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  • Department of Neurology, USA
  • Title:Astrocyte-Microglia Interaction in a Mouse Model of Neuromyelitis Optica.
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Abstract:
Neuromyelitis optica (NMO) is a severe inflammatory autoimmune CNS disorder triggered by binding
of an IgG autoantibody to the aquaporin 4 (AQP4) water channel on astrocytes. Activation of cytolytic
complement has been implicated as the major effector of tissue destruction that secondarily involves
myelin. However, cellular and molecular mechanisms that precede the cytolytic astrocyte-centered
lesion of NMO are largely unknown. We investigated early precytolytic events in the evolving
pathophysiology of NMO in mice by continuously infusing IgG (NMO patient serum–derived or AQP4-
specific mouse monoclonal), without exogenous complement, into the spinal subarachnoid space.
Using this novel mouse model of NMO, we found that motor impairment and sublytic NMOcompatible immunopathology were IgG dose dependent and AQP4 dependent. By selectively deleting
microglia, we demonstrated an unanticipated central role for microglia in NMO pathogenesis that
involves early complement component signaling. In vivo spinal cord imaging revealed a striking
physical interaction between microglia and astrocytes that required signalling from astrocytes by the
C3a fragment of their upregulated complement C3 protein. Astrocytes remained viable but lost AQP4.
Furthermore, despite astrocyte activation and AQP4 downregulation by NMO-IgG, microglial activation
and interaction with astrocytes, and motor impairment were attenuated in mice lacking C3aR.
Therefore, previously unappreciated crosstalk between astrocytes and microglia involving earlyactivated CNS-intrinsic complement components and microglial C3a receptor signaling appears to be a
critical driver of the precytolytic phase in the evolving NMO lesion, including initial motor impairment.
Our study highlights the role of astrocyte-microglia interaction in NMO and suggests microglia as a
therapeutic target in the treatment of NMO.
Biography:
Dr. Long-Jun Wu received his PhD of Neurobiology from University of Science and Technology of China in 2004. He did his postdoc trainings at University of Toronto (2004-2008) and Harvard Medical School (2008-2011). He was an Instructor at Harvard Medical School (2011-2012) and then an Assistant Professor at Rutgers University (2012-2016). Currently, he is Professor and Consultant at Department
of Neurology, Mayo Clinic. His research focuses on the neuroimmune interaction, particularly the function of microglia, in normal and diseased brain. He has published more than 130 peerreviewed articles, including those in Nature Neuroscience, Neuron, Science Translational Medicine, Nature Communications, Journal of Clinical Investigation, PNAS, PLoS Biology, eLife, Cell Reports, Journal of Neuroscience, etc. His work is impactful in the field with more than 9000 citations and H index of 50 in Google Scholar (03/2021). He serves as a standing member for NIH CMBG study section and ad hoc reviewer for three other study sections. He is an Associate Editor for Frontiers of Neuroscience, Molecular Brain, Neuroscience Bulletin, and he is also served in editorial boards for a number of journals including Glia, Brain Behavior and Immunity, Molecular Pain, Neural Plasticity etc.

