Scientific Program

Conference Series Ltd invites all the participants across the globe to attend 4th International Conference on Epilepsy & Treatment Zurich, Switzerland.

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Scientific Program Day 1
Scientific Program Day 2

Day 1 :

Keynote Forum

Alain L Fymat

International Institute of Medicine and Science, USA

Keynote: A disrupted blood brain barrier may allow potentially new epileptic treatments

Time : 09:30-10:10

Conference Series Epilepsy 2018 International Conference Keynote Speaker Alain L Fymat photo
Biography:

Alain L Fymat is a Medical-Physical Scientist and an Educator who was educated at the Universities of Bordeaux and Paris-Sorbonne, France, and the University of California at Los Angeles. He is the Current President/CEO and Professor at the International Institute of Medicine & Science. He was formerly Professor of Radiology, Radiological Sciences, Radiation Medicine (Oncology), Critical Care Medicine, and Physics at several US and European Universities. His current research interests lie at the interface between science and medicine (Neurological Disorders; Precision Medicine; Nanobiotechnology; Nanomedicine; Genetics/Epigenetics/Ecogenetics; and Drug Delivery across the brain protective barriers). He has extensively published ~350 scholarly publications and lectured in several national and international academic, professional, governmental and industrial venues. He is a Board Member of several institutions, and Editor-in-Chief, Honorable Editor or Editor of twelve scientific journals.

Abstract:

There are approximately 400 known neurological disorders (including some which may be better classified as mental disorders). Some of these disorders may be due to a disruption or failure of the blood brain barrier (BBB) such as, importantly, epilepsy (a group of neurological disorders characterized by chronic or acute seizures caused by inflammation). Epileptic seizures are the result of excessive and abnormal nerve cell activity in the brain cortex. As of 2015 about 39 million people have epilepsy with nearly 80% of the cases occurring in the developing world and 125,000 having died of it. Common among older people, epilepsy will become more prevalent as a result of the growing aging population. The cause of most cases of epilepsy is still unknown through a process known as epileptogenesis. Nonetheless, there are both genetic and acquired causes, with interaction of these factors in many cases. To date, nearly all the genes discovered to be involved in human epilepsies encode subunits of ion channels, both voltage-gated and ligand-gated. Known genetic mutations are directly linked to a small proportion of cases. Established acquired causes include serious brain trauma, stroke, tumors, infective lesions, and birth defects. Seizures are controllable with medication in about 70% of cases. Inexpensive options are often available. In those whose seizures do not respond to medication, surgery, neurostimulation, or dietary changes may be considered. In its integral form, the BBB is a selective filter that allows passage of essential nutrients, water, some gases, lipid-soluble molecules, hydrophobic molecules (O2, CO2, hormones) and also allows transport of metabolic products to the brain (glucose with specific proteins). It restricts diffusion of microscopic objects (e.g. bacteria) and large hydrophilic molecules and prevents entry of polar and lipid-insoluble substances, and lipophilic neurotoxins. Of interest here are those epileptic treatments rendered possible by the delivery of therapeutic drugs through the disrupted blood brain barrier.

 

Break: Networking & Refreshments 10:10-10:30 @ Europa Foyer

Keynote Forum

Chandramohan Wakade

Augusta University, USA

Keynote: Niacin attenuates inflammatory cytokine upregulation in PD mediated through GPR109A

Time : 10:30-11:10

Conference Series Epilepsy 2018 International Conference Keynote Speaker Chandramohan Wakade photo
Biography:

Chandramohan Wakade has been engaged in the field of CNS injury and its amelioration for number of years. The focus of his research includes trauma to the nervous system and neural repair. He has worked on various animal stroke models including MCAo, SAH and TBI models in rats and mice. His recent work focuses on studying role of inflammation in CNS injury and neurodegenerative diseases in patients.

 

Abstract:

Neuroinflammation is central in Parkinson’s disease (PD) pathology. Microglia derived inflammatory cytokines are known to be involved in progressive degeneration of substantia nigra (SN) neurons. We have demonstrated upregulation of anti-inflammatory receptor GPR109A in blood (PD patients) as well as in SN (post-mortem PD patient samples). Up-regulation of GPR109A may be a part of body’s defense mechanism. Niacin (vitamin B3) acts on GPR109A to reduce the inflammation in PD. To understand the cellular mechanisms involved in the anti-inflammatory action of niacin here we utilize lipopolysaccharide (LPS) induced inflammatory cascade in RAW 267.4 cells. These cells are macrophages that resemble microglial lineage. LPS is known to trigger inflammatory cytokines production such as IL1-b, IL-6 and TNF-a via NF-kB pathway. NF-kB is the transcription factor and the translocation of its p65 unit to nucleus is an essential step in the inflammatory cascade. Here we demonstrate inhibition of pNF-kB translocation by niacin in RAW 267.4 cells via GPR109A. However, in the absence of GPR109A, niacin failed to block the translocation of pNF-kB and the subsequent production of inflammatory cytokines in RAW 267.4 cells. This anti-inflammatory action of niacin via GPR109A might be beneficial in PD to alleviate motor and non-motor symptoms.

 

Keynote Forum

Alcibiades J Rodriguez

NYU School of Medicine, USA

Keynote: Case presentations: sleep phenomena or seizures

Time : 11:10-11:50

Conference Series Epilepsy 2018 International Conference Keynote Speaker Alcibiades J Rodriguez photo
Biography:

Alcibiades J Rodriguez has obtained his Medical degree from the University of Panama, School of Medicine, Republic of Panama. He trained in Neurology at Tuft University, Boston, MA. He completed two fellowships, Clinical Neurophysiology/EEG track and Sleep Medicine at Mayo Clinic Rochester, MN. He is the Medical Director of the NYU Sleep Disorders Center, treating people with epilepsy and sleep disorders using electroencephalography (EEG) and video-EEG monitoring. He is board certified in Neurology, Clinical Neurophysiology, Epilepsy and Sleep Medicine. His research focuses on the effect of seizures and epilepsy on sleep. He has written multiple articles and book chapters related to distinguishing seizures that occur while a person is awake from those that occur during sleep. He has also written about differentiating between a sleep disorder and seizures. He collaborates with the National Institutes of Health on several projects related to sleep and neurodevelopment. He is honorary member of the Sleep-Wake Disorders Study Group of the Spanish Neurological Society, helping to organize and teach an annual sleep medicine course for general practitioners, residents, and fellows. He is Advisor and Consultant for Sleep Medicine for the Neurology and Neurosurgery Institute Prof. Dr. Jose Rafael Estrada Gonzalez, Havana City, Cuba. He has been invited to lecture nationally and internationally. He was Vice Chair of the Lifelong Learning Development Committee of the American Academy of Sleep Medicine and Member of the Education Committee of the World Sleep Society.

 

Abstract:

Background: Epilepsy and sleep are closely related. Not only sleep or lack of sleep can influence EEG and seizures, but seizures can have an impact in sleep consolidation and architecture. Beyond that, the differential diagnosis of nocturnal paroxysmal events include seizures and parasomnias (abnormal sleep behavior). These phenomena may co-exist.

Objective: The goal of the presentation is to discuss different cases of seizures and sleep events, which may overlap or be in the differential diagnosis.

Methods: We will present several video-EEG/sleep cases in order to discuss differential diagnosis of these events. Audience participation will be encouraged.

Conclusion: We hope to clarify similarities and differences, as well as point out strategies to distinguish seizures vs. sleep phenomena.

 

  • Parkinsons Disease | Insights and Therapeutics: Parkinsons Disease | Neurosurgery
Location: Athens
Speaker

Chair

Alain L Fymat

International Institute of Medicine and Science, USA

Speaker

Co-Chair

Jae Moon Lee

Kainos Medicine Inc., South Korea

Session Introduction

Laurice Yang

Stanford University, USA

Title: Diagnosis and treatment for dystonia

Time : 11:50-12:15

Speaker
Biography:

Laurice Yang earned a Master’s Degree in Health Administration at the University of Southern California where she received the high honor as a Dean Merit Scholar. She went on to obtain her Medical Degree from the University of Vermont and completed her Neurology Residency at the University of Southern California where she was appointed Neuroscience Chief Resident and spent the year revamping the entire medical student/resident education curriculum. She completed her clinical training as a Movement Disorders Fellow at the University of California in Los Angeles under Dr. Jeff Bronstein. She is a board-certified Neurologist, specializing in the diagnosis of movement disorders including Parkinson’s disease, atypical parkinsonian disorders, essential tremor, and Huntington’s disease. She has an interest in dystonia and spasticity and has been trained to perform botulinum toxin injection under ultrasound guidance to better ensure accuracy and efficacy with each procedure. She has also presented lectures on topics in dystonia, education, and healthcare administration for CME (Continuing Medical Education) faculty development courses and at the American Academy of Neurology.

Abstract:

Dystonia is a characterized by intermittent, abnormal and often repetitive muscle contractions. The diagnosis of dystonia can often be difficult to assess due to the variability and complexity of the disease. During this lecture, we will first review the historical context of how dystonia was discovered and how the clinical understanding of dystonia had evolved over the last several decades. We will discuss the clinical characteristics of the most common types of dystonia and review how to accurately describe and categorize this very complex disease. We will also review the medical treatment options and discuss the efficacy of botulinum toxin as well as techniques on how to be more accurate during the injection procedure. We will explore the other types of treatment such as sensorimotor retraining therapies, which takes advantage of the neuroplasticity of the brain to help “relearn” normal movement. And lastly, we will explore the surgical options that are available now as well as other types of procedures that could supplement the current treatment options. The learning objectives for this presentation are: Understanding the main diagnostic components of dystonia; being familiar with the different types of dystonia; describing medical and surgical treatment; and describing sensorimotor retraining and its role in those who have dystonia.

