07:30-08:30
|
E-Poster Presentations (Exhibition Area)
|
MULTIPLE SCLEROSIS (MS) | HALL A
|
|
08:30-10:10
|
DIAGNOSIS
|
Chairs:
|
Anastasios Orologas, Greece
|
08:30-09:20
|
Are the 2017 MS McDonald criteria too liberal and should be more restrictive?
|
|
Capsule: The 2017 revisions of the McDonald criteria for the diagnosis of MS were mainly designed to facilitate an earlier MS diagnosis thus marginalizing the clinically isolated syndrome. While the criteria are easy to use and highly sensitive, they lack specificity and may bear the risk of MS overdiagnosis, exposing patients to unnecessary, expensive and sometimes dangerous therapy.
|
08:30-08:40
|
Host: Ralf Linker, Germany
|
08:40-08:55
|
|
08:55-09:10
|
|
09:10-09:20
|
Discussion and rebuttals
|
|
|
09:20-10:10
|
Does OCT make VEP redundant?
|
|
Capsule: Visual evoked potentials (VEP) have traditionally been used to support the existence of subclinical involvement of the optic nerve in MS patients. The newly developed optical coherence tomography (OCT) is sensitive to anatomical changes in the retina and optic nerve. Does the OCT make the VEP obsolete or does the physiological measure add important information?
|
09:20-09:30
|
|
09:30-09:45
|
|
09:45-10:00
|
No: Mario Habek, Croatia
|
10:00-10:10
|
Discussion and rebuttals
|
10:10-10:25
|
Coffee Break
|
08:30-10:10
|
THERAPY
|
Chairs:
|
Emma Gray, UK | Anas Jouhar, Syria
|
10:25-11:15
|
Should new therapies for MS be used even with poor scientific support?
|
|
Capsule: Over the past three decades, numerous drugs were approved for MS, but in many patients the disease is not fully controlled. In this session, the debaters will outline the pros and cons of using interventions based on limited scientific evidence, such as high dose vitamin D or hyperbaric oxygen (HBO).
|
10:25-10:35
|
Host: Olaf Stuve, USA
|
10:35-10:50
|
Yes: Richard Nicholas, UK
|
10:50-11:05
|
No: Konrad Rejdak, Poland
|
11:05-11:15
|
Discussion and rebuttals
|
|
|
11:15-12:05
|
Newly diagnosed MS patients should be started on aggressive therapy.
|
Capsule: Early treatment is claimed to improve long-term prognosis in MS. Recent studies also suggest that early aggressive therapy with potent immunosuppressive drugs (“induction therapy”) may improve long-term outcomes and perhaps lower the risk of conversion to secondary-progressive MS. Should newly diagnosed MS patients be started on such aggressive therapies? Do the potential benefits always outweigh their risks?
|
|
11:15-11:25
|
Host: Jera Kruja, Albania
|
11:25-11:40
|
|
11:40-11:55
|
|
11:55-12:05
|
Discussion and rebuttals
|
12:05-12:15
|
Short Break
|
12:15-13:15
|
Industry Supported Symposium
|
13:15-14:15
|
Lunch Break
|
13:15-14:15
|
Meet the Expert
|
14:15-15:45
|
DISEASE COURSE
|
Chairs:
|
Jelena Drulovic, Serbia | Melchor Rodrigo, Argentina
|
14:15-15:00
|
Are MS patients at increased risk for developing cancer?
|
|
Capsule: Whether people with MS are at higher risk of developing cancer has not been definitively established. The increased rate of general comorbidity would indicate a higher risk of cancer. On the other hand, some registers and large cohort studies have not found an association. Could it be that there is higher risk of specific cancers, but not all cancers? And can newer highly potent immunosuppressive treatments modify the long term risk?
|
14:15-14:25
|
Host: Cris Constantinescu, UK
|
14:25-14:40
|
|
14:40-14:55
|
|
14:55-15:00
|
Discussion and rebuttals
|
15:00-15:45
|
MS is a primary progressive disease in all cases, but some patients have superimposed relapses.
