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.

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.

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.