5^th World Congress on Neurology and Therapeutics March 14-16, 2016 London, UK

Biography:

Geoffrey Burnstock completed his PhD at King's College and University College London. He was head of the Department of Zoology, Melbourne University (1964-1975) before moving to London to head the Department of Anatomy and Developmental Biology, UCL until 1997. He is currently the President of the Autonomic Neuroscience Centre, University College Medical School, UK. He is a Fellow of the Australian Academy of Sciences (1971), Royal Society (1986) and Academy of Medical Sciences (1998). He was awarded the Royal Society Gold Medal (2000) and has over 1520 publications and an H-index of 135.

Abstract:

The concept of purinergic neurotransmission (i.e. neurally released ATP acting as an extracellular signaling molecule) was proposed in 1972. Later it was recognized as a co-transmitter in most, if not all, nerves in the peripheral and central nervous systems, acting on post- and also pre-junctional membranes, at autonomic neuro-effector junctions and ganglionic and central synapses. ATP and its breakdown product adenosine also act as trophic factors during development and regeneration. Brief background information is given about ATP storage, release and ecto-enzymatic breakdown. Purines and pyrimidines have key roles in neurotransmission and neuro-modulation, with their effects being mediated by P1 (adenosine), P2X ion channel and P2Y G protein-coupled receptors. There is coverage of neuron-glia interactions and of purinergic neuro-effector transmission to non-muscular cells. Purinergic mechanisms and specific receptor subtypes have been shown to be involved in pathological conditions, including brain trauma and ischemia, epilepsy, visceral and neuropathic pain, neurodegenerative diseases associated with neuro-immune and neuro-inflammatory reactions, as well as neuropsychiatric diseases, including depression, anxiety and schizophrenia. Specific purinergic receptor subtypes, notably A2A, P2X4 and P2X7 are being explored as therapeutic targets for the treatment of these conditions.

Biography:

Shao-Jun Tang completed his PhD from the University of Toronto in Canada in 1998 and Post-doctoral studies from the HHMI/California Institute of Technology in USA in 2001. He is currently the William Willis Jr. MD PhD Distinguished Professor in Neuroscience and the Director of Neuroscience Graduate Program in the University of Texas Medical Branch

Abstract:

Neuropathic pain is a common neurological disorder in HIV-1/AIDS patients. Current therapies for HIV-associated neuropathic pain are largelyineffective. Multiple etiological factors may contribute to the pathogenesis of this pain syndrome, including HIV-1 infection and antiretroviral medicine. Analysis of the pain neural pathway in postmortem tissues of HIV-infected patients leads to identifying specific neuropathologies that may causally link to pain development in the patients.We are interested in understanding the pathogenic mechanism for the ultimate development of rationale-based therapeutic approaches. Our work has been focused on identifying the HIV-1 pathogenic factor and elucidating the molecular and cellular processes through which the factor causes neuropathic pain. We have undertaken an interdisciplinary approach in this research, including analyzing postmortem nervous tissues from HIV-1/AIDS patients, generating clinically relevant rodent models, and determining the molecular, cellular, behavioral and electrophysiological abnormalities in the model. Our results indicate that HIV-1 gp120 is a relevant viral factor for the HIV neuropathic pain. We also identify that that Wnt signaling in the pain neural circuit plays a key role in mediating the activity of gp120 to cause major neuropathologies of HIV-associated pain such as neuro-inflammation, astroglial reaction and neuropathy.Our studies may provide novel insights into the molecular, cellular and circuitry mechanisms of HIV-associated neuropathic pain.

Biography:

Dr. Ramel Carlos has been working as a neurologist in the Island of Guam for the past 13 years. He completed his Neurology residency and Epilepsy and Clinical Neurophysiology fellowship training at Wake Forest University, Winston Salem, North Carolina, USA. Noel Bien Carlos is currently a Neuroscience student at the University of Southern California in Los Angeles, California. He is actively involved in clinical and laboratory research.

Abstract:

The risk of cardiovascular and cerebrovascular diseases, as well as neurodegenerative diseases such as dementia and Parkinson disease (PD) increases with aging. Numerous researches have shown that these vascular diseases may be influential in increasing the risk of developing neurodegenerative diseases. This study aims to determine the occurrences of vascular diseases in patients with dementia and PD in the Island of Guam. This is a retrospective review of medical records of patients in the only Neurology Clinic in Guam with the diagnosis with dementia and PD from August 2006 to December 2014. There were 348 patients with dementia and 206 patients with PD. The mean age of diagnosis for patients with dementia is higher for both genders than PD patients. There were more females (60%) diagnosed with dementia while more males (61%) have PD. Hypertension, diabetes mellitus, hyper-lipidemia, heart disease and stroke were identified in 76%, 49%, 60%, 30%, and 35% of patients with Dementia, respectively. In addition, Hypertension, Diabetes Mellitus, Hyperlipidemia, Heart Disease and Stroke were identified in 80%, 50%, 58%, 21%, and 29% of patients with PD, respectively. There is an increased occurrence of various vascular diseases in patients with dementia and PD in Guam. It is recommended to optimally control these vascular diseases early on at the diagnosis to potentially prevent progression of neurodegenerative diseases. It is also recommended to implement an awareness program in Guam to educate the public in prevention and treatment of vascular diseases, which are highly prevalent in neurodegenerative diseases.