  • Department of Neurological Surgery at Montefiore Medical Center, USA
  • Title:We Aim to Characterize The Incidence, Risk for Mortality, and Identify Risk Factors for Mortality in Patients Presenting With Hemorrhage and COVID-19.
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Abstract:
Methods: This retrospective cohort study included a cohort of patients admitted to one of three major hospitals of our healthcare network including, an academic medical center and comprehensive stroke center, which ac- cepts transfers for complex cases from eight community hospitals, during March 1 to May 1, 2020. All patients that received imaging of the neuroaxis and had positive PCR testing for COVID-19 were identified and reviewed by an attending neuroradiologist. Demographics and comorbidities were recorded. Biomarkers were recorded from the day of the hemorrhagic event. Vital signs from the day of the hemorrhagic event mechanical ventilation orders at admission were recorded. Imaging findings were divided into 5 subtypes; acute subdural hematoma (SDH), subarachnoid hemorrhage (SAH), multi-compartmental hemorrhage (MCH), multi-focal intracerebral hemorrhage (MFH), and focal intracerebral hemorrhage (fICH). Outcomes were recorded as non-routine dis- charge and mortality.
Results: We found a total of 35 out of 5227 patients with COVID-19 that had hemorrhage of some kind. Mortality for the entire cohort was 45.7 % (n = 16). SDH patients had a mortality rate of 35.3 % (n = 6), SAH had a mortality of 50 % (n = 1), MCH patients had a mortality of 71.4 % (n = 5), MFH patients had a mortality of 50 % (n = 2), fICH patients had a mortality of 40 % (n = 2). Patients with severe pulmonary COVID requiring mechanical ventilation (OR 10.24 [.43−243.12] p = 0.015), with INR > 1.2 on the day of the hemorrhagic event (OR 14.36 [1.69−122.14] p = 0.015], and patients presenting with spontaneous vs. traumatic hemor- rhage (OR 6.11 [.31−118.89] p = 0.023) had significantly higher risk for mortality.
Conclusions: Hemorrhagic presentations with COVID-19 are a rare but serious way in which the illness can manifest. It is important for neurosurgeons to realize that patients can present with these findings without primary pulmonary symptoms, and that severe pulmonary symptoms, elevated INR, and spontaneous hemor- rhagic presentations is associated with increased risk for mortality.
Biography:
Dr. David Altschul, MD: Chief of Cerebrovascular Neurosurgery, Leo M. Davidoff Department of Neurological Surgery at Montefiore Medical Center, Albert Einstein College of Medicine Surgical Director of the Advanced Comprehensive Stroke Center at Montefiore Health System

  • Second Hospital of Hebei Medical University , China
  • Title:Development and Validation of a Predictive Model for The Diagnosis of Neural Antibody-Mediated Epilepsy/ Seizure in Patients with New-Onset Seizure or Established Epilepsy.
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Abstract:
Purpose: Currently, the diagnosis of neural antibody-mediated epilepsy/seizure (NAME/
S)relies heavily on neural antibody testing, which is time-consuming, costly and introduces
diagnostic delays. A statistical tool to predict the probability of a patient with NAME/S is
lacking. We aimed to construct a predictive model to help clinicians expedite the diagnostic
process.
Methods: We retrospectively recruited subjects (206 in the development group and 62 in the
validation group) with new-onset seizures or established epilepsy suspected to have presented
with antibody-mediated seizures between January 2014 and December 2019. We collected
data about demographics, medical history, clinical manifestations and follow up. Binary
logistic regression was used to select potential predictors for the construction of a predictive
model. Five-fold cross and bootstrap validation were applied to avoid overfitting.
Concordance index, calibration plots and decision curve analysis were used to assess its
performance.
Results:The model, incorporating presence/absence of tumour, psychiatric/cognitive/
emotional changes, language disturbances, sensory auras, tonic-clonic seizures, multiple
seizure events, hyponatremia and MRI inflammation, was visualized as a nomogram. The
crude and adjusted concordance indices were both 0.88 with a cut-off value of 0.62,
sensitivity of 83.2% and specificity of 77.4%. The slope and intercept of the calibration curve
were 0 and 1, respectively. The model also showed good performance in the validation group
with a concordance index of 0.82, cut-off value of 0.33, sensitivity of 75.5% and specificity
of 73.1%. The slope was 0.86 and the intercept was 0.039. Decision curve analysis showed
that the model was useful with an optimal threshold probability of >4% in both groups.
Conclusions: Despite limitations such as sample volume and selection bias in subject
enrolment, this model may be used to estimate the individualized probability of having
NAME/S, deserving further exploration and validation.
Biography:
Dr.Wenlin Zhang He is a neurologist with an interest in the study of epilepsies. He work as an attending doctor in the department of Neurology,Second Hospital of Hebei Medical University. He received his Bachelor , Master’s and PhD degree in neurology in China

