Hall A :: PARKINSON'S DISEASE & MOVEMENT DISORDERS

       

Session (1)	MOVEMENT DISORDERS
08:30-10:30
Chairpersons:	Kemal Bayulkem, Turkey; Weidong Le, China
Capsule:	The nosology of progressive supranuclear palsy (PSP) is based on clinical and pathological criteria.  Are pathological changes by themselves sufficient to define a disease?
08:30-09:30	Debate: Is the division of PSP into PSP parkinsonism and Richardson syndrome clinically useful and helpful?  Yes: Pettarsup Wadia, India No: Umaiorubahan Meenakshisundaram, India Commentator: John Duda, USA
Capsule:	Several animal models of Parkinson's disease (PD) have been developed and are still useful in developing dopaminergic drugs.  Their usefulness in understanding the pathogenesis of PD is however still unproven
09:30-10:30	Debate: Are animal models useful in understanding PD?  Yes: Daniel Truong, USA No: Heinz Reichmann, Germany  Commentator: Weidong Le, China
10:30-11:00	Coffee Break
Session (2)	ETIOLOGY OF PARKINSON'S DISEASE (PD)
11:00-13:00
Capsule:	Sporadic PD was found to have several risk factors, both clinical and genetic.  Which are more important?
Chairpersons:	Beom Jeon, Korea; Zhenwin Zhang, China
11:00-12:00	Debate: Is the etiology of sporadic PD predominantly environmental or genetic? Environmental: Heinz Reichmann, Germany Genetic: Ovidiu Bajenaru, Romania Commentator: Roongroj Bhidayasiri, Thailand
12:00-13:00	Debate: Is PD in boxers just a coincidence? Yes: Daniel Truong, USA No: Roongroj Bhidayasiri, Thailand Commentator: Haibo Chen, China
13:00-14:00	Lunch Break
Session (3)	TREATMENT OF PARKINSON'S DISEASE
14:00-16:00
Capsule:	There is still no consensus regarding the treatment of PD.  Several opinion leaders suggest that treatment with MAOB inhibitors should be a first line approach.  On the other hand, dyskinesias cause by l-dopa may be prevented if dopaminergic drugs are administered in a continuous delivery system: None of the claims are sufficiently supported by data
Chairpersons:	Daniel Truong, USA; Shengdi Chen, China
14:00-15:00	Debate: After years of thought, is MAOB-inhibition still considered to be neuroprotective? Yes: Heinz Reichmann, Germany   No: Jose Martin Rabey, Israel  Commentator: Umaiorubahan Mennakshisundaram, India
15:00-16:00	Debate: Will continuous dopaminergic stimulation (CDS) prevent motor complications?  Yes: Alberto Albanese, Italy No: Jose Martin Rabey, Israel Commentator: Dirk Dressler, Germany
16:00-16:30	Coffee Break
Session (4)	THERAPY: TRADITIONAL AND FUTURE
16:30-18:30
Chairpersons:	Zhong Pei, China; Xiaomin Wang, China
Capsule:	Alpha-synuclein is a marker of pathology in PD, and SYNA mutations are associated with some cases of familial PD.  However, the causative role of alpha-synuclein in the sporadic disease is still unclear
16:30-17:30	Debate: Is the accumulation of alpha-synuclein detrimental and a valid targetfor intervention in PD? Yes: John Duda, USA No: Piu Chan, China Commentator: Lea Grinberg, USA
Capsule:	Eastern medicine gains wide acceptance in the West, but reliable data on its efficacy is slow to accumulate
17:30-18:30	Debate: Are ayurveda medicine and accupuncture efficacious therapies in PD? Pro: Horst Przuntek, Germany Con: Beom Jeon, Korea Commentator: Jeffery Schwartz, USA

     

Hall B :: MULTIPLE SCLEROSIS

       