Kambiz Hassanzadeh

Kurdistan University of Medical Sciences, Iran

Title: The role of oxidative stress and inflammation in Parkinson’s disease: Current knowledge and future therapeutic strategies

Time : 12:15-12:40

Speaker
Biography:

Kambiz Hassanzadeh is the Associate Professor and Head of Cellular and Molecular Research Center at Kurdistan University of Medical Sciences, Iran. He teaches Pharmacology and Neuroscience courses to Medical and PhD students and does research in the field of Neuroscience with more than 60 publications. During recent years, he has been interested in doing research on molecular nature of neurodegenerative diseases, especially Parkinson’s disease. He also researches on antioxidant agents on animal models of Parkinson’s disease.

Abstract:

Current Parkinson’s disease (PD) therapies are focused on maintaining dopamine levels of brain at normal range. Although, this approach is fairly useful to control and manage Parkinson’s disease symptoms, it has some disadvantages. Previous studies indicate that levodopa and other dopaminergic medications accelerate neuronal degeneration in some parkinsonian brains via production of free radicals and reactive oxygen species (ROS). This is in addition to the main oxidative and inflammatory processes of the PD. Additionally, patients need higher doses of drugs over the time which it implies some serious side-effects including motor and non-motor signs. Oxidative stress and inflammation are considered as the leading cause and progression in many diseases, especially those that are associated with aging such as Parkinson’s disease. During the recent years, interest in administration of neuroprotective factors such as anti-oxidants, anti-inflammatory drugs and neurotrophic factors for management of PD is popularly increasingly. According to the above literature, it is important to understand the mechanism of action of these neuroprotective factors and investigate the new and more effective ones. On the other hand, neuroinflammation is one of the serious complications of PD which is usually developed due to protein aggregates and dopaminergic cell deaths. Therefore, here we review the pathways of these two important aspects of PD (oxidative stress and neuroinflammation) to understand what is happening inside a PD brain and we discuss about the benefit of anti-oxidants and anti-inflammatory drugs based on our recent studies in this area.

Break: Lunch Break 12:40-13:20 @ La Place AB

Byung-Jun Park

Daejeon University, South Korea

Title: HEPAD, a novel therapeutic approach of Parkinson’s disease

Time : 13:20-13:45

Speaker
Biography:

Byung-Jun Park completed his PhD and Korean Doctor in Medicine Degree at the College of Korean Medicine, Daejeon University, Daejeon, South Korea. He has opened a Young Jin Korean Medicine Clinic, and his clinical speciality has been the treatment of Parkinson’s disease and movement disorders since 1995. He has published multiple papers on Parkinson’s disease in reputable journals and is a Member of the Movement Disorder Society. He was listed in the Marquis Who’s Who in the World in 2017–2018.

Abstract:

Parkinson’s disease (PD) is a neurodegenerative disorder involving abnormal body movements. The degenerative loss of dopaminergic neurons in the substantia nigra leads to the onset of PD symptoms, including slow movement, tremor, stiffness, and abnormal posture. Because L-3,4-dihydroxyphenylalanine (L-DOPA) treatment is very effective for symptom inhibition, it is the most widely prescribed treatment of patients with PD. However, long-term L-DOPA treatment is not recommended because of its serious side effects, including dyskinesia. Moreover, L-DOPA does not prevent the progression of PD. Therefore, a novel therapeutic approach is greatly needed for PD. Hepad, a herbal medicine, consists of six Korean medicinal herbs that were selected based on Korean medicine theory. The treatment of patients with PD using Hepad has been clinically effective. In addition, Hepad treatment reduces the required doses of conventional PD drugs, and some patients were able to terminate conventional PD treatments without additional symptom manifestation. A preclinical study has reported that Hepad prevents neuronal cell death by suppressing the production of reactive oxygen species. These neuroprotective effects of Hepad have also been observed in animal experiments. Hepad treatment in a PD animal model increased dopaminergic neuron number and dopamine levels in the substantia nigra to similar or higher levels than those in L-DOPA-treated animals. Considering the complexity of PD, a multi-targeted approach with multiple compounds would be more effective than single-compound treatment. Taken together, these results suggest that Hepad, a mixed Korean herbal medicine, would be an effective treatment for patients with PD.

 

 

D’Auria Stanislao

Ospedale Santa Maria della Misericordia di Udine, Italy

Title: Steering stimulation and directional leads- a recent reliable concept to improve follow-up in implanted patients: A preliminary experience

Time : 13:45-14:10

Speaker
Biography:

D’Auria Stanislao  graduated in Medicine in 2003 did a specialization in Neurosurgery in 2008 from Second University of Naples, School of Medicine. Since 2008, he works as a Neurosurgeon at the Department of Neuroscience of Santa Maria della Misericordia in Udine, Italy. His fields of interests are Functional Neurosurgery and Neuromodulation and Neuro-Oncology. He has published more than eight papers in reputed journals and has been involved in many international congresses.

Abstract:

In the last 20 years, thanks to technological development and still ongoing innovations in features and materials of implantable devices, deep brain stimulation (DBS) has become one of the most effective, reliable and safe surgical procedure for treatment of many different movement disorders.  The clinical condition that has been better treated with such a technique is Parkinson’s disease. Nevertheless, many other diseases today are good indications for DBS like dystonia, essential tremor and Giles de la Tourette syndrome. Many papers say that DBS is like a “gold standard” in patients affected by dystonia or Parkinson's disease when pharmacological intake alone doesn't work or has lots of troublesome collateral effects. Since 2010, we started to use a stereotactical frameless technique. We noticed a real improvement in patients in terms of comfort, tolerability and reduced pain during surgery. At the same time, we obtained a very good precision in targeting, comparable to those of classical frame based surgery. Innovations, mostly in hardware such as leads, extentions and IPG, go on. We recently started to implant a new lead's generation named, “directional leads”. This lead has many different splitted contacts that allows the clinicians to steer the electrical field mostly wherever they want through the nervous tissue, obtaining clinical effect far from brain area, so as to avoid collateral effects. Since March 2016, we have performed 14 bilateral implantations for Parkinson’s disease and dystonia. At the time of reglage, when collateral effects like motor evoked unwanted responses or limbic effects have been elicited, switching the “hemi-contacts” allowed to make them disappear without any reduction in the desired beneficial effect. An issue we faced, was how to standardize all implanted patients, a shared rotational position of leads. As such, the clinicians can establish a number for any single contacts in order to compare results in different patients and in the single one over time as well. We also did not have an X-ray checking system in the Nexframe device, like basically any head-mounted and pin-fixed traditional stereotactical system has in itself. In other words, we needed a method that allowed to figure out the position of leads. We took two markers behind the ears to allineate during intraoperative X-ray checking. This brought to correct alignment of the lead's reference markers visible at the top of the whole group of contacts. In conclusion, even though the number of patients is low, we believe that directional leads bring to excellent results in terms of shaping of stimulation. They are a powerful tool in the hand of programmer clinicians, potentially able to improve the outcome of the patients. Splitting of contacts gives the chance to get a higher number of contacts allowing the clinician to choose among many stimulation's combination. Moreover, directional leads technology gives us the possibility to steer and deform the tridimensional electrical field shape. Warping and bending of electrical field, brings to a better results for patients, both lessening side effects and enhancing the positive benefits of stimulation. Our easy and reliable intraoperative tecnique is effective to correctly alineate in the same orientation the two leads of both sides.

  • WORKSHOP
Location: Athens
Speaker

Chair

Alain L Fymat

International Institute of Medicine and Science, USA

Speaker

Co-Chair

Jae Moon Lee

Kainos Medicine Inc., South Korea

Session Introduction

Selver Burcu TellioÄŸlu

Tarsus State Hospital , Turkey

Title: Clinical and neuropsychological study of natural course of light cognitive failure, alzheimer disease and parkinson dementia

Time : 14:10-15:10

Speaker
Biography:

Abstract:

Objective: 

The Objective of this study is to examine the natural courses of Alzheimer Disease (AD), Light Cognitive Failure (LCF) and Parkinson ‘s Dementia (PD) cases free of any therapeutic procedure and with neuropsychological test series; to determine the transformation ratio of these cases to dementia and to examine the courses of clinical factors. 

Tools and Method: 

120 patients consisting of 72 AD, 16 PD and 32 LCF patients and 24 healthy controls who are the spouses of the patients or healthy volunteers, who have applied to Mersin University Faculty of Medicine Education and Research Hospital Neurology Department between years 2007 and 2016, have been included in the research.

Patients have been invited to control visits once every 6 months and healthy individuals have been invited to control visits once a year.

