of the principles of classic Newtonian physics. Thus, terms having intrinsic experiential content (e.g. feeling, observing and effort) are not included as primary causal factors. This theoretical perspective is dictated by ideas about the natural world that have been known to be fundamentally incorrect for more than three-quarters of a century. Contemporary physical theory differs profoundly from classic Newtonian physics on the important matter of how the consciousness of human agents enters into the causal dynamics of empirical phenomena. The new quantum principles contradict the older idea that mechanical processes alone can account for all observed empirical data. Contemporary quantum physical theory brings directly and irreducibly into the overall causal structure certain psychologically described choices made by human agents about how they will act. This key development is applicable to neuroscience, and it provides neuroscientists and neurologists with an alternative conceptual framework for describing neural processes. The new framework, and specifically the well described physical principle known as quantum Zeno effect, enables scientists and clinicians to better understand the neuroplastic mechanisms relevant to the growing number of studies demonstrating the capacity of directed attention and mental effort to systematically alter brain function. Clinical neurophysiological and neuropsychological findings from research on depression, attentional deficits, placebo effect, stroke, and normal human psychology will be discussed and elucidated in light of this theoretical paradigm shift. |
| |
|
| 10:30-11:00 |
Coffee Break
|
| Session 34 |
Prevention in Alzheimer's Disease |
| 11:00-13:15 |
|
| Capsule: |
A moderator and four experts debating a hot topic. The ambition: To walk away with one or two positions on very concrete proposals on how to fix a particular problem ... continued |
| Moderator:: |
M. Krams, USA |
| Speakers: |
S. Greenfield, UK; A. Grieve, UK; H. Hampel, Germany; E. Karran, UK; L. Middleton, UK
|
|
There is a time lag of years, may be decades before the initial occurrence of histopathological hallmarks of Alzheimer’s disease is followed by clinical manifestations of the disease. This begs the question when to initiate pharmacological interventions aiming at modifying the underlying disease: should we treat or should we prevent?
In this session we will discuss how to make Alzheimer Prevention trials a mainstream effort in the clinical development of disease modifying treatments against Alzheimer’s disease:
• The underlying biology: Which targets are of interest?
• The patient population: Whom to select and how?
• The endpoint: How to observe? A GPS system built of biomarker satellites.
• The clinical trial methodology: A cross between epidemiological natural history study and a pharmacological intervention trial
• The political and regulatory landscape: Educating the environment
Experts from different backgrounds (neuroscience, medicine, epidemiology, statistics and drug development) will present a short position statement, followed by a structured debate with an ambition to identify solutions on how to make prevention trials happen. |
| |
|
|
Sunday, March 11
Hall B
Section Heads: M. Dalakas, Greece & USA & H.-P. Hartung, Germany (Neuroimmunology)
|
| Session 35 |
New Players |
| |
Partially supported by Electrocore Medical |
| 08:30-09:00 |
|
| Chairperson: |
J. Ranxha, Albania
|
| 08:30-09:00 |
Development of a non-invasive vagus nerve stimulator for the treatment of acute and chronic migraines: Preliminary animal and human data
B. Simon, USA
|
| 10:30-11:00 |
Coffee Break
|
| Session 36 |
|
| 11:00-13:15 |
|
| Capsule: |
THe field of neuroimmunology is rapidly progressing and attracts more attention. However, the exact role of immune processes as friends or foes is still debated. Several immunomodulatory therapies are available, and the suitability of each and their preferences need to be discussed |
| Chairperson: |
H.-P. Hartung, Germany; M. Levite, Israel
|
| 11:00-11:45 |
Debate: Neuroimmune diseases - IVIg vs. plasmaphersis
IVIg: M. Dalakas, Greece & USA
Plasmaphersis: A. Chaudhuri, UK
|
| 11:45-12:30 |
Debate: Are immune processes beneficial in neurodegeneration diseases?
Yes: E. Meinl, Germany
No: A. Chaudhuri, UK
|
| 12:30-13:15 |
Debate: Treatment of inflammatory myopathies: IVIg vs. immunosuppresants
Yes: M. Dalakas, Greece & USA
No: R. Mantegazza, Italy
|
| 13:15-13:30 |
POSTER AWARDS AND CLOSING CEREMONY
Hall A
|
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