  • Tel Aviv University, Israel
  • Title:A New Homozygous HERC1 Gain-of-Function Variant in MDFPMR Syndrome Leads to mTORC1 Hyperactivation and Reduced Autophagy During Cell Catabolism.
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Abstract:
The giant 532 kDa HERC1 protein is a ubiquitin ligase that interacts with tuberous sclerosis complex subunit 2 (TSC2), a negative upstream regulator of the mammalian target of rapamycin complex 1 (mTORC1). TSC2 regulates anabolic cell growth through its influence on protein synthesis, cell growth, proliferation, autophagy, and differentiation. TSC subunit 1 (TSC1) stabilizes TSC2 by inhibiting the interaction between TSC2 and HERC1, forming a TSC1-TSC2 complex that negatively regulates mTORC1. HERC1-TSC2 interaction destabilizes and degrades TSC2. Recessive mutations in HERC1 have been reported in patients with intellectual disability. Some patients exhibit epilepsy, macrocephaly, somatic overgrowth, and dysmorphic facial features as well. Here we describe two sisters from a consanguineous marriage with a novel homozygous missense variant in the C-terminal HECT domain of HERC1 [chr15:g63,907,989C>G GRCh37.p11 | c.14,072G>C NM_003922 | p.(Arg4,691Pro)]. Symptoms compris global developmental delay, macrocephaly, somatic overgrowth, intellectual disability, seizures, schizoaffective disorder, and pyramidal tract signs. We functionally assessed the HERC1 mutation by investigation of patient and control fibroblasts under normal and nutrient starving conditions. During catabolic state, mTORC1 activity remained high in patient fibroblasts, which stands in stark contrast to its downregulation in controls. This was corroborated by an abnormally high phosphorylation of S6K1-kinase, a direct downstream target of mTORC1, in patients. Moreover, autophagy, usually enhanced in catabolic states, was down-regulated in patient fibroblasts. These data confirm that the missense variant found in both patients results in a gain-of-function for the mutant HERC1 protein.

  • Institute of Chronic Illnesses, USA
  • Title:A Prospective Longitudinal Cohort Study of Childhood Measles-Mumps-Rubella (MMR) Vaccination and Seizures
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Abstract

Measles is a highly contagious rash illness that was estimated to annually infect about 500,000 Americans with about 1,000 persons developing encephalitis with permanent brain damage prior to routine measles vaccination. Starting in the late 1980s/early 1990s, Measles-mumps-rubella (MMR) vaccination was routinely recommended for administration to American children at 12 through 15 months. A comprehensive meta-analysis by the Cochrane Review examined MMR vaccine safety. It was identified that the onset of febrile seizures was significantly increased from 6 to 11 days post-MMR vaccination in children 12 to 23 months, but post-marketing MMR safety studies were inadequate. As a result, a prospective longitudinal cohort study of children within the Independent Healthcare Research Database (IHRD) was undertaken to examine the onset of new seizures from 6 to 11 days post-MMR vaccination. The IHRD is composed of non-identifiable healthcare records generated from the Florida Medicaid system. A vaccinated cohort of 23,486 children continuously enrolled in the IRHD from birth until 10 years-old, receiving at least one dose of MMR vaccination between 12 through 16 months, and not diagnosed with a seizure prior to their first MMR vaccination was examined. An unvaccinated cohort of 41,725 children continuously enrolled in the IHRD from birth until 10 years-old, receiving no doses of measles-containing vaccines, and were not diagnosed with a seizure prior to 12 months of age was examined. Cox proportional hazards ratio and time-trend models post-MMR vaccination compared to unvaccinated persons and in a self-controlled case-series revealed the incidence rate of an initial seizure episode with onset of symptoms from 6 to 11 days post-MMR vaccination and the incidence rate of an eventual seizure disorder among those with an initial seizure episode with onset of symptoms from 6 to 11 days post-MMR vaccination were significantly increased in all analyses undertaken. About 1 in 3,100 MMR vaccines administered to children from 12 through 16 months were attributably associated with a seizure disorder diagnosis following an initial seizure episode with an onset of symptoms from 6 to 11 days post-MMR vaccination. The observed rate of seizure disorder diagnosis post-MMR vaccination is estimated to be a > 80% reduction as compared to natural measles infection. Further, a recent long-term longitudinal cohort study of American children in the IHRD revealed that childhood MMR vaccination reduced the rate of diagnosed measles by 80% to 90%. On balance, despite the adverse neurological effects post-MMR vaccination, the routine childhood MMR vaccination program in the US is an important and effective means to control natural measles infection, but on rare occasions is associated with an increased risk of seizure disorder.