Findings:

In the patient groups, functionality and DLA scores have considerably failed in comparison with the scores of control group. In the LCF group, MMSE, forward and backward counting range, calculation, abstraction, praxis, memory of word list, understanding, construction, clock drawing scores have been higher than the other groups but lower than the control group. In the LCF group, total NPI and NPI trouble scores have been lower than the other groups.  In the PDgroup, total NPI scores have been determined to be higher than the AD and LCF groups. Total NPI trouble score has been higher for the AD group when compared with PD and LCF groups. In the LCF group, for 11 % of the patients, diagnosis have transformed to AD in the control period. In the control visits, MMSE values of the control group have risensignificantly after the second visit. In the LCF group, falls in word list memory scores which are statistically meaningful have been determined in the first and third trials.

Result: 

In our study, we determined that 11,1% of the patients with LCF cogenesis had transformation to AD, in this group no transformation to PD has been observed in the control time, no transformation in the healthy control group has been observed.

 

Break: Networking & Refreshments 15:10-15:25 @ Europa Foyer
  • Epilepsy Therapeutics
Location: Athens
Speaker

Chair

Alain L Fymat

International Institute of Medicine and Science, USA

Speaker

Co-Chair

Jae Moon Lee

Kainos Medicine Inc., South Korea

Session Introduction

Rapita Naresh Sood

McGill University, Canada

Title: Role of the mTOR signaling pathway in epilepsy specifically in eIF4ebp2 KO mice

Time : 15:25-15:50

Speaker
Biography:

Rapita Naresh Sood has completed her PhD from University of Haifa Israel and presently doing her Postdoctoral studies from Goodman Cancer Research Center, McGill University in the laboratory of Dr. Nahum Sonenberg. She has published eight papers in reputed journals and has also received the Richard and Edith Strauss Fellowship which is a McGill Internal fellowship award for one year. Also, her project on epilepsy is giving a new direction to rescue the mTOR pathway which is a new perspective for future therapy of epilepsy.

Abstract:

Epilepsy, a common neurological disorder characterized by recurrent seizures that are unpredictable and sometimes progressively severe affecting 50 million people worldwide. Mutations in TSC1/2, PTEN and FMR1 genes cause Tuberous Sclerosis, PTEN hamartoma syndrome and fragile X syndrome respectively and lead to intellectual disability, autistic-like behaviour and epileptic seizures. Mutations in these genes cause upregulation of mTORC1 signalling, however the role of mTORC1 downstream effectors, such as 4E-BPs and S6K, in the pathophysiology of the disorders is not well understood. In the current project we set out to study the contribution of cap-dependent translation and 4E-BP2, downstream of mTORC1, in the susceptibility to seizures. Our previous study showed that deletion of 4E-BP2 leads to autism-like phenotypes and imbalance of excitatory to inhibitory synaptic activity. We recently found that eIF4ebp2 KO mice show reduced threshold to seizure-inducing agent (PTZ) at concentration of 70 mg/kg IP. As part of this project we would like to see whether inhibition of eIF4A would rescue or attenuate the seizure phenotype. The first experiment we are planning is to inject intraperitoneally WT and eIF4ebp2 KO mice with vehicle and eIF4A inhibitor. The experimental studies is still going on and furthermore, is needed to understand the role of mTOR signaling pathway in epileptogenesis, and that it may be a target for the development of novel therapies that eliminate the progressive effects of seizures.

Farnaz Nikbakht

Iran University of Medical Sciences, Iran

Title: Anticonvulsant and antiepileptogenic effects of metformin

Time : 15:50-16:15

Speaker
Biography:

Farnaz Nikbakht, before obtaining her PhD degree in Human Physiology from Shiraz University in 2007, she received an award from the Iran Ministry of Health and Education; she spent six months at Flinders University, Adelaide, Australia for completing her research on degenerative diseases. Now, as the Associate Professor of Department of Physiology, Iran University of Medical Sciences, she has managed several research programs and has conducted the thesis of several Masters and PhD students in her Lab. Since 2010 she has directed a research team on Epilepsy and Alzheimer’s diseases fields in her lab. Her research leads to publishing several articles.

Abstract:

Background: Current medications for epilepsy are just anticonvulsive agents and cannot protect against epileptogenic processes. On the other hand, theses anticonvulsive drugs are ineffective for one-third of epilepsy patients. Regarding these limitations, there is an urgent and growing need for a new drug to process both properties. Metformin, a common antidiabetic drug, has been shown to act as an anticonvulsive drug in some experimental models. However, the antiepileptic properties of metformin are not yet clear.

Materials & Methods: Sixty male Wistar rats are divided randomly into four groups: control, kainate (KA group), metformin+KA group and metformin group. Temporal lobe epilepsy was induced by intracerebroventricular (ICV) microinjection of 0.5 µg KA. Metformin was orally administered, starting two weeks before epilepsy induction. Following epilepsy induction, animals were monitored for behavioral seizure severity. Epileptogenesis was assessed by evaluating four factors: Hippocampal neuronal loss and neurodegeneration using Nissl and Fluoro Jade B(5 days after surgery); Neurogenesis using BrdU (5 days after surgery); Mossy Fiber sprouting, using Timm staining (30 days after surgery) and; EEG (30 days after surgery).

Results: Metformin as an anticonvulsant drug: the latency to seizure and the seizure severity were both reduced significantly, following metformin treatment (P<0.001). Metformin as antiepileptic drug: According to the Nissl and Fluoro-Jade B staining, the best protected areas in the hippocampus after metformin administration were CA3 and hilus (P<0.00). Behavioral EEG monitoring revealed that metformin-treated rats displayed spontaneous seizures at lower frequencies compared with epilepsy group. Metformin alone increased the neurogenesis which was even greater than Ka-induced neurogenesis. However, metformin-treated rats after epilepsy showed the immigration of new neurons to the hilar and CA3 areas. Metformin also reduced significantly mossy fiber sprouting.

Conclusion: Altogether we conclude that metformin acts not only as an anticonvulsant but an antiepileptogenic drug. 

 

Abraham Ratna Joseph Nayakanti

Avalon University School of Medicine, Curacao

Title: Anencephaly a chance of teratogenicity by Antiepileptic drugs during organogenic period

Time : 16:15-16:40

Speaker
Biography:

Abraham Ratna Joseph Nayakanti is an Assistant Professor in the Human Structure and Function Department, Avalon University School of Medicine, Curacao. He is a PhD Scholar in the Department of Anatomy in the Field of  Embryology of Renal Morphogenesis and Histogenesis, Faculty of Medicine at Vinayaka Missions University  and has completed his Master’s degree in Medical Anatomy at SVIMS University, India and has more than six years of teaching experience in various medical universities in India and abroad with presentations and publications in various international conferences and medical journals of anatomy and research. He has Successfully comleted Online course in Essential Skills in Medical Education, given by Association of Medical Education in Europe (AMEE) under Dundee University, Scotland.

Abstract:

Neural tube defects are very rare untill they are found in repeated deliveries. During routine collection of fetuses for the morphometrical and histological studies of renal developmental study, we found a rare anomaly with the defective closure of the cranial neuropore resulting in anencephaly. The case study consists of Intra uterine dead fetus with anencephaly which has spontaneously aborted. Service of Salem Polyclinic Hospital, in giving male aborted fetus for the study with the parent consent is appreciable. The diagnosis of suspected anencephaly was made on average at 21.3 weeks of gestation. The crown rump length was 14 cm and the crown heel length measurement of the fetus was 22 cm. In general there are various conginetal neural anomalies which appear to be similar to anencephaly.

Arindam Ghosh Mazumder

CSIR- Institute of Himalayan Bioresource Technology, India

Title: Exploring the anti-seizure potential of selective PI3K inhibitor in zebrafish model of pentylenetetrazole induced seizure

Time : 16:40-17:05

Speaker
Biography:

Arindam Ghosh Mazumder is a Senior Research Fellow, currently pursuing his PhD from CSIR-Institute of Himalayan Bioresource Technology, Palampur, Himachal Pradesh, India. He was awarded DST-INSPIRE Fellowship for pursuing PhD, sponsored by the Department of Science and Technology (DST), Government of India, 2013.

 

 

Abstract:

The role of mammalian target of rapamycin (mTOR), an evolutionary serine/threonine protein kinase, has been well documented in several disorders. In epilepsy research, mTOR pose as a very exhilarating target, as inhibition of its hyperactivation has been found to be effective in suppression of epilepsy and epileptogenesis. However the precise mechanism for the aberrant expression of mTOR, leading to the overexpression of its downstream genes, still remains blurred. Preclinical and clinical studies have revealed that decrease in PI3K/AKT/mTOR pathway hyperactivation have considerably reduced seizures. Hence, our study was designed to explore the anti-seizure potential of selective PI3K inhibitor (morpholine containing compound) on zebrafish model of pentylenetetrazole induced seizure. Zebrafish larvae of 7 days post fertilization were subjected to different concentrations of the selective PI3K inhibitor, following which they were exposed to pentylenetetrazole and recordings were scored on a 3 point scale. The best therapeutic concentration was selected and it was tested on adult zebrafish. Furthermore, fish brains were isolated and expressions of genes were studied in comparison to the epileptic fish. The results showed that the inhibitor distinctly reduced the seizure state in both larvae and adult fish in combination to decreasing the expression of various genes of the PI3K/AKT/mTOR pathway. These findings concluded that selective PI3K inhibitor has anti-seizure potential and can be explored in the near future as a potential antiepileptic.