|
|
Capsule: Patients with clinically isolated syndrome have been shown to have significant cortical changes in their brains. Subcortical asymptomatic alterations have also been described. Does that mean that MS is basically a degenerative disease with superimposed clinical flare-ups (“relapses”) as epiphenomena or is MS an inflammatory disease of the brain with only secondary degeneration?
|
15:00-15:10
|
Host: Bart van Wijmeersch, Belgium
|
15:10-15:25
|
Yes: Antonio Scalfari, UK
|
15:25-15:40
|
|
15:40-15:45
|
Discussion and rebuttals
|
15:45-16:00
|
Coffee Break
|
16:00-18:45
|
COGNITION IN MS AND FAKE NEWS
|
Chairs:
|
Manuel Seijo-Martinez, Spain
|
16:00-16:55
|
We are well enough equipped to identify fake news in MS therapy before they can cause harm.
|
|
Capsule: Fake news are news stories or hoaxes created to deliberately misinform or deceive readers. Information that patients with MS read online, and especially in their social media feeds is often inaccurate or untrue. Misinformation about MS therapies have also been disseminated to care providers.
|
16:00-16:10
|
Host: Nikos Evangelou, UK
|
16:10-16:25
|
Yes: Klaus Schmierer, UK
|
16:25-16:40
|
No: Radu Tanasescu, UK
|
16:40-16:55
|
Discussion and rebuttals
|
|
|
16:55-17:50
|
Cognitive decline is sufficient to define transition to secondary progressive multiple sclerosis (SPMS).
|
|
Capsule: There is no biomarker that indicates when a patient has transitioned from relapsing-remitting MS (RRMS) to SPMS, and consequently SPMS is a retrospective diagnosis, based primarily on motor disability. The period of diagnostic uncertainty separating RRMS and SPMS diagnoses often lasts years. Is cognitive decline sufficient to define this change?
|
16:55-17:05
|
Host: Dimitrios Karusis, Israel
|
17:05-17:20
|
Yes: Klaus Schmierer, UK
|
17:20-17:35
|
No: Thomas Berger, Austria
|
17:35-17:50
|
Discussion and rebuttals
|
17:50-18:45
|
In MS patients with significant cognitive decline, drug treatment should be modified.
Capsule: Approximately 50% of people with MS become unemployed with a median EDSS of 3.0-3.5. They usually acquired hidden disabilities related to cognitive impairment. Should MS specific drug treatment be modified in patients with cognitive decline whose EDSS is otherwise unchanged?
|
17:50-18:00
|
Host: Laszlo Vecsei, Hungary
|
18:00-18:15
|
Switch to a new agent: Ron Milo, Israel
|
18:15-18:30
|
Not so fast: Amos Korczyn, Israel
|
18:30-18:45
|
Discussion and rebuttals
|
STROKE | HALL B
|
|
08:30-10:10
|
NEUROIMAGING IN ACUTE ISCHEMIC STROKE
|
Chairs:
|
Maia Beridze, Georgia | Nataliia Chemer, Ukraine
|
08:30-09:20
|
Is penumbral imaging mandatory for potential thrombectomy in patients arriving beyond six hours?
|
|
Capsule: There is general agreement amongst stroke experts that patient selection is essential for successful thrombectomy is essential. The introduction of penumbral imaging may allow for improved patient evaluation but comes at a higher cost. Is there sufficient evidence that such imaging is made mandatory prior to initiation of treatment?
|
08:30-08:40
|
|
08:40-08:55
|
Yes: Krassen Nedeltchev, Switzerland
|
08:55-09:10
|
No: Ashfaq Shuaib, Canada
|
09:10-09:20
|
Discussion and rebuttals
|
|
|
09:20-10:10
|
Do diffusion weighted imaging (DWI) negative strokes exist?
|
|
Capsule: Stroke is a clinical entity. Its exact identification is crucial as therapeutic options nowadays are associated with some risks. DWI MRI is considered the best imaging technique for the confirmation of acute ischemic stroke (AIS). Sensitivity, however, is not perfect, with debatable underlying reasons, raising the question: Do AIS with negative DWI imaging really exist?