Biography
Dr.David A. Geier received a BA in biology and a minor in history from the University of Maryland, Baltimore County (UMBC). He undertook graduate studies at the Foundation for Advanced Education in the Sciences at the National Institutes of Health and at the George Washington University. He has coauthored more than 150 publications in academic journals and medical textbook chapters and been an invited presenter at numerous prestigious academic conferences around the world. He was an accredited participant on behalf of the accredited non-governmental organization, CoMeD, Inc, at multiple intergovernmental negotiating committee meetings of the United Nations Environmental Programme to help prepare a global legally binding treaty on mercury, the “Minamata Convention on Mercury”, to help reduce global human mercury exposure and harm. He is the co-founder and currently co-director of the non-profit Institute of Chronic Illnesses, Inc.

  • Institute of Chronic Illnesses, USA
  • Title:A Prospective Longitudinal Cohort Study of Childhood Measles-Mumps-Rubella (MMR) Vaccination and Seizures
  • Time :

Abstract

Measles is a highly contagious rash illness that was estimated to annually infect about 500,000 Americans with about 1,000 persons developing encephalitis with permanent brain damage prior to routine measles vaccination. Starting in the late 1980s/early 1990s, Measles-mumps-rubella (MMR) vaccination was routinely recommended for administration to American children at 12 through 15 months. A comprehensive meta-analysis by the Cochrane Review examined MMR vaccine safety. It was identified that the onset of febrile seizures was significantly increased from 6 to 11 days post-MMR vaccination in children 12 to 23 months, but post-marketing MMR safety studies were inadequate. As a result, a prospective longitudinal cohort study of children within the Independent Healthcare Research Database (IHRD) was undertaken to examine the onset of new seizures from 6 to 11 days post-MMR vaccination. The IHRD is composed of non-identifiable healthcare records generated from the Florida Medicaid system. A vaccinated cohort of 23,486 children continuously enrolled in the IRHD from birth until 10 years-old, receiving at least one dose of MMR vaccination between 12 through 16 months, and not diagnosed with a seizure prior to their first MMR vaccination was examined. An unvaccinated cohort of 41,725 children continuously enrolled in the IHRD from birth until 10 years-old, receiving no doses of measles-containing vaccines, and were not diagnosed with a seizure prior to 12 months of age was examined. Cox proportional hazards ratio and time-trend models post-MMR vaccination compared to unvaccinated persons and in a self-controlled case-series revealed the incidence rate of an initial seizure episode with onset of symptoms from 6 to 11 days post-MMR vaccination and the incidence rate of an eventual seizure disorder among those with an initial seizure episode with onset of symptoms from 6 to 11 days post-MMR vaccination were significantly increased in all analyses undertaken. About 1 in 3,100 MMR vaccines administered to children from 12 through 16 months were attributably associated with a seizure disorder diagnosis following an initial seizure episode with an onset of symptoms from 6 to 11 days post-MMR vaccination. The observed rate of seizure disorder diagnosis post-MMR vaccination is estimated to be a > 80% reduction as compared to natural measles infection. Further, a recent long-term longitudinal cohort study of American children in the IHRD revealed that childhood MMR vaccination reduced the rate of diagnosed measles by 80% to 90%. On balance, despite the adverse neurological effects post-MMR vaccination, the routine childhood MMR vaccination program in the US is an important and effective means to control natural measles infection, but on rare occasions is associated with an increased risk of seizure disorder.