Biography:

Suzanne L Tinsley received her PT degree from Texas Woman’s University and earned her PhD in Neuro-pharmacology from Louisiana State University Health Sciences Center. She received her Board Certification in Neurologic Physical Therapy from ABPTS. She has been on faculty at LSU-Health since 1988 and currently holds the position of Associate Professor. She has published a Pharmacology Text book for physical therapy education. She has an active clinical research program in the area of neurological rehabilitation. She has presented her clinical and basic science research in state, national and international scientific forums.

Abstract:

Individuals that suffer from neurological deficits often experience foot drop and knee instability during gait, related to a lack of active control of lower extremity muscles. These impairments combined, significantly hinder gait activity and may place the individual at an increased risk for falls. In order to compensate, individuals will often develop compensatory movements that often produce a greater energy cost. Common solutions for foot clearance and knee instability are the use of an ankle-foot orthosis (AFO) and/or functional electrical stimulation (FES) on lower extremity musculature. Advancements in technology have produced FES systems for the lower extremity that can produce a functional gait cycle. This descriptive study evaluates the BioNesss L-300 Plus® system effectiveness for individuals with neurological gait deficits. Two participants with neurological impairments, using a repeated measures within-subject design, took part in one session of motion analysis data collection measuring joint angles at the hip, knee and ankle. The resulting joint angles were compared during 4 phases of the gait cycle in three different environments: without FES, with BioNesss L-300® (calf only), and with BioNesss L-300 Plus® (calf and thigh). Study results indicate improved joint angles and more activity in hip musculature with the using the BioNesss L-300 Plus® system for both participants as well as immediate improvements in gait speed. These findings indicate a possible improved and more efficient gait pattern, as well as more appropriate joint angles in all phases of the gait cycle by utilizing both the BioNesss L-300 Plus® system

Biography:

Dr. Gratwicke qualified in medicine from the University of Oxford, and undertook post-graduate training in neurology at the National Hospital for Neurology and Neurosurgery in Queen Square, London. He is a practicing neurologist both at NHNN, Queen Square and St. George’s Hospital in south London, with specialist interests in movement disorders, dementia and neurodegenerative diseases. He is concurrently completing a PhD at UCL’s Institute of Neurology where he works within the Unit of Functional Neurosurgery, delivering both a specialist academic and clinical DBS service to patients. He has published a number of highly cited papers in reputed journals discussing cognitive network dysfunction in dementias and the use of cognitive neuromodulation as a therapy to counter this.

Abstract:

Dementia remains one of the major challenges facing western society with an estimated 80 million people due to be affected by 2040. Despite this only a handful of modestly effective symptomatic therapies exist. Recent trials of pharmacologic agents aimed at reducing aggregation of pathogenic proteins have proved ineffective, likely because of the heterogeneity of the genetic and molecular pathology underlying dementia syndromes, and novel approaches are therefore needed. Brain stimulation therapies can avoid these difficulties by modulating the disease process downstream at the neural network level, aiming to restore cognitive processing patterns and thereby relieve symptoms. In this presentation I will discuss how improved understanding of cognitive brain networks can be harnessed for development of novel brain stimulation therapies for dementia, with a particular focus on the use of deep brain stimulation. I will cover both basic scientific and clinical aspects of this approach, and discuss the results of two clinical trials recently completed in our unit. I will also look to the future and discuss how cognitive neuromodulation can be advanced further through improved understanding of brain functioning, from both empirically driven and computationally driven approaches.

Biography:

Sybille Krauß studied biotechnology at the Technische Fachhochschule Berlin until 2002. As graduate student she worked at the Max Planck Institute for Molecular Genetics and received her PhD in 2005. After this, she conducted research as postdoc at the Charité in Berlin in the group of Prof. Susann Schweiger. Since 2010 Sybille Krauß is groupleader at DZNE in Bonn.

Abstract:

Polyglutamine diseases are monogenic diseases that are caused by elongation of CAG repeat motifs translating into elongated polyglutamine (polyQ) stretches on the protein level. Aggregation polyQ proteins in the central nervous system of patients is a hallmark of polyQ diseases. Based on the neurotoxic function of these proteins produced from expanded CAG repeats, a reduction of these proteins will be beneficial in the disease context. In line, reduction of polyglutamine protein in disease models for polyglutamine diseases improved the disease phenotype. But how is the protein synthesis rate from expanded CAG repeat mRNAs regulated? One mechanism that we have recently identified to play a role in regulating the translation of huntingtin (HTT) mRNA with expanded CAG repeats involves the MID1-PP2A complex. Mutant HTT mRNA binds to a protein complex containing the MID1 protein, the catalytic subunit of protein phosphatase 2A (PP2Ac), and 40S ribosomal S6 kinase (S6K) in a CAG repeat length-dependent manner. Strikingly, binding of the MID1 protein complex to mutant HTT mRNA results in an increased translation and subsequently aggregation of mutant HTT. Interestingly, this sequestration of MID1 to expanded CAG repeats does not seem to be limited to mutant HTT mRNA, but is also seen on other mRNAs with expanded CAG repeats such as mutant ATXN3. This makes the MID1-RNA-protein complex a very interesting target to prevent formation of pathological accumulations of mutant polyQ protein in polyQ disorders.