|
09:20-09:30
|
Host: Olena Tsurkalenko, Ukraine
|
09:30-09:45
|
Yes: Jonathan Streifler, Israel
|
09:45-10:00
|
No: Krassen Nedeltchev, Switzerland
|
10:00-10:10
|
Discussion and rebuttals
|
10:10-10:25
|
Coffee Break
|
10:25-12:05
|
HEART AND BRAIN
|
Chairs:
|
Zdravka Poljakovic, Croatia | Aleksandras Vilionskis, Lithuania
|
10:25-11:15
|
Should all patients with embolic stroke of undetermined source (ESUS) be anticoagulated?
|
|
Capsule: ESUS patients are more likely to have a cardioembolic source of stroke, so may benefit from anticoagulation. However, studies to date have not supported anticoagulation in all patients with ESUS. Are there robust reasons that they should be anticoagulated?
|
10:25-10:35
|
Host: Natan Bornstein, Israel
|
10:35-10:50
|
Yes: David Spence, Canada
|
10:50-11:05
|
No: Jonathan Streifler, Israel
|
11:05-11:15
|
Discussion and rebuttals
|
|
|
11:15-12:05
|
Is left atrial appendage closure is underutilized for stroke prevention in atrial fibrillation?
Capsule: The majority of embolic strokes patients with nonvalvular atrial fibrillation are associated with left atrial thrombi, and left atrial appendage closure may be suitable alterative to chronic anticoagulation.
|
11:15-11:25
|
Host: George Chrysant, USA
|
11:25-11:40
|
|
11:40-11:55
|
No: Roni Eichel, Israel
|
11:55-12:05
|
Discussion and rebuttals
|
12:05-12:15
|
Short Break
|
12:15-13:15
|
Industry Supported Symposium
|
13:15-14:15
|
Lunch Break
|
13:15-14:15
|
Meet the Expert
|
14:15-15:45
|
ACUTE ISCHEMIC STROKE (AIS) MANAGEMENT
|
Chairs:
|
Fenny Yudiarto, Indonesia | Michael Chopp, USA
|
14:15-15:00
|
Mobile stroke units (MSU) are useful and cost effective for patients with AIS.
|
|
Capsule: IV tPA was approved as an effective treatment for AIS within 4.5 hours. It also was shown that the sooner the tPA is administered the better are the chances of beneficial outcome – “Time is Brain". Therefore, MSU with CT scan were introduced with the ability to give tPA in the ambulance and by that to save time. It is still unsettled whether MSU actually have an impact on patients’ outcome and are cost effective. This debate will try to shed light on this controversial issue.
|
14:15-14:25
|
Host: Joanna Wojczal, Poland
|
14:25-14:40
|
Yes: Silke Walter, Germany
|
14:40-14:55
|
No: Krassen Nedeltchev, Switzerland
|
14:55-15:00
|
Discussion and rebuttals
|
|
|
15:00-15:45
|
Does the main benefit of AIS come from tPA or stroke unit care?
|
|
Capsule: The presence of a dedicated stroke unit allows for the management of all patients with suspected AIS. Treatment with tPA can only be offered to a smaller subset of AIS patients but the improvement in some treated patients can be very significant. In an era of limited resources, should we focus on ensuring that all AIS patients be admitted to a stroke unit or recommend fast triage methods for timely thrombolysis?
|
15:00-15:10
|
|
15:10-15:25
|
tPA: Gary Ford, UK
|
15:25-15:40
|
Stroke unit: Ashfaq Shuaib, Canada
|
15:40-15:45
|
Discussion and rebuttals
|
15:45-16:00
|
Coffee Break
|
16:00-17:30
|
SECONDARY STROKE PREVENTION
|
Chairs:
|
Dalius Jatuzis, Italy
|
16:00-16:45
|
Should statins be given to people over age 80 for stroke prevention?
|
|
Capsule: There is considerable evidence that the use of statins results in reduction of cardiovascular morbidity and mortality. Long-term treatment with statins can lead to side effects including muscle and liver damage. Clinical trials evaluating the efficacy of statins have mostly enrolled subjects less than 75 years of age. Can we extrapolate the evidence to older individuals in whom the risk of side-effects may be higher?