Biography

Dr. Mark R. Geier received a BS in zoology, a PhD in genetics, and a MD from the George Washington University and is a Fellow of the American College of Epidemiology. He was a research scientist in the Laboratory of General and Comparative Biochemistry at the National Institute of Mental Health, National Institutes of Health for 10 years. He was an assistant professor in the Department of Gynecology and Obstetrics at the Johns Hopkins School of Medicine and an assistant research professor in the Department of Psychiatry at the Uniformed School of the Health Sciences. He practiced clinical medicine for more than 30 years. He has coauthored more than 200 publications in academic journals and medical textbook chapters and been an invited presenter at numerous prestigious academic conferences around the world. He was an accredited participant on behalf of the accredited non-governmental organization, CoMeD, Inc, at multiple intergovernmental negotiating committee meetings of the United Nations Environmental Programme to help prepare a global legally binding treaty on mercury, the “Minamata Convention on Mercury”, to help reduce global human mercury exposure and harm. He is the co-founder and currently co-director of the nonprofit Institute of Chronic Illnesses, Inc.

  • University of San Martín, Argentina
  • Title:
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Abstract

Depression affects hundreds of people. Despite its complex etiology, it is accepted that chronic stress is a key factor in its onset. Since stress main effects occur in the brain, an inaccessible area, we focused in detecting stress molecules in peripheral fluids such as blood or saliva. We have shown that the neural glycoprotein M6a can be detected in serum. M6a contributes to the neuronal plasticity promoting neurite and filopodium growth
and synaptogenesis (Alfonso 2004, Brocco 2010, Formoso 2016). Next, we demonstrated that M6a is carried in extracellular vesicles (EVs). EVs are delivered by cells in physiological and pathological conditions, can be isolated from almost all fluids and are used in the diagnosis of several diseases. Then, we showed that M6a-carrying EVs, but not EVs without M6a, induced a phenotypical change in COS-7 cells observed as filopodium formation. This indicates that M6a coupled to EVs might participate in cellular communication and contribute to cellular plasticity maintenance. Since M6a has also been related to several neuropsychiatric disorders, we studied serum M6a levels in chronically stressed animals. We found that stress altered M6a levels in blood. Thus, we proposed M6a as a putative stress biomarker (Monteleone, 2017). Furthermore, using patient saliva samples we showed that M6a levels positively correlated with the scores for the perceived stress scale in individuals diagnosed with depression. This reinforces the idea of M6a as a stress-responsive protein whose levels changes when the individual experiences stress. In addition, saliva samples of depressed patients treated with classic antidepressants (SRI) or with benzodiazepines differed in their M6a levels with respect to untreated patients. This suggests a potential use of M6a for evaluation of antidepressant treatment efficacy (Monteleone 2020). These findings encourage us to continue the study of M6a as a putative stress biomarker and also to determine if EVs can per se be messengers of the stress signal.

Biography

Dr Melisa Monteleone is an Argentinian molecular biologist. She is a researcher from the National Council for Scientific and Technological Research (CONICET) at the Institute for Research in Biotechnology in the Neurobiology of Stress laboratory from the University of San Martin (UNSAM). She obtained her Ph.D. in molecular biology and biotechnology from the UNSAM and received a postdoctoral training with Dr Alberto Frasch in the field of neurobiology. She has centered her research on the role of chronic stress, prenatal and during adulthood, on individual genetics, epigenetics and behavioral alterations and how these effects could be detected in a simple way using extracellular vesicles. She is also a teaching assistant in the B.Sc. career of UNSAM and a member of the B.Sc. student tutoring and mentoring committee.

  • Instituto de Investigation Medica M y M Ferreyra, INIMECCONICET, Argentina
  • Title:PERK Signaling Mediates Neurite Atrophy and Apoptosis in a GM2-Gangliosidosis
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Abstract