Biography:

Dr Oliver Tolson completed his medical degree at Newcastle University Medical School, following completion of his Masters in Research in 2014. He was awarded a Wolfson Intercalated Award in 2013 to fund this research into fatigue and autonomic dysfunction in multiple sclerosis.

Abstract:

Background: Fatigue is a common debilitating symptom of multiple sclerosis (MS) but its pathophysiology remains poorly understood. Recent studies in a variety of diseases have shown dysfunction of the cardiovascular autonomic nervous system correlates with fatigue severity. Objectives: To investigate the prevalence of fatigue and orthostatic intolerance in a representative MS cohort. To objectively assess fatigued secondary-progressive patients for cardiovascular autonomic dysfunction. Methods: Fatigue severity and orthostatic intolerance were measured using validated questionnaires in 144 patients (85.2% response). Subsequently, 11 fatigued secondary-progressive MS patients underwent objective assessment of resting heart rate variability (HRV) and blood pressure variability (BPV). Results: Fatigue was identified in 74.8% of MS patients, with fatigue severity significantly higher in secondary-progressive patients. Moderate orthostatic intolerance was identified in 54.3% of patients and correlated significantly with fatigue (r=0.49, p<0.0001). Objective assessment revealed significant reductions in low-frequency HRV and BPV in the fatigued secondary-progressive group versus controls. A substantial reduction was seen in low-frequency systolic BPV (33.6% versus 48.9%, p=0.03), an established marker of sympathetic vasomotor function. Furthermore reductions in this parameter correlated significantly with orthostatic symptoms (r=−0.87, p=0.0007) and fatigue severity (r=−0.66, p=0.03). Conclusions: Fatigue severity correlates significantly with increasing orthostatic intolerance. Additionally, fatigued secondary-progressive patients have objective evidence of sympathetic vasomotor dysfunction.

Biography:

Bulent Unay has completed his PhD from Medical School and currently working as Child Neurology Professor in Department of Pediatrics. He had the position of Research Fellow in Epilepsy Center, Children’s Hospital; University of Pittsburgh from 2004 to 2005. He is the Director of Department of Child Neurology. He has published more than 65 peer reviewed medical articles and book chapters on many topics including epilepsy, evoked potentials and cerebral palsy.

Abstract:

Occipital intermittent rhythmic delta activity (OIRDA) may be present either in physiological or pathological conditions. Absence seizures present as brief episodes of staring and unresponsiveness and are characterized by an abrupt cessation of activity and impairment of consciousness. Generalized 2.5–4 Hz spike and wave discharges are electrographic pattern of absence epilepsy. OIRDA occurs usually in children. OIRDA was described in patients with epilepsy, particularly with generalized syndromes, such as absence epilepsy. In this report we present a patient with absence epilepsy who have OIRDA findings in their EEG recording and discussed the clinical importance of OIRDA in children. Posterior slow activity on EEG was initially described in children with behavior problems. Throughout the years, the range of clinical interpretation of this pattern by researchers varied to suggesting non-specific, metabolic, epileptic and structural. 7-year old boy who met the diagnostic criteria for absence epilepsy admitted to epilepsy center of university hospital. Absence was defined based on ILAE classification. OIRDA was defined as intermittent monomorphic rhythmic delta activity with maximal amplitude over the occipital regions ranging from 1-4 Hz. He had one record of awaken EEG where OIRDA was reported and sleep EEG was normal. OIRDA ranged from 1-2 Hz to 2-3 Hz in same record. In previous studies, OIRDA was found in 3-4 % of children. OIRDA may not be associated to structural lesions and was described in patients with absence seizures by Cobb in 1945. Recently (2003) Gullapali and Fountain reported a series of 77 patients with OIRDA and found seizures to be more frequent than in the control group. Some authors consider OIRDA as a good prognosis factor in patients with absences.

Biography:

Hanan Galal Azouz has completed her Doctorate Degree of Pediatrics in 1994 from Alexandria University and PhD of health of children with special needs from Ain Shams University, Egypt. She is Professor and Head of Neuro-pediatrics and Behavioral Pediatrics unit in Faculty of Medicine, Alexandria University. She supervised over 30 researches and shared in adaptation of guidelines for ADHD and ASD in Alexandria. She is a member in ICNA and was the secretary of congress of Egyptian Society of Child Neuro-Psychiatry and Pan-Arab Child Neurology Association. She has published more than 10 papers in reputed journals

Abstract:

Autistic spectrum disorder (ASD) is a neuro-developmental disorder characterized by a behavioral phenotype that includes qualitative impairment in the areas of language development or communication skills, social interactions and reciprocity and restricted repetitive behavior. Normal function of the auditory sensory organs and the central auditory pathways is a prerequisite for the normal development of language. In autism, deficits in language, particularly delays in language acquisition, are the principal early manifestation of the disorder. The range of language abilities varies from total muteness to the use of an apparent grammatically complex language. The auditory profile at different levels of the auditory system in children with ASD and the role of (Central) auditory processing (CAP) disorder as an essential pathology of the autistic disorder or as an associated co-morbidity was studied on thirty children, as well as the correlation between CAP findings and the language delay in these cases. 40% of the children with ASD were hyper-responsive to auditory stimuli according to the Sensory checklist for auditory skills. ABR showed inter-peak latencies (IPLs) I–V and III–V of both ears were significantly prolonged in the ASD group in addition to absolute latency of wave I of the left ear and absolute latency of wave V in right ear were significantly prolonged in the ASD group. The results concluded that (central) auditory processing disorder is an essential pathology of the autistic disorder. Autistic children possess a dysfunctioning or an immature central auditory nervous system at both the brainstem and cortical levels.

Biography:

Natalia Vérez Cotelo has completed her PharmD from Santiago de Compostela University and Post-doctoral studies from Universidad Nacional de Educación a Distancia (UNED) School of Phsycology. She is member of Berbés Group, a Pharmaceutical Research and Education organization. She has published more than 25 papers in reputed journals and has been serving as Pharmacist in National Health Service in Spain.

Abstract:

In Spain, as in other Mediterranean countries, family caregivers play an essential role in caring for patients with Alzheimer’s disease (AD). Given the high demands on caregivers of AD patients, they may experience physical, psychological or social consequences as a result of caregiving. Several factors are associated with the onset of caregiver burden, including the social support available, AD patient’s health, and the place where they live. A cross-sectional study with 175 family informal caregivers was conducted at a community pharmacy and in family caregivers associations in Galicia (Spain). Demographic variables were collected, and the following questionnaires were administered: the Beck Depression Inventory-II, STAI-Anxiety Questionnaire, Zarit Burden Scale, family APGAR scale, and the Duke-UNC questionnaire. The typical caregiver profile consists of a 56-year old women with a primary education who belongs to a functional family. Nearly a half (48%) of caregivers had a high perception of burden, with anxiety in 37% of caregivers and symptoms of depression in 25%. Family caregivers usually went to the same pharmacy (93%), were treated with psychotropic drugs (39%) and interacted with the pharmacist (90%). The caregivers from cities of The Atlantic Ocean zone presented a major level of overload and anxiety that those of the interior of Galicia. The caregiver members of family caregivers associations showed major overload and anxious symptoms that those who aren´t members of any association. The cultural standard, a good familiar function and the social received support act as "protective" factors. This study confirmed that pharmacists can help caregivers finding signs of psychopathology in order to improve their psychological health.

Biography:

Prof. Villa graduated in Biological Sciences (D.Sc.) and in Medicine and Surgery (M.D.); he is Associate Professor of Pharmacology at University of Pavia. His research activities on the cerebral energy metabolism evaluated by the Functional Proteomics and Metabolomics are about the Physiopathology and Pharmacology of the Central Nervous System in experimental conditions of hypoxia, ischemia, hyperammoniemia, hypoglycemia; molecular mechanisms of aging and drugs' interference; the study of Parkinson’s disease and drugs' actions in Dementia, clinical studies on Molecular Medicine and Human Genetics on patients affected by Dementias and Ischaemia. He published 349 total papers (IF about 350) and has been officially invited to 214 Congress since 1993.

Abstract:

Acute ischaemic stroke (AIS) is a leading cause of death and disability worldwide. Its incidence and prevalence increase considerably with age and numbers of patients will grow in the future. AIS is caused by the abrupt occlusion of an intracranial vessel resulting in reduced blood flow to the brain region supplied. The ischemic core (which is irreversibly lesioned) is surrounded by the penumbra region with less severe flow reduction, lower functional impairment and potential recovery; so, the fundamental treatment of AIS relies on prompt recanalisation and reperfusion of the threatened ischemic penumbra, that however is potentially salvageable. With this aim, intravenous thrombolysis with recombinant tissue plasminogen activator (rtPA) remains the current strategy. However, thrombolysis is underused, owing to various exclusion criteria that limit the number of treated patients. Other thrombolytics are under investigation. Endovascular therapy with mechanical recanalisation devices is increasingly applied; moreover, hypertension and hyperglycemia are acute complications to be treated in AIS. Our study analyzes the current status, the problems, the perspectives of the pharmacological therapy for AIS.