Session (5)	WHAT IS MULTIPLE SCLEROSIS (MS)
08:30-10:30
Capsule:	Is MS one disease or many? Are the different phenotypes we perceive in terms of course representative of different pathologies or pathogeneses? Secondary progressive MS usually evolves from relapsing disease whereas primary progressive MS starts with progression, yet their courses seem identical and a significant number of primary progressive patients develop relapses and have enhancing lesions on MRI – are the entities really different?  Up until recently, Devic’s disease (now known as neuromyelitis optica or NMO) was considered a variant of MS – though clearly now it can be differentiated from it. Some cases of MS presenting mostly with spinal cord and optic nerve involvement can test negative for NMO antibodies yet may still have NMO – how do we distinguish these from MS?
Chairpersons:	Ariel Miller, Israel; Xiaojun Zhang, China
08:30-09:30	Debate: Is the Asian optico-spinal MS a distinct entity or part of the NMO spectrum? Part of the spectrum: Brian Weinshenker, USA A distinct entity: Jun-ichi Kira, Japan Commentator: Kazua Fujihara, Japan
09:30-10:30	Debate: Is MS an inflammatory or a primary neurodegenerative disease? Inflammatory: Jacek Losy, Poland Degenerative: Abhijit Chaudhuri, UK Commentator:  Olaf Stuve, USA
10:30-11:00	Coffee Break
Session (6)	MULTIPLE SCLEROSIS TREATMENT
	(partially sponsored by an unrestricted grant from Teva)
11:00-13:00
Capsule:	The story of chronic cerebro-spinal venous insufficiency (CCSVI) continues to loom strong fueled by a desire by patients and advocates to treat “blocked veins” and feel well, but there continues to be a lack of solidifying scientific evidence that it even exists let alone warranting treatment, especially since deaths and complications are now being reported. Also lacking are the strong evidence-based studies supporting the use of immunosuppressants for the treatment of aggressive MS, yet they continue to be used worldwide and now may pose a threat to safety in the use of newer agents such as natalizumab
Chairpersons:	Jera Kruja, Albania; Xiao Kun Qi, China
11:00-12:00	Debate: Venous obstruction is of primary importance in MS pathogenesis  Yes: Jerzy Kotowicz, Poland No: Olaf Stuve, USA Commentator: Joanna Wojczal, Poland
12:00-13:00	Debate: The treatment of MS with immunosuppressants  Pro: Abhijit Chaudhuri, UK  Immunosuppressors have a dubious past and an uncertain future: Joab Chapman, Israel  Commentator: Xiaojun Zhang, China
13:00-14:00	Lunch Break
Session (7)	THERAPIES OF MULTIPLE SCLEROSIS
14:00-16:00
Capsule:	The horizon is bright when it comes to the future of MS treatment with numerous new agents with varied mechanisms completing late stage trials or early stage proof of principle studies. Faced with an ever expanding tool chest, how is the neurologist to decide what to use and when to use them? Move slowly and escalate to more powerful agents that have more safety issues only when first line agents fail to contain the disease, or recognize a more advanced condition from the start and begin with the power agents?
Chairpersons:	Xie Peng, China; Zbigniew Stelmasiak, Poland
14:00-15:00	Debate: Should MS be treated by escalation or induction therapy? Escalation: Mark Freedman, Canada Induction: Ron Milo, Israel
15:00-16:00	DRUG UPDATES & NEW PLAYERS IN MS Alemtuzumab: Tjalf Ziemssen, Germany Betaferon: Douglas Goodin, USA Daclizumab: Olaf Stuve, USA  Fingolimod: Ariel Miller, Israel Laquinimod: Ariel Miller, Israel  Ocrelizumab: David Leppert, Switzerland Teriflunomide: Mark Freedman, Canada
16:00-16:30	Coffee Break
Session (8)	BIOMARKERS AND NEW THERAPIES
16:30-18:30
Capsule:	Which patient is likely to progress and who will be “benign” ? How do you know when a therapy is working before a patient falters beyond the means of a treatment to help? Short of waiting for progression or relapses, is there a way of telling whether one drug is better than another? Are there markers that indicate whether a particular therapy might be futile while another is ideal? These are but some of the hopes of a MS “biomarker”
Chairpersons:	Chuntao Lai, China; Erik Larssen, Sweden
16:30-17:30	Debate: Biomarkers can be useful for diagnosis and prognosis in MS NFH & gMS: Mark Freedman, Canada NMO ab's, JC virus & IFN ab's: Ariel Miller, Israel Commentator: David Leppert, Switzerland
17:30-18:30	Debate: Are the new oral medications superior to current treatments? (Partially supported by Bayer) Yes: Brian Weinshenker, USA No: Douglas Goodin, USA Commentator: Cheng Zhang, China

        

HALL C :: HEADACHE

       