GM2-gangliosidosis, a subgroup of lysosomal storage disorders, is caused by deficiency of hexosaminidase activity, and comprises the closely related TaySachs and Sandhoff diseases. The enzyme deficiency prevents normal metabolization of ganglioside GM2, usually resulting in progressive neurodegenerative disease. The Endoplasmic Reticulum (ER) plays a critical role in a variety of cellular processes. A disturbance of any of these functions imposes stress to the ER and subsequently leads to accumulation of unfolded protein in the lumen organelar. This condition activates a signal transduction pathway called the Unfolded Protein Response (UPR) that attempts to restore homeostasis in the ER, but if the stress persists the signaling switches and induce apoptosis. The molecular mechanisms whereby GM2 accumulation in neurons triggers neurodegeneration remain unclear. We found that ganglioside GM2 accumulation in the ER induce decrease in the luminal Ca2+ content. This in turn activate PERK (protein kinase RNA [PKR]-like ER kinase) signaling, one of UPR branches, which shows two phases: one acute,
where the cytoprotective calcineurin is up regulated, and another where is enhanced the expression of pro-apoptotic transcription factor C/EBP homologous protein (CHOP). Moreover, we present evidence showing that pharmacological as
well as molecular modulation of PERK signaling changes the vulnerability of neurons to undergo neurite atrophy and apoptosis.

Biography

Dr . Mariana Bollo graduated as a Microbiologist at the National University of Rio IV,Argentina and obtained her Ph.D. in Biology Sciences at the same University in 2003. Then, she was a post-doctoral fellow in the Department of Physiology, University of Texas Health Science Center at San Antonio (UTHSCSA), USA. She is currently Associate Researcher (Faculty e.q.) of the National Council for Scientific and Technical Research (CONICET), Argentina. Her laboratory focuses on understanding the signaling pathway underlying the calcium regulation of Endoplasmic Reticulum perturbation and its relationship to pathological conditions. One specific area of research is an investigation of the underlying protective mechanisms mediated by Calcineurin β and moderated cytosolic Ca2+ rise after brain injury. A second area of research focused on the role of the unfolded protein response (UPR) in change the susceptibility of neurons to undergo apoptosis in GM2-gangliosidosis.

  • State University of Maringa, Brazil
  • Title:Juvenile Physical and Psychological Stress has Opposite Effects on the Hippocampus of Adult Rats - Unsuccessful and Successful Adaptation
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Abstract

Studies point out that predictable stress models with a short time duration do not lead to a toxic effect, on the contrary, they cause adaptation and can collaborate to elucidate the mechanisms of resilience. This study investigated the long-term behavioral and neuroanatomical effects in two low-stress models (psychological and physical) experienced in the early phase. Male Wistar rats (n=42) were arranged into three groups: Control (C), Physical Stress (Restraint) e Psychological Stress (Predator-Cat). As juvenile (P25 to P27), each group was submitted to the respective stress model, and their behavior was analyzed on P60. The Elevated Plus Maze (EPM) test was used to verify the anxiety-like behavior exhibited by the rats, and Novel Object Preference Task was used to verify their memory in three different instants: after 15 minutes (T1), 24 hours (T2), and 72 hours (T3). On P80, after perfusion, their brains were prepared and the sections were processed to verify the hippocampus volume which were analyzed through the Nissl staining method, and the hippocampus’ dendritic spine in their regions CA1, CA3, and dentate gyrus (DG) was analyzed through Golgi-Cox.
The data obtained in the EPM revealed no effect on exploration in the open and closed arm and anxiety index, thus suggesting resistance to develop anxious behavior in both types of stresses. Regarding their cognitive behavior, there was no significant effect on the rats’ performance in the memory tests, in all tests T1, T2, and T3, therefore suggesting that both types of stresses had no long-term impact.
The neuroanatomical analysis revealed that there was no change in the volume of the hippocampus, this result was obtained by analyzing the surface area of the neurons layer in the regions CA1, CA3, as well as DG. However, the analysis of dendritic spines revealed a pattern of biological responses: while the Physical Stress decreased the dendritic spines’ density, the Psychological Stress increased it, in comparison to the control group. These effects were observed in three analyzed regions, CA1, CA3, and DG hipocampus’. Our data suggest that physical stress has a negative long-term effect, whereas, the psychological stress causes effect considered a successful adaptation, and the next question is answer why.

Biography

Dr.Silvana Regina de Melo (Neuroanatomy- State University of Maringa -Brazil) since 1991,she received the Ph.D in Biological Science from State University of São Paulo (Brazil), a Post-doc position in Neuroscience from University of Lethbridge (Canada), and Philipps-Universität Marburg (Germany).The main research activities are in the fields about brain plasticity relatet to stress and resilience.