Biography:

Abstract:

Background: Impairment in cognitive functioning and motor activity are commonly encountered in patients affected by multiple sclerosis (MS). Objective: To investigate the effect of enhanced environment on cuprizone mouse model of demyelination. Methods: C57BL/6 male mice were divided into cuprizone only (Cup-O), cuprizone housed in EE (Cup-EE) and control groups (9 to 10 per group). Environmental enhancement continued for a period of nine weeks. Neurobehavioral tests were conducted after a six-week period of 0.2% cuprizone-enriched diet. All mice were assessed for cognitive performance in the Morris water maze, motor function in rotarod and exploratory behavior in open field test. Results: Cup-EE performed significantly better in fields of spatial learning and memory and motor functioning when compared to Cup-O as evident by Morris water maze (p<0.001) and rotarod (p<0.05) results. Open field test results failed to show an anxiety-like behavior in cuprizone mouse model. Conclusion: Environmental enhancement can improve MS-associated cognitive and motor deficits. Insights gained from these results facilitate the exploration of non-medical modes of intervention as an emerging adjuvant therapy in MS.

Biography:

Dr. Wang is Director of Neuroapoptosis Drug Discovery Laboratory, Department of Neurosurgery, Brigham and Women’s Hospital/Harvard Medical School. Dr. Wang received her PhD from Hebrew University of Jerusalem. She did her postdoctoral training at University of Michigan and Harvard Medical School. Dr. Wang has published about 80 peer-reviewed articles and has served as the Guest Editor, Executive Associate Editor-in-Chief, Handling Editor, and Editorial Board Member for a number of peer-reviewed journals, as well as the scientist reviewer for institutes or foundations including NIH, DOD, BSF, and others, and invited reviewer for 41 peer-reviewed journals.

Abstract:

Inappropriate activation of the cell death program drives the progression of amyotrophic lateral sclerosis (ALS) and Huntington’s disease (HD), as well as increases damage from ischemic stroke. Pharmacological and genetic interventions that inhibit caspases have been shown to slow neurodegeneration in animal models of these chronic illnesses and to lessen the impact of acute brain injury. As in other cells, most physiological pathways leading to cell death include changes in the integrity of mitochondria. Release of mitochondrial cytochrome c into the cytoplasm, often as a consequence of the mitochondrial permeability transition, links upstream events in cell death pathways to activation of capsases that ultimately destroy the cell’s vital structures. Consequently, blocking the release of mitochondrial cytochrome c is the promising strategy to prevent the pathological death of motor neurons, striatal and cortical neurons that cause ALS, HD, and brain injury. We have selected several promising compounds for their ability to prevent cytochrome c release from mitochondria in cultured neurons, drug candidates including melatonin, N-acetyl-L-tryptophan, and N-acetyl-serotonin. Subsequent experiments have shown that these potently neuroprotective agents all exhibit anti-apoptotic activity when used to treat cultured neurons and that they decrease the impact of ALS in mSOD1G93A transgenic ALS mice, or HD in R6/2 transgenic strain whose syndrome resembles HD, or the middle cerebral artery occlusion (MCAO) in C57BL/6 mice that models stroke. The findings may suggest these therapies to be tested in human ALS, HD or stroke patients.

Biography:

The pathogenesis and management of intractable epilepsy (IE) remain a challenge to neuroscientists even today. Electrical stimulation techniques like vagal nerve and deep brain stimulations have assumed significant role as adjunctive therapies. The author postulates pedunculopontine nucleus (PPN) stimulation as an adjunctive therapy in IE, essentially based on the strong antiepileptic property of rapid eye movement (REM) sleep controlled by acetylcholine neurons (AChN) in the PPN, the stimulation of which is found to induce and enhance REM sleep. Even the severe EEG abnormalities (hypsarrhythmia) in West syndrome (WS) disappear during REM sleep; furthermore, in autopsy examination of cases of WS, the number of AChN in PPN in particular have been found to be reduced with relative preservation of other neurons, suggesting a specific involvement of AChN in epileptogenesis. Adrenocorticotrphic hormone is believed to decrease intractable spasms in WS not only through hypothalamo-hypophyseal-adrenal axis but also through a direct action on the pontine tegmentum probably via REM sleep and the anticonvulsant, lamotrigine, is also found to block alpha4beta2nAChRs-mediated currents. Therefore, PPN stimulation is postulated for inducing and enhancing the genesis of REM sleep throughout the night sleep time that is composed mainly of non-rapid eye movement fraction during which the susceptibility to seizure generation and occurrence is known to be enhanced. Involvement and functioning of the PPN in locomotion have formed the basis of its stimulation in controlling gait impairment in Parkinson’s disease. Based on the novel technique, a patent-application has been filed in the United States Patent and Trademark Office.

Abstract:

The pathogenesis and management of intractable epilepsy (IE) remain a challenge to neuroscientists even today. Electrical stimulation techniques like vagal nerve and deep brain stimulations have assumed significant role as adjunctive therapies. The author postulates pedunculopontine nucleus (PPN) stimulation as an adjunctive therapy in IE, essentially based on the strong antiepileptic property of rapid eye movement (REM) sleep controlled by acetylcholine neurons (AChN) in the PPN, the stimulation of which is found to induce and enhance REM sleep. Even the severe EEG abnormalities (hypsarrhythmia) in West syndrome (WS) disappear during REM sleep; furthermore, in autopsy examination of cases of WS, the number of AChN in PPN in particular have been found to be reduced with relative preservation of other neurons, suggesting a specific involvement of AChN in epileptogenesis. Adrenocorticotrphic hormone is believed to decrease intractable spasms in WS not only through hypothalamo-hypophyseal-adrenal axis but also through a direct action on the pontine tegmentum probably via REM sleep and the anticonvulsant, lamotrigine, is also found to block alpha4beta2nAChRs-mediated currents. Therefore, PPN stimulation is postulated for inducing and enhancing the genesis of REM sleep throughout