|
16:00-16:10
|
|
16:10-16:25
|
Yes: David Spence, Canada
|
16:25-16:40
|
|
16:40-16:45
|
Discussion and rebuttals
|
|
|
16:45-17:30
|
Should symptomatic extracranial vertebral artery stenosis be stented?
|
|
Capsule: Stenosis in the vertebro-basilar system accounts for about one quarter of all posterior circulation strokes. The risk profile is similar to that seen for carotid stenosis. Recent phase 2 trials have shown that extracranial vertebral stenosis can be stented with low risk but whether this reduces recurrent stroke risk compared with best medical therapy alone remains controversial. The debate will consider whether based on current evidence stenting should be recommended for recently symptomatic extracranial vertebral artery stenosis.
|
16:45-16:55
|
Host: Hugh Markus, UK
|
16:55-17:10
|
Yes: Laszlo Csiba, Hungary
|
17:10-17:25
|
No: Hrvoje Budincevic, Croatia
|
17:25-17:30
|
Discussion and rebuttals
|
17:30-19:00
|
ANTITHROMBOTIC TREATMENTS
|
Chairs:
|
|
17:30-18:15
|
Should TIA patients be routinely treated chronically with both aspirin and clopidogrel?
|
Capsule: In some studies, dual antiplatelet therapy has benefits in the short term compared to single agents. However, the duration of benefit may be limited, and there may be some patients who would not benefit. In addition, dual therapy carries risk of complications, particularly hemorrhage. Is there sufficient evidence to recommend long-term dual antiplatelet therapy for all patients with TIA or minor strokes?
|
|
17:30-17:40
|
|
17:40-17:55
|
|
17:55-18:10
|
No: David Spence, Canada
|
18:10-18:15
|
Discussion and rebuttals
|
|
|
18:15-19:00
|
In the presence of cerebral microbleeds (CMBs), antithombotic therapy should be avoided.
|
Capsule: The presence of microbleeds (detected only with MRI) is associated with increased risk of hemorrhagic and perhaps of ischemic stroke. The risk depends on the location and number of microbleeds. How dangerous is antithrombotic therapy in patients with microbleeds? The session provides an overview about the pros and cons.
|
|
18:15-18:25
|
Host: David Werring, UK
|
18:25-18:40
|
|
18:40-18:55
|
No: Laszlo Csiba, Hungary
|
18:55-19:00
|
Discussion and rebuttals
|
ALZHEIMER’S DISEASE (AD) AND DEMENTIA | HALL C
|
|
08:30-10:10
|
PRECLINICAL AND EARLY ALZHEIMER’S DISEASE (AD)
|
Chairs:
|
Martin Rossor, UK | Shira Knafo, Spain
|
08:30-09:20
|
Is subjective cognitive impairment itself a prelude to dementia?
|
|
Capsule: In a chronic medical condition, early diagnosis becomes an issue when treatment is available that can alter its course. Regarding AD, there is hope that novel prevention strategies will have the capacity of slowing down the neurodegeneration. Such treatments may provide greatest benefit to patients at the stage of absent or minor cognitive impairment. This debate will focus on the central question, can (and should) AD be diagnosed in the stage of subjective cognitive deficits, although disease-modifying interventions are still unproven?
|
08:30-08:40
|
Host:
|
08:40-08:55
|
|
08:55-09:10
|
|
09:10-09:20
|
Discussion and rebuttals
|
|
|
09:20-10:10
|
Is cognitive reserve just a buzzword lacking scientific value?
|
|
Capsule: The concept of reserve was established to account for the observation that a given degree of neurodegenerative pathology may result in varying degrees of symptoms in different individuals. There is a large amount of evidence on risk and protective factors for neurodegenerative diseases and dementia, yet the biological mechanisms that underpin the protective effects of certain lifestyle and physiological variables remain poorly understood, limiting the development of more effective strategies. This debate will focus on the important question, is reserve just another buzzword or is the phenomenon supported by convincing scientific evidence.