  • Gamal Abdel Nasser University of Conakry, Guinea
  • Title:What is the Nutritional Status of your Patients Suffering from Stroke
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Abstract

Strokes can significantly affect the autonomy and the ability of the patient to feed properly. Malnutrition after strokes increases the length of stay in hospital, increases mortality and aggravates disability. Nutritional support is a therapeutic that can be useful in the management of strokes and during the rehabilitation period. It may help to reduce the occurrence of complications due to the physical dependence associated with this condition. The objective of our study was to evaluate, through a questionnaire, the opinion of prescribing doctors working in the Department of Neurology of The FANN National Teaching Hospital in Dakar. The interest of the question resides in the fact that the Center does not have a dedicated nutritionist for inpatients. This was an opinion poll about their concerns about the nutritional status of patients in the therapeutic projects they propose during the stroke. The type of the chosen opinion poll was elementary, type random. The questionnaire was individual and consisted of five items of single-response and multiple-choice questions. The results of this study reveal that while the nutritional status of patients with limited autonomy in the service was a concern in the intentions of the prescribers, in practice it was not taken into account in therapeutic projects. To date, no structured protocol is available in cases of proven nutritional deterioration in patients. Nutritional management must be integrated into the overall management of Neurology patients, particularly in elderly victims of strokes.

  • Guangzhou Medical University, China
  • Title:Electrical status Epilepticus in Sleep Affects Intrinsically Connected Networks in Patients with Benign Childhood Epilepsy with Centrotemporal Spikes
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Abstract

Background: Although outcomes of benign childhood epilepsy with centrotemporal spikes (BECTS) are frequently excellent, some atypical forms of BECTS, especially electrical status epilepticus in sleep (ESES), are characterized by worse outcomes and negative impacts on cognitive development.Methods: To explore specific ESES-related brain networks in BECTS patients, we used resting-state functional magnetic resonance imaging (fMRI) to scan BECTS patients with ESES (n = 9), BECTS patients without ESES (n = 17) and healthy controls (n = 36). Unbiased seed-based whole-brain functional connectivity (FC) was adopted to explore the connectivity mode of three resting-state cerebral networks: the default mode network (DMN), salience network (SN), and central executive network
(CEN).Results: Compared with the other two groups, BECTS patients with ESES showed FC in the SN or in the CEN decreased, but not in the DMN. Moreover, we found the FC in the CEN in BECTS patients without ESES decreased when compared with controls. Our currently intrinsically defined anticorrelated networks strength was disrupted in BECTS and connote greater deactivation than the results from functional connectivity for a seed region in the BECTS children.Conclusion: These results indicated that the BECTS children with ESES showed brain activity altered in the CEN and the SN. The difference of impairment in the SN and CEN may lead to improve understand the underlying neuropathophysiology, and to assess the activity of BECTS patient with ESES, which is crucial for measuring disease
activity, improving patient care and assessing the effect of antiepilepsy therapy.

Biography

Dr.Hongsheng Liu was born in Hubei Province, China in 1972. He received the B.S. degrees in clinical medicine from Tongji Medical University, Wuhan, in1995, the M.S. degrees in imaging and nuclear medicine from China Medical University, Shenyang, in 2003, and the M.D. degree in imaging and nuclear medicine from Southern Medical University, Guangzhou, in 2010. From February to August 2007, he was a visiting scholar, Astrid Lindgrens Children’s Hospital, Karolinska University. From 2011 to 2017, he was director of MRI Department of Guangzhou Women and Children Medical Center. Since 2017, he has been director of Radiology Department of Guangzhou Women and Children Medical Center. He is the editor-in-chief of “Fetal Magnetic Resonance Imaging Diagnostics”, more than 70 articles, and more than 8 scientific research projects. His research interests include gynecology and pediatrics imaging diagnosis, especially in children’s central nervous system, bones and fetus. He held more than 3 national continuing education courses, such as New advances in pediatric neuroimaging diagnosis.He is deputy leader of Gynecology and Pediatrics Group of Guangdong Radiological Society and member of more than 9 societies.