  • Novel Therapeutics | Parkinsons Disease | Managing life with Parkinsons Disease
Location: Athens
Speaker

Chair

Ramon Bautista

University of Florida Health Science Center, USA

Speaker

Co-Chair

Byung-Jun Park

Daejeon University, South Korea

Session Introduction

Sebastian Knöbel

Miltenyi Biotec GmbH, Germany

Title: Towards a cell therapy for Parkinson’s Disease: Fully integrated closed system expansion and differentiation of pluripotent stem cells to mesencephalic dopaminergic progenitor cells

Time : 10:35-11:00

Speaker
Biography:

Sebastian Knöbel is a trained Biologist and received his PhD at the RWTH Aachen University in 2006. He joined the Miltenyi R&D Department as Research Scientist in 2007.  In his current position as Manager, he heads the Media Development Group and Research Groups for pluripotent, mesenchymal stem cells generating tools and protocols for the isolation, culture and modulation of cells for research and translational applications. His current research includes many aspects of regenerative cell therapy with a focus on the manufacturing of pluripotent stem cell derived cell types.

Abstract:

Pluripotent stem cell (PSC) derived cell products hold great promise for future clinical use in a variety of indications like type i diabetes, cardiomyopathies, macular dystrophies and Parkinson’s disease. For Parkinson’s disease trials, grafted human fetal tissue has indicated utility of tissue or cell replacement therapy. However, the limited availability and ethical implications connected to using primary fetal material have inspired pluripotent stem cell (PSC) based approaches. In vitro differentiated mesencephalic dopaminergic (mesDA) progenitor cells grafted into the striatum have proven to, revert motor symptoms in pre-clinical animal models of Parkinson’s disease compensating for the loss of dopamine producing cells in the substantia nigra. Raising regulatory requirements for such advanced-therapy medicinal products (ATMPs) imply the need for standardized reagents and highly reproducible manufacturing procedures. Automation of PSC expansion, differentiation, and potential product optimization through cell sorting may contribute to successful and cost-effective innovative therapies. Using the versatile and integrated GMP cell processing platform, CliniMACS Prodigy®, we previously developed a cultivation and expansion workflow for PSCs. Now we have adapted the lab protocol for the differentiation to mesDA progenitor cells and have transferred it onto the device, for a medium-scale prototype manufacturing process within the closed system. Extrapolating the cell numbers retrieved from the protoype process would correspond to 150–250 patient doses per manufactured batch. To characterize the identity of the resulting progenitors, we have designed a concise marker panel for flow cytometry-based quality control (QC). Taken together, we have developed a method for adherent, closed-system cultivation of PSCs and differentiation to dopaminergic progenitor cells in combination with comprehensive QC assays.

Anita Haahr and Dorthe Sørensen

VIA University College, Denmark

Title: Coping with Parkinsons disease in everyday life: A metasynthesis

Time : 11:00-11:25

Speaker
Biography:

Anita Haahr—RN, MScN, PHD—is a Senior Lecturer at the School of Nursing, Aarhus, Denmark and an Adjunct Lecturer at the Department of Health, section for Nursing, Aarhus University, Denmark. The focus of her research is living and coping with life with PD from a patients and spouses perspective. She has done research within this area for more than a decade and has published several papers on the subject.

Abstract:

Parkinson’s disease (PD) is the second most common chronic progressive neurodegenerative disease affecting more than 10 million people worldwide. The main features of PD are tremor, bradykinesia, rigidity and at the later stage, postural instability. As the disease progresses, non-motor symptoms such as neuropsychiatric symptoms, depression, anxiety, cognitive challenges, sleep disturbances and fatigue may also appear. Thus, living with PD strongly affects daily living and as the disease progresses, individuals living with PD may experience the disease as limiting on a daily basis, requiring the development of individual ways of coping with the disease to maintain an active everyday life. The aim of the study was to identify coping in daily life in individuals with PD as it is described in the existing literature, ultimately to be able to describe coping patterns and challenges, in order to uncover the needs of the individual living with PD, to support their efforts in managing daily life with the disease. In this presentation, we unfold the results of a literature review performed as a meta-ethnographic metasummary and metasynthesis. A thorough literature search was conducted and adhering to the JBI guidelines, eligible studies were assessed for quality. A total of 13 articles were included in the study. Preliminary results shows the overarching motivation for coping with PD to be “striving for normalcy” and “preserving the self” from before PD. These findings will be unfolded at the presentation.

Sana AlBustan

Kuwait University, Kuwait

Title: Parkinson disease: A study of public awareness in Kuwait

Time : 11:25-11:50

Speaker
Biography:

Sana A. AlBustan is a young researcher  in the Department of Communication Disorders Sciences, College of Life Sciences, Kuwait University. She earned her Ph.D from the Department of Speech, Language and Hearing Sciences, College of Public Health and Health Professions, University of Florida. Her clinical internship and practicums were in Florida hospitals, public schools and private clinics. In May,2017, Dr. AlBustan  published “Kuwaiti Teachers' Perceptions of Voice Handicap” in the Journal of Voice . In December 2017,  she published” Towards a Standard Arabic System Usability Scale: Psychometric Evaluation using Communication Disorder App” in the International Journal of Human–Computer InteractionThe intended study would shed a light on Parkinson Disease (PD)in Kuwait. This study will represent the levels of awareness and knowledge among general people about PD that are currently not very well documented in Kuwait. A questionnaire will be developed  for this current study by the researcher that would consist of a structured item questionnaire that would compose of both open-ended and close-ended questions would be given to 50 males and  50 females after a committee of professionals in  the field approve the questionnaire. Questions will be devolved to address  various aspects of the  definition PD,  onset of PD, cause, treatment, and hereditariness Demographic data with participants demographic features such as age, gender, occupations, qualifications and educational level will also be considered and addressed in this research. SPSS analysis procedures will be used to examine and analyze the participants responses The study is still in its pre implementation stage progress. The researcher anticipates her results will be consistent with other researchers findings. The primary goal of this study is  to investigate the level of public awareness and knowledge of PD and facilitate the level of awareness and the services offered by governmental and private medical facilities in the Kuwait

 

Abstract:

The intended study would shed a light on Parkinson Disease (PD)in Kuwait. This study will represent the levels of awareness and knowledge among general people about PD that are currently not very well documented in Kuwait. A questionnaire will be developed  for this current study by the researcher that would consist of a structured item questionnaire that would compose of both open-ended and close-ended questions would be given to 50 males and  50 females after a committee of professionals in  the field approve the questionnaire. Questions will be devolved to address  various aspects of the  definition PD,  onset of PD, cause, treatment, and hereditariness Demographic data with participants demographic features such as age, gender, occupations, qualifications and educational level will also be considered and addressed in this research. SPSS analysis procedures will be used to examine and analyze the participants responses The study is still in its pre implementation stage progress. The researcher anticipates her results will be consistent with other researchers findings. The primary goal of this study is  to investigate the level of public awareness and knowledge of PD and facilitate the level of awareness and the services offered by governmental and private medical facilities in the Kuwait

 

 

Jae Moon Lee

Kainos Medicine Inc., South Korea

Title: Development of FAF1 inhibitor KM-819 as a disease-modifying drug for treatment of Parkinson’s disease

Time : 11:50-12:15

Speaker
Biography:

Jae Moon Lee completed his PhD from Duke University and Post-doctorate from Duke University School of Medicine. He is the VP of Kainos Medicine, a clinical stage Korean biotech company. He has published more than 15 papers in reputed journals.

Abstract:

Current standard of care for Parkinson’s disease is symptomatic treatments by supplementing dopamine or dopamine agonists or analogous mechanisms, and the disease modifying treatment is one of the major unmedical needs to block the progression. KM-819 is an orally active small molecule drug developed as an inhibitor for FAF1, a proapoptotic protein, targeting various degenerative diseases. It has shown superior efficacy of neuroprotection in cell models and of dopaminergic neuron protection in midbrain in various animal models of Parkinson’s disease as well as improvement of behavioral tests, suggesting this drug has potential capability of slowing or stopping the progression of the disease. It has also shown inhibition of alpha-synuclein accumulation in cells. We have completed Phase 1 clinical trial for KM-819, randomized, double-blind, placebo-controlled study. The study is divided into part A (single ascending dose) and part B (multiple ascending dose) for evaluation of safety, tolerability, and pharmacokinetics as well as various pharmacodynamics markers for KM-819 in healthy volunteers. The study results showed no drug-related serious AEs and high safety profile in human. Also, the PK study showed dose-proportional exposure with higher in elderly group, ideal for Parkinson’s drug. We are currently planning for phase 2 in patients focusing on investigation of the drug’s efficacy of slowing down or halting the progression of the disease.

Break: Lunch Break 12:15-12:55 @ La Place AB
  • Poster Presentations
Location: zurich

Session Introduction

Limin Shi

Qingdao University, China

Title: Ghrelin enhances the excitability of nigral dopaminergic neurons by inhibition of A-type potassium channels
Biography:

Limin Shi completed her PhD from Qingdao University. She is an Associate Professor of the Department of Physiology and Pathophysiology in Qingdao University.
She has published more than 10 papers in reputed journals.

