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«Program Feb 21 (Fri).. 08 Feb 22 (Sat).. 10 Feb 23 (Sun).. 12 Abstract Feb 21 (Fri).. 15 Feb 22 (Sat).. 59 Feb 23 (Sun).. 79 Acknowledgements ...»

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Table of Contents

Introduction ………………………………………………………………………… 05

Information ………………………………………………………………………… 07

Program

Feb 21 (Fri) …………………………………………………………… 08

Feb 22 (Sat) …………………………………………………………… 10

Feb 23 (Sun) …………………………………………………………… 12 Abstract Feb 21 (Fri) …………………………………………………………… 15 Feb 22 (Sat) …………………………………………………………… 59 Feb 23 (Sun) …………………………………………………………… 79 Acknowledgements …………………………………………………………… 103

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-5- Takamatsu Parkinson Disease Foundation President Mitsutoshi Yamamoto, MD, PhD Director, Takamatsu Neurology Clinic President, Takamatsu Parkinson Disease Foundation Co-President Nobutaka Hattori, MD, PhD Professor of Neurology Department of Neurology Juntendo University International Advisory Board David J Burn Newcastle upon Tyne Werner Poewe Innsburck Olivier Rascol Toulous Heinz Reichmann Dresden Anthony Schapira London EK Tan Singapore Louis Tan Singapore Eduardo Tolosa Barcelona Genjiro Hirose Kanazawa Shigeki Kuzuhara Mie Eldad Melamed Tel-Aviv Yoshikuni Mizuno Tokyo Ruey-Meei Wu Taipei The local organizing committee Chair Mitsutoshi Yamamoto Co-Chair Nobutaka Hattori Member Kazuko Hasegawa Kenichi kashihara Seiji Kikuchi Jun-ichi Kira Sadako kuno Yasuyuki Okuma Norihiro Suzuki Ryousuke Takahashi Atsushi Takeda Hidehiro Mizusawa Miho Murata Hirohisa Watanabe Fumihito Yoshii Yoshio Tsuboi Operating committee Chair Hirohisa Watanabe Member Masaaki Hirayama Tadashi Ichikawa Katsuo Kimura Ryouichi Kurisaki Tetsuya Maeda Suguru Nishida Hidemoto Saiki Kazuto Yoshida

-6- Information Registration Information Registration: on-site only available Pre-registration is appreciated.

No discount for pre-registration is available

Registration Times:

Feb 21(Fri) 08:20-18:40 Feb 22(Sat) 08:30-17:30 Feb 23(Sun) 08:30-15:40

Registration Fee:

Until January31 Until February10 Onsite Medical student free free 3,000 Trainee/Co-medical 5,000 6,000 7,000 Neurologist 15,00020,000 25,000

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Notice to Speaker and Chair (presentation material) Your presentation can be pre-checked and accepted in PC desk located in 6th floor on conference hall.

Internet Service A wireless internet service is available.

Official Language is English (Day1,2) Social event Reception: 18:30-20:30 free of charge on Feb. 21, 2014 “Mykeila” near congress venue 5 minutes walk Symposium dinner: 20:00-22:00 at Japanese restaurant Ryoutei “ Ni-cho” Seats is still available (¥10,000JPY) Notice Recoding and Photos are strictly prohibited.

The eating and drinking in the hall is prohibited.

(Only the PET bottle can be brought in.)

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13:00-13:30 Lunch Chair Ruey-Meei Wu & R.Bhidayasiri 13:30-14:00 FTD and parkinsonism Ruey-Meei Wu 14:00-14:30 Drug-induced parkinsonism E.Melamed

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Luncheon seminar 共催:日本ベーリンガーインゲルハイム Chair D.Burn 12:30-13:30 Hyposmia and cholinergic deficiency in A.Takeda Parkinson Disease

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10:00-10:30 coffee break Chair H.Tachibana & S.Orimo 10:30-11:00 Rehabilitation in PD from walking to T.Ichikawa speech : the state of the art 11:00-11:30 Excersie and cognition in PD and AD R.Kurisaki

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What is Atypical Parkinsonism?