Biography:

Dr Harinder Jaseja has worked as Professor in Physiology in G R Medical College, India and is presently consultant to Vellore EEG Center, Gwalior, India. Ranked Second in Epilepsy Research in India, he has published novel guidelines for management of patients with cerebral palsy. He has also published pedunculopontine nucleus stimulation (PPNS) as a novel adjunctive therapy and an innovative strategy for selection of deep brain stimulation parameters (DBSPs) in patients with intractable epilepsy. He has filed patent applications separately for PPNS and DBSPs selection-mode. He has published more than 70 international papers and is member of several editorial boards.

Abstract:

Deep brain stimulation (DBS) of anterior thalamic nucleus (ATN) is establishing as an effective adjunctive therapy for patients with intractable epilepsy (IE) not suitable for epilepsy brain surgery and/or vagal nerve stimulation. The judicious selection of DBS parameters (DBSPs) plays a crucial role in the success of ATN-DBS. Conventionally, DBSPs are selected by trial and error requiring multiple sessions and hospital visits warranting a strong need for optimization of the DBSPs with objective assessment of its effects. The author presents an EEG-guided novel and superior approach to the selection of effective DBSPs targeted to induce EEG-desynchronization, which is known to exert potent antiepileptic influence with possibly possession of an additional anti-kindling effect that can suppress or even arrest the ongoing process of epileptogenesis in the patients with intractable epilepsy in addition to exercising control over the intractable seizures. It is further claimed that the innovative EEG-guided approach can successfully optimize the DBSPs resulting in (a) minimum sessions of DBSP adjustments reducing the frequency of hospital visits (b) minimum side effects and (c) minimum consumption of the device battery thus prolonging its life. Preliminary results of the clinical application of the novel approach in the selection of the DBSPs in a small case series have been very promising and encouraging despite which it is strongly recommended that well designed large sized studies are required for its validation and successful clinical outcome. An application for patenting the novel approach has been filed in the United States Patent and Trademark Office.

Biography:

Syeda Nadia Nadeem is 24 years old and completing final year of medical school at University of Liverpool. She is has a strong interest in neurology, especially stroke medicine and most recently worked alongside acclaimed stroke consultants at the Walton Centre, Liverpool. She is also a representative of the Neurology Society in Liverpool and has taught numerous medical students on the topic of stroke and neurology .

Abstract:

Background: Acute ischaemic stroke is the second leading cause of death worldwide. It creates a massive burden not only on the patients’ life but society as a whole. There has been many advancement in stroke management over the past few decades but 2015 has shown giant leaps in this. Up till now, thrombolysis was the main stroke treatment but recently several randomised controlled trials have emerged to demonstrate the efficacy behind using thrombectomy and how it will lead us into the future by treating ischaemic stroke quicker and more effectively than ever before. Aim: To perform a systematic review of the new trials, which compare thrombectomy to best medical care. Furthermore, to critically analyse the current thrombectomy guidelines across UK and Europe in order to develop a thrombectomy best practice protocol, which can be used as a guide worldwide. Method: Numerous articles which highlight the use of thrombectomy compared to thrombolysis alone in acute ischemic stroke were reviewed. Most recent UK and Europe guidelines for thrombectomy use were compared and critically appraised. Results and Conclusion: Results show that thrombectomy used with thrombolysis reduces mortality rates, and improves patients’ functional independence and vessel reperfusion rates significantly from 37% to 100% compared to thrombolysis alone. Current European recommendations complies with these results and forms relevant guidance, whereas, the UKs guidelines are incompatible, lacking structure and recent evidence. As a result, this review has created a new protocol which encompasses the trial results and European recommendations, in the hope to assist physicians worldwide.

Biography:

Abstract:

Forty-two albino male rats aged between 30 and 40 days (weighted 200 g to 250 g) were used in the present study. The left sural nerves of 36 rats were subjected to crush injury at 1 to 6 weeks intervals using 6 animals at each interval. The right and left sural nerves of the rest 6 rats were used as a control. After 2 weeks of the crush injury, the endoneurium showed channel-like spaces that were lined by the collagen bundles with fibroblast-like cells processes. These channels contained degenerated myelin and were connected with the subperineurial spaces. Some of the flattened fibroblast-like cells were arranged in several layers in the subperineurial space, forming barrier-like cellular sheets localizing the endoneurial edema in these spaces. Fibroblast-like cells also wrapped the regenerating nerve fibers by their branching cytoplasmic processes. At the end of the third week, the flattened fibroblasts formed nearly continuous sheets in the subperineurial space. Macrophages were frequently noticed between these cellular barrier-like sheets and in the subperineurial and perivascular spaces. Conclusion: it could be concluded that the endoneurial fibroblast-like cells form barrier-like cellular sheets that localized the endoneurial edema in the subperineurial space and create also the endoneurial channel-like spaces containing degenerated myelin and endoneurial edema helping the resolution of such edema.