Abstract:

Ghrelin, an endogenous ligand for growth hormone secretagogue receptor (GHS-R, a G-protein-coupled receptor), is a
28-amino-acid peptide that regulates growth hormone secretion, food intake, reward-seeking behavior and memory
performance. In the substantia nigra pars compacta (SNc), ghrelin electrically activates dopaminergic neurons, and increases
dopamine concentration in the striatum. However, how ghrelin enhances neuronal excitability remains largely unknown. In
the present study, we focus on A-type potassium channels (IA), which has a wide expression on dopaminergic neurons and
plays a key role in pacemaker control. Brain slices of the SNc were prepared from C57BL/6 mice of postnatal 15–20 days. The
effects of ghrelin on spontaneous firing and IA current of dopaminergic neurons were observed by whole cell patch clamp
technique. IA specific blocker 4-AP (1 mM) significantly enhanced the spontaneous firing of dopaminergic neurons, whereas
further application of ghrelin (100 nM) had no additional effect on neuronal firing. The application of ghrelin reversibly and
significantly decreased the amplitude of IA to 54% of control. Application of H89 (1 μM, PKA selective blocker) did not alter the
IA current or the response to ghrelin. However, GF109203X (5 μM, PKC inhibitor) abolished ghrelin-induced inhibition of IA.
To assess the involvement of the possible PKC specific subspecies, we then used Gö6976 (20 nM, conventional PKCs selective
inhibitor) and rottlerin (10 μM, PKCδ selective inhibitor). Our results showed that bath application of Gö6976 or rottlerin
alone had no effect on the IA currents, whereas rottlerin totally abolished the IA current response to ghrelin. Therefore, our
findings indicate that inhibition of IA may contribute to the ghrelin-induced excitation of dopaminergic neurons. Ghrelin
reduces IA by activation of PKCδ pathway.

Junxia Xie

Qingdao University, China

Title: The Kv7/KCNQ channel blocker XE991 protects nigral dopaminergic neurons in the 6-hydroxydopamine rat model of Parkinson’s disease
Biography:

Limin Shi completed her PhD from Qingdao University. She is an Associate Professor of the Department of Physiology and Pathophysiology in Qingdao University.
She has published more than 10 papers in reputed journals

Abstract:

Ghrelin, an endogenous ligand for growth hormone secretagogue receptor (GHS-R, a G-protein-coupled receptor), is a
28-amino-acid peptide that regulates growth hormone secretion, food intake, reward-seeking behavior and memory
performance. In the substantia nigra pars compacta (SNc), ghrelin electrically activates dopaminergic neurons, and increases
dopamine concentration in the striatum. However, how ghrelin enhances neuronal excitability remains largely unknown. In
the present study, we focus on A-type potassium channels (IA), which has a wide expression on dopaminergic neurons and
plays a key role in pacemaker control. Brain slices of the SNc were prepared from C57BL/6 mice of postnatal 15–20 days. The
effects of ghrelin on spontaneous firing and IA current of dopaminergic neurons were observed by whole cell patch clamp
technique. IA specific blocker 4-AP (1 mM) significantly enhanced the spontaneous firing of dopaminergic neurons, whereas
further application of ghrelin (100 nM) had no additional effect on neuronal firing. The application of ghrelin reversibly and
significantly decreased the amplitude of IA to 54% of control. Application of H89 (1 μM, PKA selective blocker) did not alter the
IA current or the response to ghrelin. However, GF109203X (5 μM, PKC inhibitor) abolished ghrelin-induced inhibition of IA.
To assess the involvement of the possible PKC specific subspecies, we then used Gö6976 (20 nM, conventional PKCs selective
inhibitor) and rottlerin (10 μM, PKCδ selective inhibitor). Our results showed that bath application of Gö6976 or rottlerin
alone had no effect on the IA currents, whereas rottlerin totally abolished the IA current response to ghrelin. Therefore, our
findings indicate that inhibition of IA may contribute to the ghrelin-induced excitation of dopaminergic neurons. Ghrelin
reduces IA by activation of PKCδ pathway

Jun Wang

Qingdao University, China

Title: The effects of 6-OHDA on iron metabolism in astrocytes are mediated by hypoxia-inducible factors
Biography:

Jun Wang completed her PhD from Qingdao University and Post-doctorate from the University at Buffalo, USA. She is a Professor at the Department of Physiology
and Pathophysiology in Qingdao University. She has published more than 30 papers in reputed journals.

Abstract:

Disrupted iron homeostasis in the substantia nigra (SN) is involved in Parkinson's disease (PD). When loaded with iron,
neurons and microglia die, but astrocytes have a high iron tolerance and can proliferate in the same situation. Our previous
studies have shown that in astrocytes, expression of divalent metal transporter 1 (DMT1) and iron export protein ferroportin1
(FPN1) are both upregulated after 6-hydroxydopamine (6-OHDA) treatment, but the mechanisms remain unclear. Hypoxiainducible
factors (HIFs) are known to be important in regulating iron homeostasis. Binding of HIF-2α to the promoter region
of the hypoxia response elements (HREs) of DMT1 and FPN1 increases their expression. However, as yet it is unclear if HIFs are
involved in the regulation of DMT1 and FPN1 expression in astrocytes treated with 6-OHDA.Using western blots, we observed
HIFs, DMT1 and FPN1 expressions in primary cultured astrocytes and SH-SY5Y neuron cell lines treated with 6-OHDA,
inhibitors of HIF-1α and HIF-2α, protein kinase C (PKC) inhibitor and PKC activator, radical scavenger and inducible NO
synthase (iNOS) inhibitor. The ferrous iron traffic of astrocytes was determined by measuring the quenching or reversing of
calcein fluorescence. In this study, we found that protein levels of HIF-1α and HIF-2α in astrocytes were significantly increased
by treatment with 6-OHDA, whereas expression did not change in dopaminergic neurons. Furthermore, using inhibitors
of HIF-1α and HIF-2α, we observed that an HIF-2α inhibitor markedly reduced the up-regulation of DMT1 and FPN1 by
6-OHDA and decreased ferrous iron influx and efflux. However, there was no effect following treatment of astrocytes with the
HIF-1α inhibitor. We found that PMA activated HIF-2α, leading to increased expression of DMT1 and FPN1. Activation of
HIF-2α by PMA and 6-OHDA was blocked by Bisl preventing downstream activation of DMT1 and FPN1. Likewise, N-acetyll-
cysteine (NAC) or Nω-Nitro-L-arginine methyl ester hydrochloride (L-NAME) were found to block HIF-2α activation by
6-OHDA. Our data indicate that HIF-2α, but not HIF-1α, regulates expression of DMT1 and FPN1 in astrocytes. Furthermore,
we conclude that PKC pathway, reactive oxygen species (ROS) and reactive nitrogen species (RNS) were involved in HIF-2α
activation.

Chansik Hong

Chosun University, South Korea

Title: Increased TRPC5 glutathionylation contributes to striatal neuron loss in Huntington’s disease
Biography:

Chansik Hong completed his PhD from Seoul National University and Post-doctorate from Seoul National University, College of Medicine. He is an Associate
Professor in the Physiology Department at Chosun University, College of Medicine. He has published more than 25 papers on ion channels in reputed journals

Abstract:

Aberrant glutathione or Ca2+ homeostasis due to oxidative stress is associated with the pathogenesis of neurodegenerative
disorders. The Ca2+-permeable TRPC channel is predominantly expressed in the brain which is sensitive to oxidative
stress. However, the role of the TRPC channel in neurodegeneration is not known. Here, we report a mechanism of TRPC5
activation by oxidants and the effect of glutathionylated TRPC5 on striatal neurons in Huntington’s disease. Intracellular
oxidized glutathione leads to TRPC5 activation via TRPC5 S-glutathionylation at cysteine-176/cysteine-178 residues. The
oxidized glutathione-activated TRPC5-like current, results in a sustained increase in cytosolic Ca2+, activated calmodulindependent
protein kinase and the calpain-caspase pathway, ultimately inducing striatal neuronal cell death. We observed
an abnormal glutathione pool indicative of an oxidized state in the striatum of Huntington’s disease transgenic (YAC128)
mice. Increased levels of endogenous TRPC5 S-glutathionylation were observed in the striatum in both transgenic mice and
patients with Huntington’s disease. Both knockdown and inhibition of TRPC5 significantly attenuated oxidation-induced
striatal neuronal cell death. Moreover, a TRPC5 blocker improved rearing behaviour in Huntington’s disease transgenic mice
and motor behavioural symptoms in littermate control mice by increasing striatal neuron survival. Notably, low levels of
TRPC1 increased the formation of TRPC5 homotetramer, a highly Ca2+-permeable channel, and stimulated Ca2+-dependent
apoptosis in Huntington’s disease cells (STHdhQ111/111). Taken together, these novel findings indicate that increased TRPC5
S-glutathionylation by oxidative stress and decreased TRPC1 expression contribute to neuronal damage in the striatum and
may underlie neurodegeneration in Huntington’s disease.

Kim KT

Pohang University of Science and Technology, South Korea

Title: VRK2 mRNA stability and polyQ-huntingtin aggregation
Biography:

Kim K T completed his PhD from the University of Massachusetts, Amherst in 1989. During 1982–1985, he worked as a Research Investigator at Genetic Engineering
Research Center, Korea Institute of Science and Technology. From 1997–1998, he was a Visiting Scientist at the Department of Physiology & Biophysics at the
University of Washington. His major stream of research involves the modulation of second messengers in neuronal cells, regulation of neurotransmitter secretion,
and transcriptional regulation of the enzymes involved in the biosynthesis of neurotransmitters.