Werner Poewe Dept of Neurology, Innsbruck Medical University The term ‚Atypical Parkinsonism’ is being used to describe a heterogeneousgroup of neurodegenerative conditions, where the clinical motor syndrome of parkinsonism is associated with additional clinical features not typically seen in ‚classical’ idiopathic Parkinson’s Disease (PD). The textbook listings of the atypical parkinsonian disorders usually include the Multiple System Atrophy (MSA) and Dementia with Lewy Bodies (DLB) which – like PD – are associated with synuclein pathology, as well as Progressive Supranuclear Palsy (PSP) and Corticobasal Degeneration (CBD), where tau-positive neuronal inclusions are the pathological hallmark. The clinical qualifyer of ‚atypical’ features, however, maybe imperfect for several reasons: first, some ‚atypical’ features used to distinguish these conditions from PD may also occur in post-mortem confirmed PD – including early severe dementia, autonomic dysfunction, dystonia and poor Levodopa response (Hughes et al., Brain, 2002). Second, some patients suffering from one of these types of ‚atypical parkinsonism’ may not show any of the defining atypical features. This is best exemplified by the parkinsonian variants of MSA or PSP which can be associated with a sustained meaningful response to Levodopa. In addition, PSP-P patients may show classical rest tremor and a rather benign course of disease progression with absence of early falls and supranuclear gaze palsy,mimicking the clinical signature of PD. Likewise, MSA-P patients may present with asymmetric or even unilateral parkinsonism without significant autonomic dysfunction. These typical-PD-look-alike presentations are the prime source of diagnostic difficulty in atypical parkinsonism. Finally, DLB in particular does not have any features which in themselves are at all ‚atypical’ for PD. In fact, everything listed in the





- 16 clinical diagnostic criteria is also a classical symptom in PD dementia, such that the only clinical anchor of DLB is the timing of dementia diagnosis relative to the diagnosis of parkinsonism (i.e. the ‚one-year-rule’).

Nevertheless, classifying certain features, drug-responses and modes of progression as ‚atypical’ for PD is highly useful for alerting clinicians to consider or reconsider initial diagnostic classifications and to plan diagnostic work-up. Misclassifications of patients with degenerative parkinsonian disorders will, however, continue to occur – particularly in early disease stages - until there are sensitive and specific biomarkers enabling secure discrimination between these conditions.

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The definition of Parkinson Disease Eduardo Tolosa, MD Parkinson disease definition: An insidious unilateral onset of bradykinesia, rigidity and rest tremor between ages of 30 and 85 years. Mild male preponderance,no more than one affected first degree relative. Spread to involve other side within 3 years, but disability remains asymmetrical throughout. Good sustained response to l-dopa with eventual emergence of psychomotor fluctuations and dyskinesias. Increasing gait, balance and speech problems after 5 years disease Death on average 14 years after diagnosis (may be over 30 years in young-onset cases).

Whether presence of Lewy bodies in the central nervous system or the presence of certain non motor symptoms are part of the definition of Parkinson disease is a matter of debate which I will discuss in my presentation.

- 18 Bioskech Prof. Eduardo Tolosa MD, FRCP February 2014 Eduardo Tolosa obtained his MD degree from the University of Barcelona and received his neurological training at the University of Minnesota Hospital in Minneapolis. He is Professor of Neurology at the University of Barcelona and Director of the Parkinson Disease Research Program at the University of Barcelona Hospital. He is a founding member and past president of the Movement Disorder Society. He is also past president of the European Neurological Society. Prof. Tolosa was certified as a neurologist by the American Board of Neurology and Psychiatry and is currently a Fellow of the American Academy of Neurology, the American Neurological Association and the Royal College of Physicians. He is the recipient of the American Academy of Neurology 2014 Movement Disorders Research Award.

Professor Tolosa’s research interests are in movement disorders and particularly in issues related to experimental therapeutics, etiology and pathophysiology of various Parkinson syndromes. In the area of experimental therapeutics, he was involved in pioneering studies defining mechanisms underlying levodopa-related motor fluctuations, and his team has been among the first in Europe to evaluate the efficacy of novel surgical strategies for Parkinson’s disease, such as subthalamic nucleus stimulation, subcutaneous dopamine agonist infusions and intraduodenal infusions of levodopa.