Biography:

Dr. Ferrari graduated with honour in Biological Sciences (BSc) and in Experimental and Applied Biology (MSc); she earned the PhD in Biomedical Sciences and is Researcher at Laboratory of Pharmacology and Molecular Medicine of Central Nervous System (CNS). Dr Ferrari’s researches are about CNS Physiopathology and Pharmacology: (a) the study of drugs’ interference on the energetic state of cerebral tissue in healthy and physiopathological experimental conditions, like physiological aging and cerebral ischemia and recovery; (b) Molecular Medicine and Functional Proteomic clinical studies on patients with a diagnosis of Cerebral Ischemia; (c) experimental studies of pharmacological effects of antidepressants on brain energy metabolism. This scientific research activity is documented by 36 publications (IF about 46.5).

Abstract:

Stroke is the third cause of death worldwide and the main cause of chronic, severe adult disability. The current therapy aims at restoring cerebral blood flow within a narrow time window in order to prevent damaging the penumbra which surrounds the infarct core. Intravenous thrombolysis remains the fundamental treatment worldwide, though not ideal for various restrictions and complications limiting to 10% or less the percentage of patients treated within the appropriate time window. Neuroprotection is an alternative or adjunct approach to thrombolysis, targeting cerebral parenchyma in the acute ischemic phase. In the past decades, the efficacy and safety of numerous candidate neuroprotective agents were shown in various animal stroke models. However, in clinical trials, promising pre-clinical studies have not been translated into positive outcomes. Our study analyze the possible reasons for this failure and the new approaches and recommendations to overcome it, as well as novel strategies targeting additional events in ischemia cascade. Finally, the neurorepair strategy will be described with special emphasis on the role of cell-based therapies and ischaemic conditioning.

Biography:

Abstract:

Background and Objective: Depression is a common disabling symptom of multiple sclerosis (MS) with a lifetime prevalence of 50%. The aim of this study is to investigate the impact of induced depression on cuprizone mouse model of demyelination. Methods: Mice were divided into cuprizone with no intervention (Cup-O), cuprizone undergoing induced depression (Cup-Dep) and control groups (9 to 10 per group). Depression was induced by repeated open-space forced swim and was implemented 6 days prior to the testing period. Multiple sclerosis was induced by continuously feeding six-week-old C57BL/6 male mice a 0.2% cuprizone-enriched diet. Spatial learning and memory were tested using Morris water maze while rotarod was used to assess motor function. Results: Cognitive and motor deficits were established in cuprizone mouse model of demyelination as Cup-O had worse results than control group in Morris water maze (p<0.001) and rotarod (p<0.05). Induced depression was seen to exaggerate the aforementioned deficits; Cup-Dep showed a significantly declined performance in Morris water maze (p<0.001) and rotarod (p<0.05) in comparison to Cup-O. Conclusion: Depression can further worsen the natural disease course of MS model. Therefore depression-ameliorating measures should be considered as a part of MS management plan based on the results of this study.

Biography:

O. Nuri Ozgirgin is involved in Otology and Neurotology. Currently being the President of European Academy of Otology and Neurotology. His interests are particularly on Vestibular Medicine. He is the Chairman of the Vertigo Academy International and Editor in Chief of the Journal of International Advanced Otology.

Abstract:

Vestibular diagnosis becomes a challenge for many cases. Even the patient history maintains the basic and most important part of diagnosis, we still need further tests. Understanding and evaluating the vestibulo-ocular reflex added considerably to correct diagnosis. Before the application of sophisticated examinations, evaluation of nystagmus, in the Office or bedside gives important clues. However, we shall need sophisticated tests fort he final diagnosis in some cases. Following evaluation by videonystagmography techniques, inclusion of video head impulse tests, vestibulo-evoked myogenic responses will create a new dimension. Within this lecture new techniques of vestibular evaluation methods will be emphasized.

Biography:

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Biography:

James Gratwicke qualified in Medicine from the University of Oxford and undertook Post-graduate training in Neurology at the National Hospital for Neurology and Neurosurgery in Queen Square, London. He is a practicing neurologist both at NHNN, Queen Square and St. George’s Hospital in South London, with specialist interests in movement disorders, dementia and neurodegenerative diseases. He is concurrently completing a PhD at UCL’s Institute of Neurology where he works within the Unit of Functional Neurosurgery, delivering both a specialist academic and clinical DBS service to patients. He has published a number of highly cited papers in reputed journals discussing cognitive network dysfunction in dementias and the use of cognitive neuro-modulation as a therapy to counter this.