|
09:20-09:30
|
|
09:30-09:45
|
Yes: Panteleimon Giannakopoulos, Switzerland
|
09:45-10:00
|
No: Irena Rektorova, Czech Republic
|
10:00-10:10
|
Discussion and rebuttals
|
10:10-10:25
|
Coffee Break
|
10:25-12:05
|
PATHOPHYSIOLOGY OF AD
|
Chairs:
|
Xao-Ping Wang, China
|
10:25-11:15
|
The development in understanding AD has not made an impact on patient care.
|
|
Capsule: AD is characterized by cognitive deterioration, but non-cognitive behavioral symptoms are also frequent and often associated with more suffering than cognitive decline. Treatment of those symptoms may be difficult and challenging, and there is insufficient evidence to support treatment decisions. This debate will focus on the question whether the improved understanding of AD pathology has improved patient care and treatment, including non-cognitive symptoms.
|
10:25-10:35
|
|
10:35-10:50
|
Yes: Judith Aharon, Israel
|
10:50-11:05
|
|
11:05-11:15
|
Discussion and rebuttals
|
|
|
11:15-12:05
|
Vascular lesions contribute to AD pathology.
|
|
Capsule: Over several years, evidence has been accumulating that suggests vascular disease impacts on common causes of dementia, in particular AD. Modifiable vascular risk factors such as hypertension, diabetes, dyslipidemia and adiposity are all linked to AD. However, it is unclear whether these factors contribute to or promote AD pathology itself or just add vascular damage.
|
11:15-11:25
|
Host: Nick Fox, UK
|
11:25-11:40
|
|
11:40-11:55
|
No: David Knopman, USA
|
11:55-12:05
|
Discussion and rebuttals
|
12:05-12:15
|
Short Break
|
12:15-13:15
|
Industry Supported Symposium
|
13:15-14:15
|
Lunch Break
|
13:15-14:15
|
Meet the Expert
|
14:15-15:45
|
RISK AND PROTECTIVE FACTORS
|
Chairs:
|
Yvonne Freund-Levi, Sweden
|
14:15-15:00
|
Does aerobic exercise protect cognition?
|
|
Capsule: Lifestyle changes have been suggested for dementia prevention. Physical activity engagement has repeatedly been associated with preserved cognition and lower risk for cognitive decline and dementia among older adults. Whether physical activity is neuroprotective or if it mitigates enhanced risk for dementia via other factors is less well understood. This debate will discuss whether physical activity protects cognitive function and whether we know enough about the phenomenon to design effective interventions.
|
14:15-14:25
|
Host: Miia Kivipelto, Sweden/UK
|
14:25-14:40
|
|
14:40-14:55
|
No: Naji Tabet, UK
|
14:55-15:00
|
Discussion and rebuttals
|
|
|
15:00-15:45
|
Is deafness a causative risk factor to dementia?
|
|
Capsule: Hearing loss is associated with increased risk for dementia. Other data suggest that there may be a causal link between deafness and cognitive decline but hearing loss may merely be an early symptom of neurodegenerative changes.
|
15:00-15:10
|
|
15:10-15:25
|
Yes: Sergi Costafreda, UK
|
15:25-15:40
|
|
15:40-15:45
|
Discussion and rebuttals
|
15:45-16:00
|
Coffee Break
|
16:00-17:30
|
NEW DEFINITIONS AND APPROACHES
|
Chairs:
|
Homa Ebrahimi, Iran
|
16:00-16:45
|
Is the new NIA-AA research definition of AD helpful?
|
|
Capsule: The 2011 NIA-AA definition of AD was based on clinical symptoms. However, the new 2018 definition eliminates the use of clinical phenotypes and rather depends on biological manifestations like whether amyloid-β (Aβ) and tau pathology or neuroimaging evidence of neurodegeneration exist, regardless of clinical manifestations. Is this change useful?
|
16:00-16:10
|
Host: Edson Amaro, Brazil
|
16:10-16:25
|
Yes:
|
16:25-16:40
|
|
16:40-16:45
|
Discussion and rebuttals
|
|
|
16:45-17:30
|
Will big data help us to find cure for dementia?
|
|
Capsule: In recent years there has been a surge towards big data approaches in AD, following a general trend in other disciplines. However, not everyone is convinced and the debate on the merits of big data for identifying effective treatments for AD is in full swing. That big collections might generally be useful is not the issue. It was suggested that we can let the data speak for itself. But what does the amassed data actually explain about the underlying pathophysiology and how can it help us identify new drug targets? This debate will focus on the promise of big data initiatives for finding a cure for AD.