  • Weill Cornell Medical College, Qatar
  • Title:Complementary and Alternative Medicine (CAM ) for Epilepsy Treatment in the Middle East and North Africa (MENA) Region
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Abstract

Introduction
The aim of this study is to provide the reader with a review on Complementary andAlternative Medicine (CAM) treatment in epilepsy in the Middle East and North Africa(MENA) region, describe the extent and factors associated with its use among patients with epilepsy (PWE), and recommend how effectively we will be able to reduce this alarming use .
Material and Methods
Retrospective literature search from 1945 to December 2019, regarding CAM use in the MENA region , using electronic databases (PubMed, Scopus, Google Scholar,Web of Science ) identified pertinent articles for review.
Conclusion
The use of CAM and consultation of traditional healers for the treatment of epilepsy has so far been widespread practice for centuries in the MENA region. Lack of health professionals and non-adherence to conventional epilepsy treatment are strongly associated with the use of CAM. Improvement in the level of knowledge of epilepsy among PWE, healthcare professionals, including traditional healers, will educate PWE and their caregivers on potentially unsafe practices and promote adherence to Antiseizure Drugs (ASDs). Additionally, randomized controlled trials are needed to study the role and value of various CAM treatment options in PWEs

Biography

Dr Boulenouar Mesraoua is Consultant Neurologist at Hamad Medical Corporation at the Neuroscience Department at Hamad Hospital and also Associate Professor of Clinical Neurology at Weill Cornell Medical College Qatar. He graduated as a Medical Doctor from the University of Oran, Algeria. He then moved to Belgium, the City of Liege, for a Residency in Internal Medicine and Neurology at Liege University. After getting the Belgian Board of Neurology (with high marks),he went to the National Hospital for Nervous Diseases, Queen Square, London,United Kingdom, for a fellowship in Clinical Neurophysiology, under Pr Willison, He had also further training in Epilepsy and Continuous EEG Monitoring for two years in the Neurophysiology department of Zurich, Switzerland under late Pr Hans Gregor Wieser, an internationally known clinical epileptologist. He was until recently Director of the Neurology Fellowship Program at the Neurology Section and is an active member of the Comprehensive Epilepsy Program at Hamad General Hospital, Doha, Qatar. He is also Assistant Director of the Residency Program at the new Qatar Medical School. His main interests are Epilepsy, Multiple Sclerosis and Clinical Neurology. He is the Chairman and the Organizer of the well known Qatar Epilepsy Symposium. He is running yearly for the past 14 years and which is considered a landmark in the Gulf region. He has also started last year, together with other epileptologists from Qatar and the region and elsewhere, a yearly International Epilepsy School Course,which was attended by many neurologists from the Area. Both scientific events are under the umbrella of the international League against epilepsy (ILAE) and the Eastern Mediterranean Region (EMR). Internationally he is an active and elected member of the Commission on Eastern Mediterranean Region(EMR)a regional branch of the International League Against Epilepsy (ILAE), where he represents the Middle East and North Africa(MENA ) and where he hold the position of chief of the Epilepsy Epidemiology Section.He is a member of the American Academy of Neurology, the Europeen Academy of Neurology and the American Epilepsy Society. His main objectives are to encourage frequent gathering of the epileptologists/neurologists from the MENA region and the rest of the world , promote Epilepsy Teaching in the MENA Region, and encourage multicenter studies involving neurologists and epileptologists in the MENA region, particularly epilepsy epidemiological studies. He is the recipient of two research Grants, as the Lead Principal Investigator (750.000 USD and 250.000 USD) from the Qatar National Research Fund (QNRF) and the Hamad Hospital Internal Research Grant (IRGC), on the following topics : “Continuous EEG Monitoring in the ICU “ and on “Alpha-lactoalbumin , proof of concept in the treatment of epilepsy”.He is the author and co-author of many peer reviewed publications and four book chapters in the field of Epilepsy and Clinical Neurology.