Abstract:

Dementia remains one of the major challenges facing western society with an estimated affected people of 80 million by 2040. Despite this, only a handful of modestly effective symptomatic therapies exist. Recent trials of pharmacologic agents aimed at reducing aggregation of pathogenic proteins have proved ineffective, likely because of the heterogeneity of the genetic and molecular pathology underlying dementia syndromes and therefore, there is a need for novel approach. Brain stimulation therapies can avoid these difficulties by modulating the disease process downstream at the neural network level, aiming to restore cognitive processing patterns and thereby relieve symptoms. In this presentation, I will discuss how improved understanding of cognitive brain networks are harnessed for development of novel brain stimulation therapies for dementia, with a particular focus on the use of deep brain stimulation. I will cover both basic scientific and clinical aspects of this approach, and discuss the results of two clinical trials recently completed in our unit. I will also look to the future and discuss how cognitive neuro-modulation can be advanced further through improved understanding of brain functioning, from both empirically driven and computationally driven approaches

Biography:

Sybille Krauß studied Biotechnology at the Technische Fachhochschule Berlin until 2002. As a graduate student, she worked at the Max Planck Institute for Molecular Genetics and received her PhD in 2005. After this, she conducted research as Post-doc at the Charité in Berlin in the group of Prof. Susann Schweiger. Since 2010 she is group leader at DZNE in Bonn.

Abstract:

Polyglutamine diseases are monogenic diseases that are caused by elongation of CAG repeat motifs translating into elongated polyglutamine (polyQ) stretches on the protein level. Aggregation of polyQ proteins in the central nervous system of patients is a hallmark of polyQ diseases. Based on the neurotoxic function of these proteins produced from expanded CAG repeats, a reduction of these proteins will be beneficial in the disease context. In line, reduction of polyglutamine protein in disease models for polyglutamine diseases improved the disease phenotype. But how is the protein synthesis rate from expanded CAG repeat mRNAs regulated? One mechanism that we have recently identified to play a role in regulating the translation of huntingtin (HTT) mRNA with expanded CAG repeats involves the MID1-PP2A complex. Mutant HTT mRNA binds to a protein complex containing the MID1 protein, the catalytic subunit of protein phosphatase 2A (PP2Ac), and 40S ribosomal S6 kinase (S6K) in a CAG repeat length-dependent manner. Strikingly, binding of the MID1 protein complex to mutant HTT mRNA, results in an increased translation and subsequent aggregation of mutant HTT. Interestingly, this sequestration of MID1 to expanded CAG repeats does not seem to be limited to mutant HTT mRNA, but is also seen on other mRNAs with expanded CAG repeats such as mutant ATXN3. This makes the MID1-RNA-protein complex a very interesting target to prevent formation of pathological accumulations of mutant polyQ protein in polyQ disorders.

Biography:

Guy H Fontaine has made 15 original contributions at the inception of pacemakers since early 60s. He has serendipitously identified Arrhythmogenic Right Ventricular Dysplasia in the late 70s. He has published more than 900 scientific papers including 201 book chapters. He was the reviewer of 17 journals in Clinical and Basic Science. He served during 5 years as a Member of the Editorial Board of Circulation. He has been invited to give 11 master lectures of 90 minutes each during three weeks in the top universities of China (2014).

Abstract:

Objective: The purpose of this work was to confirm on a pig model, the previous work performed on a rabbit model (ReSS 2012) to demonstrate induction of both brain and general hypothermia used for the first time in OHCA patient. Material & Method: 8 Landrace pigs 39.4±3.9 kg (mean±SD) were studied under general anesthesia according to the WICCM protocol. Temperatures were measured by thermocouples every minute after each injection: Close to the injector inserted up to the nasopharynx without contact to the posterior wall, in the retrograde jugular vein, in the tympanic area, in the esophagus and in the rectum. After stabilization of temperatures, CO2 regulated at 580 psi (40 bars) was delivered for periods of 10 min. A valid data were obtained from 14 injections. We compared the drops in temperatures recorded until stabilization. In these pigs 2±1.5 injections of CO2 were delivered. In a comatose patient successfully defibrillated CO2 was injected in the fossa nasalis from a bottle of 867ml at 580 psi. Results: The initial 90% drop in temperature was detected after 4.7±1.4 min for tympanic and 9.4±4min p=0.02 for the core temperature. Temperatures recorded from the tympanic/jugular probes were identical P=1. Return to stable temperature was observed in 10-15mn. Esophagus drop in temperature was 23±10°C n=6. The drop in temperature was significantly higher in the tympanic area 0.69±0.4 °C than in the core temperature 0.36±0.15 P=0.02.The amount of extracted calories was 14.9±6.7 kilocalories. The patient recovered with absolutely no neurologic deficit despite 6mn of no flow (1224 calories extracted). Discussion: Core temperature drop was similar to that reported in pigs after nasopharynx PFC evaporation. In our experiments the lowest temperature (-30°C) was recorded, as expected, at the exit point for the gas. Significant decrease in temperature of 26°C in the esophagus was always observed. The patient was treated by pure chance but the result was impressive. Conclusion: This study confirms that CO2 expansion in the nasopharynx is effective for brain and body hypothermia in a pig model and in a fortuitous patient. This new technique which is simple, inexpensive and easy to use opens new vistas for the treatment of OHCA and Stroke which, mixed with oxygen, can be started in comatose patient even before CPR or thrombolysis.