|
16:45-16:55
|
Host: Stefano Sensi, Italy
|
16:55-17:10
|
Yes: John Gallacher, UK
|
17:10-17:25
|
No: Peter Whitehouse, USA
|
17:25-17:30
|
Discussion and rebuttals
|
17:30-19:00
|
FRONTOTEMPORAL DEMENTIA (FTD)
|
Chairs:
|
Mina Ryten, UK | Raul Arizaga, Argentina
|
17:30-18:15
|
The term Frontotemporal Dementia (FTD) is no longer of value.
Capsule: FTD is the second most common cause of young-onset dementia, which includes several distinct, heterogeneous sub-syndromes. FTD is characterized by progressive deficits in behavior, language, and executive function, but individual symptoms vary considerably and the underlying pathology is also heterogeneous. Over the last decades, the nomenclature of this group of disorders has undergone several iterations. This debate focusses on the question whether the term FTD is still relevant or if it should be replaced.
|
17:30-17:40
|
|
17:40-17:55
|
Yes:
|
17:55-18:10
|
|
18:10-18:15
|
Discussion and rebuttals
|
18:15-19:00
|
All patients with a diagnosis of FTD should have genetic testing.
Capsule: Approximately 40 percent of affected individuals with FTD have a family history that includes at least one other relative diagnosed with a neurodegenerative disorder. Three genes account for the majority of mutation-associated hereditary FTD cases, including C9orf72, GRN and MAPT and others. Furthermore, a very small percentage of people with sporadic FTD have a mutation in a known FTD gene. This debate focuses on the question if this knowledge about the genetics of FTD is reason enough to perform genetic testing (and counselling) in all patients diagnosed with the disease.
|
18:15-18:25
|
Host:
|
18:25-18:40
|
Yes: Lea Grinberg, Brazil/USA
|
18:40-18:55
|
No:
|
18:55-19:00
|
Discussion and rebuttals
|
HEADACHE | HALL D
|
|
08:30-10:10
|
SLEEP, HORMONES AND MEDICATION OVERUSE HEADACHE
|
Chairs:
|
Gabriela Mihăilescu, Romania
|
08:30-09:20
|
Estrogen containing contraceptives are safe in women with migraine with aura.
|
|
Capsule: Migraine with aura has been associated with increased risk of ischemic stroke in women. Prior studies have shown a further increase in risk in women using combined hormonal contraceptives (CHCs). This has led to guidelines recommending against use of CHCs in this population. Is this justified?
|
08:30-08:40
|
|
08:40-08:55
|
|
08:55-09:10
|
|
09:10-09:20
|
Discussion and rebuttals
|
|
|
09:20-10:10
|
Correcting the derangement in sleep architecture is sufficient to treat cluster and migraine headache without medication.
|
|
Capsule: Migraines and cluster headache patients who do not sleep well develop more frequent and severe headaches. Would optimal sleep therapies ever be good enough to take the place of medication for the treatment of these headaches, or is sleep impairment just an epiphenomenon?
|
09:20-09:30
|
Host: Jack Schim, USA
|
09:30-09:45
|
|
09:45-10:00
|
No: Oved Daniel, Israel
|
10:00-10:10
|
Discussion and rebuttals
|
10:10-10:25
|
Coffee Break
|
10:25-12:05
|
CGRP mAb’s AND MIGRAINE PREVENTION
|
Chairs:
|
Nadir Bharucha, India | Brendan Davies, UK
|
10:25-11:10
|
Peripheral trigeminal structures are the primary interaction site for CGRP antagonism in migraine prevention.
|
|
Capsule: CGRP is known to be widely distributed in the central and peripheral nervous system.The exact site of action of the mAbs to CGRP or its receptor and small molecule CGRP receptor blockers is unknown, although several studies have been done.