Abstract:

Misfolded proteins with abnormal polyglutamine (polyQ) expansion cause neurodegenerative disorders, including
Huntington's disease (HD). Recently, it was found that polyQ aggregates accumulate due to vaccinia-related kinase 2
(VRK2)-mediated degradation of TCP-1 ring complex (TRiC)/chaperonin-containing TCP-1 (CCT), which has an essential
role in the prevention of polyQ protein aggregation and cytotoxicity. The levels of VRK2 are known to be much higher in
actively proliferating cells but are maintained at a low level in the brain via an unknown mechanism. Here, we found that basal
levels of neuronal cell-specific VRK2 mRNA are maintained by post-transcriptional, rather than transcriptional, regulation.
Moreover, heterogeneous nuclear ribonucleoprotein Q (hnRNP Q) specifically binds to the 3ʹUTR of VRK2 mRNA in
neuronal cells to reduce the mRNA stability. As a result, we found a dramatic decrease in CCT4 protein levels in response to a
reduction in hnRNP Q levels, which was followed by an increase in polyQ aggregation. Taken together, these results provide
new insights into how neuronal hnRNP Q decreases VRK2 mRNA stability and contribute to the prevention of HD, while also
identifying new prognostic markers of HD.

Phil-Ok Koh

Gyeongsang National University, South Korea

Title: Quercetin prevents the ischemic injury-induced decrease of thioredoxin expression in brain tissue
Biography:

Phil-Ok Koh completed her PhD from Gyeongsang National University and Post-doctorate from University of Maryland at Baltimore, USA. She is the Professor of
College of Veterinary Medicine, Gyeongsang National University. She has published more than 180 papers in reputed journals and has been serving as an Editorial
Board Member of repute.

Abstract:

Quercetin is a bioactive flavonoid abundant in vegetables and fruits. Quercetin is an especially effective agent against
neuronal damage following global and focal cerebral ischemia. Thioredoxin has various physiological functions including
regulation of cellular redox homeostasis and apoptosis. The aim of this study was to investigate whether quercetin regulates
thioredoxin expression in focal cerebral ischemia. Male Sprague Dawley rats (210–230 g) were used for experiments and
injected with either quercetin (10 mg/kg) or vehicle via the intraperitoneal cavity one hour prior to middle cerebral artery
occlusion (MCAO). Cerebral cortex tissues were isolated 24 h after MCAO. Using a proteomics approach, thioredoxin
expression was found to be decreased in vehicle-treated MCAO animals, while treatment with quercetin attenuated this
decrease. The effect of quercetin on the MCAO-induced decrease in thioredoxin expression was confirmed by Western blot and
reverse-transcription-PCR analyses. Immunofluorescence staining showed that quercetin treatment alleviated the decrease in
thioredoxin positive cells in the cerebral cortex of animals with MCAO surgical injury. Furthermore, immunoprecipitation
analysis demonstrated that binding between apoptosis signal-regulating kinase 1 (ASK1) and thioredoxin were decreased in
vehicle-treated MCAO animals, while treatment with quercetin attenuated this effect. Our results indicate that thioredoxin
has neuroprotective functions against oxidative stress in brain ischemic injury. Maintenance of thioredoxin expression by
quercetin administration may help to prevent neuronal cell death following cerebral ischemia. Our findings suggest that
quercetin mediates its neuroprotective function by regulating thioredoxin.

Gülten Özdemir

Istanbul Eah Hospital, Turkey

Title: A case of thyroid hemiagenesis diagnosed after essential tremor symptoms
Biography:

Gülten Özdemir graduated from Selçuk University, Faculty of Medicine in 1994. she completed her specialist education in Istanbul Okmeydanı Education Research
Hospital, Department of Neurology between 2001–2016. Multiple Sclerosis, Sleep Disorders, Movement Disorders (Parkinson's disease and Parkinsonism) are
among her areas of interest. In the treatment of selected Parkinson's patients with neurostimulation between the years of 2009–2014, she worked in Istanbul
Medical Park Hospital together with Dr. Ali Zırh. He/she received a course and certificate from Christian-Albrechts-University (Kiel University) on this subject. she
has been working as a Neurology Specialist in Istanbul Physical Therapy Education Research Hospital since 2014.

Abstract:

Background: Essential tremor (ET) is a neurological disorder causing involuntary rhythmic tremors (4–12 Hz) and mostly
seen in adults of age 40 or more. ET is a clinical diagnosis and is commonly seen ipsilaterally, worsens with movement and
usually hands are involved initially. Physical and emotional stress, fatigue, low blood glucose level, alterations in temperature,
caffeinated drinks may trigger the condition. ET is not a life threatening condition but if the symptoms are severe, it may affect
the quality of life. Thyriod hormone is mainly required for growth and the development of organs including brain and skeletal
systems. Thyroid hemiagenesis (TH) is a rare, congenital disorder characterized by non-development of a lobe of the thyroid
gland.
Case: A 23 year old female patient having bilateral tremor for approximately 10 years, intensifying with motion presented to
the neurology outpatient clinic for the very first time. Muscle tone and strength, deep tendon reflexes, sensual examination,
posture, balance and coordination and walking were evaluated as part of the usual neurological examination. Routine
biochemistry, hemogram and thyroid function tests were performed and found as normal, except vitamin B12 deficiency
(176). Known disease, past surgery, exposure to heavy metals and drug use were not present in patient’s history. The patient
lacks history of alcohol and smoking; caffeine use was limited to 1–2 cups of tea/day. The patient had no family history of
essential tremor or Parkinson’s disease. The patient had strain while performing activities such as drinking water from a glass
and drawing circles. Tremor was leading to difficulty in daily life activities and functional loss. Thyroid gland ultrasonography
was performed for advanced study to enlighten essential tremor etiology: agenesis was discovered in thyroid left lobe and the
size of the right lobe was 22*12 mm.
Conclusion: This case was presented due to the lack of similar case in literature. The patient was examined for increased
essential tremor, and hemigenesis in thyroid gland was detected. Female gender and thyroid left lobe agenesis were coherent
with literature for TH. Even though no failure was found in thyroid function tests, it may have an association in cellular level
triggering essential tremor. Further studies are needed to investigate the relation between two diseaeses.

Arun Mahato

University of Helsinki, Finland

Title: Small molecule GDNF receptor RET agonist supports the survival of dopamine neurons in vitro and protects their function in 6-OHDA lesioned rat midbrain
Biography:

Arun Mahato, PhD student at Institute of Biotechnology, University of Helsinki. He is interested in studying neurotrophic factors outside nervous system which
could be neuroprotective and neurorestorative in Parkinson’s disease. He holds master’s degree in Physioology and Neuroscience from University of Helsinki.
He has received Mari Curie Fellow fellowship as well as EFMC gant to get more insight in the field of computational and medicinal chemistry which helped me in
optimization of GDNF mimetics

Abstract:

Motor symptoms of Parkinson’s disease (PD) are caused by degeneration and progressive loss of nigrostriatal dopamine
neurons and affect up to 6–7 million people world-wide. Currently no cure for this disease is available. Existing
therapeutic strategies based on dopamine replacement, alleviate PD symptoms, but do not prevent or slow down degeneration
of dopamine neurons. Glial cell line-derived neurotrophic factor (GDNF) and its closely related protein neurturin (NRTN)
can protect and repair dopamine neurons in vitro and in animal models of PD, but their clinical use is complicated because of
their low bioavailability and poor diffusion in tissues. Previously, we discovered a small molecule called BT13 that selectively
activates GDNF receptors and promotes neurite outgrowth from sensory neurons. Here, we report the ability of this molecule
to support the survival of cultured dopamine neurons only when they express GDNF receptors. In addition, BT13 activates
intracellular signaling cascades in vivo, stimulates release of dopamine and protect the function of dopaminergic neurons in
a 6-hydroxydopamine (6-OHDA) rat model of PD. In contrast to GDNF, BT13 is able to penetrate through the blood-brainbarrier
and it spreads well in brain tissue. Thus, although its solubility and stability require optimization, BT13 serves as an
excellent tool compound for the development of novel disease-modifying treatments against PD.

Semra Ari

Yunus Emre State Hospital, Turkey

Title: Parkinsonism secondary to metastatic brain tumor: A case report
Biography:

Semra Ari has completed her PhD from Atatürk University and Post-doctorate from Istanbul Medeniyet University, Training and Resource Hospital. She is now
working as a Neurologist at Yunus Emre State Hospital.

Abstract:

Objectıve: Brain tumors are rare causes of parkinsonism. The tumors causing neoplastic parkinsonism are astrocytomas,
meningiomas, craniopharyngiomas, colloid cysts and more rarely, metastatic brain tumors. Mass effect to basal ganglia takes
an essential role in the mechanism of pathological findings.
Materıals & Methods: We present an unusual case of parkinsonism secondary to a metastatic brain tumor. A 60 year old male
patient was admitted to our hospital with a history of gradually decreasing speech content, slowing of speaking, blurring of gaze
and slowing of movements for two months. The neurological examination had mask face, hypophonic speech, bradykinesia
and rigidity in the left arm and leg. Idiopathic Parkinson’s disease (IPD) was first suspected during diagnosis, but the presence
of small cell lung cancer in patient past history and a rapid progression in neurological seymptoms suggested the possibility of
secondary parkinsonism and brian magnetic resonans imaging (MRI) was performed immediately.
Results: A 27×30 mm sized lesion with very distinct edema effect and heterogeneous contrast enhancement in the right
frontoparietal area was found in MRI. The lesion was initially interpreted as a metastatic brain tumor, the patient underwent
surgery and all extrapyramidal findings were resolved.
Conclusion: Uncommon causes of parkinsonism like brain tumors may resemble clinical features of IPH; thus, we wanted
to emphasize that imaging should once again be performed for differential and accurate diagnosis and treatment planning,
espacially in cases with rapid and progressive course.