Session (9)	TRANSFORMED MIGRAINE AND NEW DAILY PERSISTENT HEADACHE
08:30-10:30
Capsule:	The term transformed migraine perfectly describes patients with episodic migraine who transform into chronic migraine.  But the IHS does not accept the term.  Should we reintroduce the term?  There has been an increased use of the diagnosis of New Daily Persistent Headache.  The etiology of this entity is unknown.  Is this a primary headache disorder or are there causative factors?
Chairpersons:	Hans L. Hamburger, The Netherlands; Shengyuan Yu, China
08:30-09:30	Debate: Transformed migraine is an accurate, descriptive term and should be incorporated into the ICHD-2 criteria Yes: Elliott Gross, USA No: Christian Lampl, Austria Commentator: Yan Sheng Li, China
09:30-10:30	Debate: New Daily Persistent Headache is a primary headache disorder Yes: Hayrunnisa Bolay, Turkey No: Robert Shapiro, USA Commentator: Dimos Mitsikostas, Greece
10:30-11:00	Coffee Break
Session (10)	EFFECTIVENESS OF COGNITIVE BEHAVIORAL THERAPY AND BOTULINUM TOXIN-A
11:00-13:00
Capsule:	There are many preventative treatments for migraine.  Behavioral medicine therapies can be helpful.  Is Cognitive Behavioral Therapy a reasonable therapy for migraine?  There is a lot of discussion about the use of botulinum toxin-A for chronic migraine and it is now approved in the USA as safe and effective for the treatment of chronic migraine, but some feel the evidence and clinical data do not support its use
Chairpersons:	Hayrunnisa Bolay, Turkey; Jing Gao, China
11:00-12:00	Debate: Cognitive Behavioral Therapy is a good treatment for migraine Yes: Frank Andrasik, USA No: Christian Lampl, Austria Commentator: Mira Kapisyzi, Albania
12:00-13:00	Debate: Botulinum toxin-A is an effective and safe treatment for chronic migraine Yes: Alexander de Ru, The Netherlands No: Robert Shapiro, USA Commentator: Alan Rapoport, USA
13:00-14:00	Lunch Break
Session (11)	WHERE IN THE BRAIN DOES MIGRAINE BEGIN: DO REGIONAL FACTORS INFLUENCE OUTCOME OF HEADACHE MANAGEMENT?
14:00-16:00
Capsule:	A heavily debated topic in migraine today is where does the first phase of the attack begin?  Some claiming the cerebral cortex and others saying that it orginates in the brain stem, or even in the periphery.  Acute care treatment of migraine is quite different in Asia from that of the USA.  Are reigional factors the cause?  Is price and availability or education to blame?
Chairpersons:	Frank Andrasik, USA; Elliott Gross, USA
14:00-15:00	Debate: Does the first phase of a migraine attack originate in the cerebral cortex or the brainstem? Cortex: Dimos Mitsikostas, Greece Brainstem: Miguel J. Lainez, Spain Commentator: Hayrunnisa Bolay, Turkey
15:00-16:00	Debate: Do regional factors influence the outcome of headache management? Yes: K. Ravishankar, India No: Miguel J. Lainez, Spain Commentator: Alexander de Ru, The Netherlands
16:00-16:30	Coffee Break
Session (12)	CGRP ANTAGONISTS; WHEN TO TAKE TRIPTANS; CEREBRAL VENOUS FINDINGS IN IIT
16:30-18:30
Capsule:	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 migraine attack.  Will it be a valuable agent or are triptans and NSAIDs all we need?  Triptans are widely thought of as the most effective medicine to give in a moderate to severe attack of migraine; but must they be given early, when the headache is mild, or can they be given later in the attack? Patients with idiopathic intracranial hypertension are sometimes found to have bilateral transverse sinus stenosis and treatment may be beneficial.  This is controversial
Chairpersons:	Miguel J. Lainez, Spain; Dimos Mitsikostas, Greece
16:30-17:15	Debate: Do we need a new mechanism of action for acute migraine treatment? Yes: Tony Ho, USA No: Hayrunnisa Bolay, Turkey Commentator: Elliott Gross, USA
17:15-18:00	Debate: Do triptans have to be given early in the attack when the headache is mild? Yes: Elliott Gross, USA No: K. Ravishankar, India Commentator: Alan Rapoport, USA
18:00-18:30	Brief Debate: Bilateral transverse sinus stenosis is a critical finding in idiopathic intracranial hypertension syndrome Yes: Hans L. Hamburger, The Netherlands  No: Betul Baykan, Turkey