|
10:25-10:35
|
Host: Fayyaz Ahmed, UK
|
10:35-10:50
|
Yes: Lars Edvinsson, Sweden
|
10:50-11:05
|
No: Dimos Mitsikostas, Greece
|
11:05-11:10
|
Discussion and rebuttals
|
|
|
11:10-12:05
|
The safety and efficacy of CGRP mAbs are known well enough for physicians to recommend them for long-term use.
|
Capsule: CGRP is a potent vasodilator and there was early concern about blocking it in patients that may have an impending stroke or myocardial infarction. CGRP is also involved in many other processes such as bone and wound healing as well as cardiovascular homeostasis and gastrointestinal function.
|
|
11:10-11:20
|
Host: Giorgio Lambru, UK
|
11:20-11:35
|
Yes: Lars Edvinsson, Sweden
|
11:35-11:50
|
No: Fayyaz Ahmed, UK
|
11:50-11:55
|
Discussion and rebuttals
|
11:55-12:15
|
How are the CGRP monoclonal antibodies being used today?
Christopher Gottschalk, USA
|
12:15-13:15
|
Industry Supported Symposium
|
13:15-14:15
|
Lunch Break
|
13:15-14:15
|
Meet the Expert
|
14:15-15:45
|
ATYPICAL MIGRAINE
|
Chairs:
|
Magda Wysocka, Poland | Teena Shetty, USA
|
14:15-15:00
|
Head injury can precipitate the onset of migraine.
|
|
Capsule: Post-trauma headache may occur in several phenotypes. Can a patient develop real migraine with or without aura, due to head trauma? This question raises clinical and legal issues.
|
14:15-14:25
|
Host: Manjit Matharu, UK
|
14:25-14:40
|
|
14:40-14:55
|
No: Anna Andreou, UK
|
14:55-15:00
|
Discussion and rebuttals
|
|
|
15:00-15:45
|
Vestibular migraine – does it exist?
|
|
Capsule: Vestibular migraine is a term used to describe episodic vertigo occurring in migraine patients; but should it be a distinct diagnosis, or simply a sensory manifestation, or even an aura, of migraine?
|
15:00-15:10
|
Host: Min Kyung Chu, South Korea
|
15:10-15:25
|
Yes: Christian Lampl, Austria
|
15:25-15:40
|
|
15:40-15:45
|
Discussion and rebuttals
|
15:45-16:00
|
Coffee Break
|
16:00-19:00
|
NON-PHARMACOLOGICAL TREATMENTS IN HEADACHE
|
Chairs:
|
|
16:00-16:50
|
Acupuncture is as effective as migraine preventive medications, with fewer unwanted adverse effects.
|
|
Capsule: In recent years the evidence base for acupuncture as a preventive treatment for migraine has grown considerably due to the publication of several large trials of high quality; however the results are still questioned and not easy to interpret.
|
16:00-16:10
|
Host: Jose Miguel Lainez, Spain
|
16:10-16:25
|
|
16:25-16:40
|
|
16:40-16:50
|
Discussion and rebuttals
|
|
|
16:50-17:40
|
Headache devices will replace medications for the acute and preventive treatment of migraine and cluster headache.
|
|
Capsule: Headache devices are proliferating rapidly in the headache medicine field; there is hope that they will provide an alternative therapeutic option for patients with migraine and cluster headache. What is the evidence?
|
16:50-17:00
|
Host: Anna Andreou, UK
|
17:00-17:15
|
Yes: Jose Miguel Lainez, Spain
|
17:15-17:30
|
No: Giorgio Lambru, UK
|
17:30-17:40
|
Discussion and rebuttals
|
|
|
17:40-18:30
|
Mushrooms extracts are a good treatment for chronic cluster headache.
|
Capsule: Psilocybin, lysergic acid diethylamide (LSD), and related psychedelic amines are reportedly effective for both preventive and acute treatment of cluster headache; but is there adequate scientific evidence to recommend it for our patients?
|
|
17:40-17:50
|
Host: Dimos Mitsikostas, Greece
|
17:50-18:05
|
|
18:05-18:20
|
No: Randall Weeks, USA
|
18:20-18:30
|
Discussion and rebuttals
|
18:30-19:00
|
The changing face of medication-overuse headache
Alan Rapoport, USA
|