Mohamed Hamdy Ibrahim

Ain Shams University, Egypt

Title: Epilepsy and treatment
Speaker
Biography:

Mohamed Hamdy Ibrahim, Egyptian, has been graduated form, Faculty of Medicine, Ain Shams University, Cairo, Egypt. He has joined the Neuropsychiatry
Residency at Ain shams University, Cairo, Egypt from 2001 till 2003, finished his MD in Neurology and got his Doctorate by 2008. He has been assigned as Lecturer
of Neurology and his main concern was in the field of neurovascular interventional radiology. He has finished his fellowship in Interventional Neurology at Zurich
University, Switzerland as F.I.N.R. by 2013. Now, he is working as an Assistant Clinical Professor of Neurology, GMU University and GMC hospital, Ajman, United
Arab of Emirates since 2010. He has some publications in many journals such as Open Journal of Medical Imaging (OJMI), The Egyptian Journal of Radiology
and Nuclear Medicine, European Journal of Neurology and Neurology of India. His interest lies in: acute stroke management, diagnostic and therapeutic digital
subtraction angiography (Special service new in UAE), nerve conduction studies, EMG, visual evoked potentials (VEP), botox injection for migraine (New in
UAE) and epilepsy management. In addition he is a Member of World Federation of Interventional and Therapeutic Neuroradiology (WFITN), Member of ESMINT
(European Society of Minimal Invasive Neurological Therapy) and Member of European Society of Neuroradiology Diagnostic and Interventional (ESNR).

Abstract:

The case study is aimed at providing a more thorough analysis of a case of epilepsy presented with an unusual aura of cough.
The study hopes to generate an interest for further studies into the topic focuses on abnormal unusual presentations of
auras. Cough as an aura is not a common presentation. Any stereotyped repeated clinical phenomenon should consider being
epileptic in origin.

Mohsen Abbasi Kangevari

Shahid Beheshti University of Medical Sciences, Iran

Title: Do mothers underestimate quality of life of their children with epilepsy?
Biography:

Mohsen Abbasi Kangevari is a fifth-year Medical student at Shahid Beheshti University of Medical Sciences. He has published two articles and has one article in
press and three articles under review. He has also co-translated the sixth edition of “Immunology & Serology in Laboratory Medicine” into Persian. His main field of
interest in research is Neuroscience and Public Health.

Abstract:

Children with epilepsy face many challenges not limited to seizures which affect their quality of life (QoL). Since mothers
of children with epilepsy become involved in seizure-related issues of their children, their reports could be valuable as a
proxy to measure QoL of children with epilepsy. This study reports whether mothers underestimated QoL of their children
with epilepsy. Mother-reported overall QoL score was measured by 76 subscales of Quality of Life in Children with Epilepsy
Questionnaire (QOLCE) which was developed by Sabaz. Beyond the 76 subscales, a question named QoL item was asked from
mothers about their children’s QoL during the previous four weeks. In response to QoL item, mothers could choose excellent
(score=90), very good (70), good (50), fair (30), and poor (10). In this study which was conducted during May to October 2017
in a children’s hospital in Tehran, we compared the overall QoL score and the score of QoL item. Participants included 223
children with epilepsy and their mothers. Among all children, 117(52.5%) were girls and the mean (SD) age of children was
6.8(6.0) years. The mean (SD) overall QoL of children was calculated 75.7(8.7) based on the 76 subscales of QOLCE. However,
the mean (SD) score of QoL item among children was 52.5(15.4), which was 30% less than the overall quality of life score.
Therefore, it could be concluded that mothers underestimated their children’s quality of life which could be due to low selfconfidence
in assessing their children.

Mohsen Abbasi Kangevari

Shahid Beheshti University of Medical Sciences, Iran

Title: Do mothers underestimate quality of life of their children with epilepsy?
Biography:

Mohsen Abbasi Kangevari is a fifth-year Medical student at Shahid Beheshti University of Medical Sciences. He has published two articles and has one article in
press and three articles under review. He has also co-translated the sixth edition of “Immunology & Serology in Laboratory Medicine” into Persian. His main field of
interest in research is Neuroscience and Public Health.

Abstract:

Children with epilepsy face many challenges not limited to seizures which affect their quality of life (QoL). Since mothers
of children with epilepsy become involved in seizure-related issues of their children, their reports could be valuable as a
proxy to measure QoL of children with epilepsy. This study reports whether mothers underestimated QoL of their children
with epilepsy. Mother-reported overall QoL score was measured by 76 subscales of Quality of Life in Children with Epilepsy
Questionnaire (QOLCE) which was developed by Sabaz. Beyond the 76 subscales, a question named QoL item was asked from
mothers about their children’s QoL during the previous four weeks. In response to QoL item, mothers could choose excellent
(score=90), very good (70), good (50), fair (30), and poor (10). In this study which was conducted during May to October 2017
in a children’s hospital in Tehran, we compared the overall QoL score and the score of QoL item. Participants included 223
children with epilepsy and their mothers. Among all children, 117(52.5%) were girls and the mean (SD) age of children was
6.8(6.0) years. The mean (SD) overall QoL of children was calculated 75.7(8.7) based on the 76 subscales of QOLCE. However,
the mean (SD) score of QoL item among children was 52.5(15.4), which was 30% less than the overall quality of life score.
Therefore, it could be concluded that mothers underestimated their children’s quality of life which could be due to low selfconfidence
in assessing their children.

Sunil Kumar Singh

King George's Medical University, India

Title: Management of status epilepticus in neurosurgical patients
Speaker
Biography:

Abstract:

Introduction: The post-operative course of patients is sometimes complicated by seizures, which in rare cases may progress to
status epilepticus. Since these patients are in a precarious condition, the development of such a complication is often disastrous
if not managed expeditiously.
Material & Methods: A retrospective study of all patients undergoing cranial surgery over the last five years in the Department
of Neurosurgery, KGMU was done. The incidence of status epilepticus and the related causes and management was studied.
Results: 3560 patients were operated during the period. Post-operative (Seven days) seizures occurred in 364 patients. Status
occurred in 58 patients. 36 of these patients had a fatal outcome while the other 22 patients responded to treatment.
Conclusions: Seven-day post-operative seizure incidence in neurosurgical patients is an uncommon event. The development
of status epilepticus in this group is even rarer but none the less is a dangerous complication associated with a poor outcome.

Jiyeon Kim

Korea University Ansan Hospital, South Korea

Title: Gaze-evoked nystagmus associated with lamotrigine toxicity
Biography:

Jiyeon Kim is currently a clinical instructor in the Department of Neurology at Korea University Ansan Hospital. She was appointed in 2016 after completion of 2-year
fellowship training in epilepsy in the Epilepsy Center at St. Mary Hospital, Seoul, Korea. Prior to her fellowship training, she completed 4-year neurology residency
training at the Eulji Hospital, Seoul, Korea. Her research focuses on clinical and neurophysiological aspects of temporal lobe epilepsy and women with epilepsy.

Abstract:

Lamotrigine (LTG) is a widely used antiepileptic drug (AED) for the treatment of partial and generalized seizures. LTG is
metabolized predominantly in the liver through glucuronidation and when administrating with hepatic enzyme-inhibiting
AED such as valproate (VPA), the serum level of LTG is increasing significantly. A 32-year-old woman with a 13-year history
of epileptic seizures admitted to the hospital for exacerbating seizures. The seizures developed secondarily generalized and
occurred several times a day. She had taken a single AED of LTG 450 mg a day. After intraveonously administration of VPA and
then maintaining dose of VPA 600 mg and lamotrigine 450 mg a day, the seizure activity was resolved. However, she developed
blurred vision, dizziness and nausea five days after medication of multiple AEDs. Neurologic examination was notable for
prominent bilateral horizontal gaze-evoked nystagmus and perverted downward saccades during head impulses for horizontal
canals. After suspicion of LTG toxicity, LTG was discontinued and replaced with levetiracetam. The dizziness and gaze evoked
nystagmus markedly improved after discontinuation of the LTG and the seizure did not occur during six months of follow-up.
Gaze-evoked nystagmus and perverted downward corrective saccades during horizontal head impulses indicate dysfunction of
the vestibulocerebellum, especially flocculus and the floccular function of gaze holding and inhibition of the AC pathway could
be disrupted by LTG toxicity. Even though LTG has been reported to be well tolerated, the risk of toxic effects could increase
when VPA is combined.

Alaa Eldeen Mahmoud Helal Helal

Helwan University, Egypt

Title: Automatic detection of epileptic discharges in long EEG recordings
Speaker
Biography:

Alaa Eldeen Mahmoud Helal Helal has completed his Master’s degree from Cairo University and Doctoral studies from Helwan University. He has published many
papers in reputed journals. In general, he is interested in Biomedical Engineering especially in biosignal processing (EEG, ECG, MEG). In his MSc study, he has
designed and implemented a smart medical device based on electrical nerve stimulation to treat the drop foot disease using the functional electrical stimulation
(FES). His Doctoral study is focused on automatic detection of epileptic waveforms in EEG signal and preventing the seizure evolution by vagus nerve stimulation
using a smart closed feed back loop system.