Other areas of current research include assessment of non-motor symptoms in asymptomatic carriers of Parkinson-associated genetic mutations and the role of neuroimaging in early detection of Parkinson disease.

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Aging and Parkinson’s disease Heinz Reichmann, MD, PhD, FRCP, FAAN Director of Department of Neurology, Technische Universitaet Dresden, Fetscherstrasse 74, D-01307 Dresden Heinz.Reichmann@mailbox.tu-dresden.de The most important risk factor for the development of Parkinson’s disease (PS) is aging.

With increasing age, more and more individuals develop a Parkinson syndrome. Thus, the question arises whether PS is an abnormal aging process of the brain. Until now, most neuroscientists claim that the cellular mechanisms which are responsible for ageing of midbrain dopaminergic neurons, are not related to those which cause dopamine neuron degeneration in Parkinson’s disease (PD). In contrast, other studies in non-human primates suggest that ageing induces a pre-parkinsonian state and that the degeneration of dopaminergic neurons in PD patients is only an accelerated form of ageing; they imply that all of us would suffer from PD if we only lived long enough.

There is also increasing evidence that there are more than 30 gene constellations which put an individuum at risk of developing PD.

Several mechanisms of accelerated cell death have been described so far, in particular RNA oxidation is more frequently observed in vulnerable neurons at an early-stage of age-related neurodegenerative disease. In contrast to normal ageing, PD patients show more alpha-synuclein accumulation in the basal ganglia and in other regions of the central and enteric nervous system. Interestingly, alpha-synuclein accumulation is infrequently seen in normal ageing brain. Some people assume that in PD patients there may be insufficient compensatory mechanisms in vulnerable brain regions, which discriminates patients with the full picture of PD from those with only Parkinsonian features such as slow gait.

Clinically, there are several interesting features which might help to distinguish normal ageing from PD. The rate of progression of white matter hyperintensities is slower in the MRI of normal old individuals compared to those with PD. Whilst the annual decrease in striatal dopamine receptor binding is approximately 0.5% in normal old

- 20 people, it is much higher (5%) in patients with PD.

Life expectancy of PD patients is only mildly reduced compared to an age-related control group. Clinically, it is rather intriguing that the decline in olfaction is faster in PD than in normal ageing. This observation correlates well with the abundance of alpha-synuclein in the olfactory bulb of normal people and patients with PD. There is a strong correlation between hyposmia or anosmia and the development of PD. There is also a significant difference, when non-motor symptoms which occur in most PD patients, are compared to age-matched controls. Non-motor symptoms are very common both in the healthy elderly and in PD patients. A significantly higher prevalence of non-motor symptoms (sexual function, perceptual problems/hallucinations, fatigue and mood changes) is observed in PD patients.

Since PD is a movement disorder and physical mobility is reduced in the elderly, it is also of interest that PD patients present with step length asymmetry and increased co-activation of agonists and antagonists when walking or performing arm motor skills.

This might also indicate that patients with PD lack compensatory mechanisms in their motor and pre-motor cortex which are still available to age-matched controls.

A large body of literature covers neuropsychological differences between normal old people and PD patients. For example, PD patients are less able to learn new tasks.

Impairments of word identification, of the number of words used and other speech abnormalities are well documented. Decision-making and executive functions (Wisconsin card sorting test) are major problems in PD patients. It is rather interesting that the theory of mind is highly impaired in PD patients which might also contribute to their social isolation in late stages of the disease. Although both controls and PD patients prefer familiar tasks to new ones, PD patients do so even more. There is also good evidence that PD has a major impact on error processing.

In conclusion, these selected examples confirm that there is a major and significant difference between normal aging and PD.

- 21 Heinz Reichmann, MD, PhD, FRCP, FAAN – biosketch Heinz Reichmann MD PhD graduated from the University of Freiburg, Germany in

1979. He spent the following four years as a research fellow at the Institute for Biochemistry, University of Konstanz, Germany and the Institute of Neurology, Columbia University, USA. This was paid for by honorary grants for excellency to Dr.

Reichmann. He returned to Germany where he held a number of positions at the University of Würzburg, becoming Professor of Neurology in 1990. In 1996, he was appointed Chairmann of the Department of Neurology at the University of Dresden, where he is now also Dean of the Medical Faculty.



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