Abstract:

Electroencephalogram (EEG) is a representative signal containing information about the cerebral cortex activities, has
been the most utilized tool to clinically assess brain functioning and the diagnosis of epilepsy. EEG morphology is
characterized by short transients and sudden waveform changes. Investigation of these rapid events is still done manually
through neurophysiologists by his/her naked eye to identify all occurrences of these electrographic abnormalities which is very
hard and may be impossible, especially with the presence of a lot of many artifacts. Because of that, automatic EEG detection
techniques have received intense attention since it aid for rapid identification of neurological abnormalities and opening a
window to analyze the mechanisms of epilepsy. The nonlinearity nature and fast transitions between non-seizure, pre-seizure,
and seizure states guide us to a promising solution in this work by combining several processing techniques to capture the
EEG features in multiple domains. The method was tested on real epileptic EEG data, giving very promising results that
allow it to offer better capabilities for assisting clinical neurophysiologists in routine EEG examinations for epilepsy diagnosis,
nominating it to find its way into routine clinical use for other neurological disorders. For its fast computation, it provides a
novel wide window for online processing of EEG data. Also, it can play a positive role for further research and applications
in cerebral activity as deep brain and vagus nerve stimulation for seizure prevention on-line by closed feedback loop system

  • Epilepsy | Epilepsy Therapeutics | Prevention and Management of Epilepsy
Location: Athens
Speaker

Chair

Ramon Bautista

University of Florida Health Science Center, USA

Co-Chair

Byung-Jun Park

Daejeon University, South Korea

Session Introduction

Matina Kampra

National and Kapodistrian University of Athens, Greece

Title: Children with epilepsy during school years: The necessity of parent – teacher cooperation and the doctor’s role

Time : 14:30-14:55

Speaker
Biography:

Abstract:

This study intends to explore the challenges faced by teachers and parents of children with epilepsy during school years. It also aims to provide useful information about the parent-teacher collaboration for the benefit of the pupils, the families and the school.

Methods: Telephone interviews were conducted based on open-ended questions, with 70 head-teachers from schools from all Greek regions. Furthermore a questionnaire was distributed to 100 Greek schools. Additionally, personal interviews took place with 91 parents of children with controlled epilepsy during their school years. The data were grouped and analyzed with the use of qualitative and quantitative analysis.

Results: 89.9% of the school staff was found to know what epilepsy is. 85.1% of the teachers were informed about pupils’ epilepsy by their parents/caregivers while 63/70 head-teachers declared that parents usually misinform the school staff about their child’s condition. 76/91 parents/caregivers personally informed only the head-teacher about their child’s condition because of fear of social stigma and bullying. 87/91 parents declared that they did not know where to seek help to cope with their child's illness apart from their doctor. 92.6% of the teachers felt insufficiently trained to deal with a seizure and 96.2% expressed the need for more formal information about epilepsy. 64/70 head-teachers and all the parents/caregivers expressed the need for inclusion of experts like social workers and nurses into the school personnel.

Conclusion: Epilepsy is a condition that affects not only the pupil with the disorder but also his/her family as well as the school staff. For the school personnel, it is very important to cooperate with the pupils’ parents/caregivers in order to handle the child’s condition properly and safely. The doctor’s guidance to the parents is crucial for their communication with the school staff.

Torie Robinson

Hospital for Neurology and Neurosurgery, UK

Title: Epilepsy - temporal lobectomy, AEDs and social stigma

Time : 14:55-15:20

Speaker
Biography:

With a corporate finance background, after her successful temporal lobectomy in 2013 and continued recovery from psychological diagnoses, Torie has became an active international public speaker and corporate consultant regarding epilepsy, disability, mental health, diversity and inclusion.

Her purposes are to enlighten the uneducated, reduce the stigma held against those with disabilities (particularly epilepsy), and hold organisations accountable for corporate social responsibility when it comes to employment.

Featuring on UK BBC London, 5Live, talkRadio, US Brain Waves Audio and Australian Noongar Radio, Torie’s BBC3 YouTube video in which she featured: “Things Not to Say to Someone with Epilepsy” has been viewed more than half a million times.

Featuring neurological professionals, patients and employers from all over the world, Torie:

  • Both founded and frequently writes for both the torierobinson.com and epilepsysparks.com blogs;
  • Co-founded the Cheeky Sparks epilepsy podcast;
  • Filmed for NHS70
  • Works with DWP (UK Government) regarding disability employment;
  • Has attended meetings within UK Parliament;
  • Is an Epilepsy Action Accredited Volunteer (Trainer), and;
  • Has featured in Huffington Post

Torie plays the piano, enjoys communicating to overseas audiences and forever learning more about neurology and cosmology.

Born in the UK, Torie grew up in both England and Australia and has worked for international firms with staff in Europe, Australia, the US and Asia. Torie lives in London with her partner.

Abstract:

Abstract:

 

Patient in early 30s with refractory, left temporal lobe epilepsy in a setting of left hippocampal sclerosis. Increase in seizure severity and freqency over 25 years, with worsening depression. Patient working in corporate environment.

Aim:

To decrease frequency and/or severity of seizures; increase quality of life and life expectancy

Treatment:

Temporal lobectomy

Facts:

Likely Cause of Epilepsy:

  • Lengthy febrile seizure aged 6months

Past AEDs tried:

  • Sodium Valproate, Levetiracetam, Phenytoin

AED side effects experienced:

  • Memory function decrease, fatigue, numbness (phenytoin), mood instability (Levetiracetam)

Seizure triggers:

  • Sleep deprevation, anxiety, forgetting AEDs

Further Diagnosis Related to Epilepsy/AEDs

  • Migraines – developing 2018
  • Mental health issues
  • Thyroid: Hyperthyroidism

Surgery Exploration Testing:

  • Video Telemetry
  • EEG
  • fMRI
  • Psychological evalutation/neuropsychology assessment inc IQ
  • Full understanding of surgery risks and potential outcomes by patient

Surgical Procedure:

  • Left Temporal Lobectomy, Feb 2013
  • CSF leak followed, leading to suture of the wound

Post-operative Diagnoses Included:

  • Severe depression, extreme problems with memory, and exhaustion (for 6-12months)
  • Blind spot in right eye
  • 5 tonic-clonic seizures post surgery, last in November 2017
  • Irregular complex partial seizures (average 4/5 per year)

Current Drugs:

  • Levothyroxine 50mg QD
  • Lamotrigine 100mg BD
  • Lacosamide 100mg BD
  • Venlafaxine 150 BD
  • Clobazam 10mg

Conclusion:

Status: outcome Engel class 2

Patient has experienced significant decrease in number and severity of seizures. Along with psychological therapy, patient’s quality of life is greatly improved. Despite continued taking of AEDs, and infrequent seizures, the results of surgery is considered to be a success by patient. Patient has greater focus, continues to travel and has supportive partner and friends.

 

  • Video Presentation
Location: Athens

Session Introduction

Elaine Wyllie

Lerner College of Medicine, USA

Title: New Opportunities in Pediatric Epilepsy Surgery

Time : 15:20-15:50

Speaker
Biography:

Elaine Wyllie, Professor, Cleveland Clinic Lerner College of Medicine, is a world renowned thought leader in neurology and epilepsy. Dr. Wyllie has been on the Castle Connolly list of America’s Best Doctors for many years, as well as on several other national and regional Top Doctors lists. Her many honors and awards include the highly competitive Award for Outstanding Work in Epilepsy Research from the American Epilepsy Society and Honorary Membership in the Canadian Association for Child Neurology.

Abstract:

New research in pediatric epilepsy surgery is providing opportunities to help more children than ever before.   Some of our most exciting results have been in children with early focal brain lesions and diffuseEEG abnormalities.  The diffuse findings on EEG reflect the evolution of the epilepsy as the early focal lesion, usually cerebral infarction or malformation of cortical development, interacts with the brain at different stages of development.  Infants with focal lesions tend to manifest with hypsarrhythmia, and the older children tend to manifest with slow spike wave complexes and other patterns, but in both age groups the epilepsy typically disappears when the lesion is removed.  Wyllie and colleagues studied 209 children with an early focal lesion who underwent epilepsy surgery, and found no significant difference in seizure outcome based on presence or abundance of generalized epileptiform discharges and EEG seizures.

A second exciting new opportunity for pediatric epilepsy surgery has emerged for children with bilateral abnormalities on brain MRI. Hallbook and colleagues reviewed preoperative MRIs in 110 children who underwent hemispherectomy at Cleveland Clinic, and found abnormalities on the contralateral side in 74%.  In a follow up study of 170 children who underwent hemispherectomy, Moosa and colleagues found that contralateral MRI findings had no significant impact on the frequency of seizure-free outcome among Cleveland Clinic’s highly selected cases.  The contralateral MRI abnormalities in these children, although not insignificant, were always less extensive and less prominent than those on the side of hemispherectomy. 

Research suggests that for patients of all ages, shorter epilepsy duration may positively affect postoperative seizure outcome.  By recognizing surgical opportunity and shortening the delay, we can help more children than ever before. 

 

Break: Networking & Refreshments 15:50-16:05 @ Europa Foyer