Scientific Program

Conference Series Ltd invites all the participants across the globe to attend 5th International Conference on Brain Disorders and Therapeutics Madrid, Spain.

Day 1 :

Keynote Forum

Eyad Faizo

BG Unfallklinik Murnau, Germany

Keynote: Neuro radio surgery: Where are we now?

Time : 09:30-10:10

Conference Series Brain Disorders 2017 International Conference Keynote Speaker Eyad Faizo photo
Biography:

Eyad Faizo is a certified licensed Medical Doctor specialized in Neurosurgery and spine surgery practicing in Murnau Hospital south Germany. He presented in international seminars, media interviews and conferences in Health Care and education. Member of the Advisory boards in many German medical companies. Member of the German
and European Neurosurgical Societies.

Abstract:

Cyberknife offers an innovative and evidence based treatment alternative for a variety of Neurosurgical tumors both Brain and Spine . Patient movement is automatically detected and corrected up to sub-millimeter accuracy. Using this ultra fast correction technology it is possible to provide high precision radio-surgical treatment of tumors without invasive Operations. Safe, accurate and painfree

Break: Networking and Refreshments Break 10:10-10:30 @ Foyer

Keynote Forum

Drini Dobi

University Hospital Center “ Mother Teresa”, Albania

Keynote: Cerebellar stroke and vertigo syndromes: Similarities and changes

Time : 10:30-11:10

Conference Series Brain Disorders 2017 International Conference Keynote Speaker Drini Dobi photo
Biography:

Drini Dobi graduated as PhD in University of Tirana, Albania in 1992, and has done the specialization course in Neurology from 1994-1998 in University Hospital Centre "Mother Teresa", Tirana Albania. After his specialization, he has done some other minispecialization course for neurorehabilitation in Instituto Carlo Besta, Milano, Italy; San Carlo, Milan, Italy and Don Carlo Gnocchi Milano, Italy and minispecialization course for neurosonology in UHC "Sestre Milosrdnice" Zagreb, Croatia. He has a lot of publications in some medical periodicals and has participated in some of AAN Annual Meetings with his works, EFNS and EAN conferences, with his works too, and some other Neurological Conferences abroad. His Master’s is in Rehabilitation in Parkinson Disease, in 2005 and PhD in Physical Rehabilitation after stroke in 2015. He is also the Member of EAN Scientific Panel of Neurorehabilitation, Scientific Panel of Neurotoxicology, and General Neurology. His field of expertise is in Neurorehabilitation and Stroke.

 

Abstract:

In generally, the symptoms of vertigo syndromes overlap with cerebellar stroke, and approximately 0.7-3% of isolated vertigo have cerebellar stroke. The clinical diagnosis is an important modality, because the computed tomography is 26% sensitive for acute stroke. Vertigo is defined as a pathologic illusion of movement. Most commonly experienced as a spinning sensation, it arises from a pathologic imbalance in the peripheral or central vestibular system. Benign paroxysmal positional vertigo is a distinct condition not typically confused with cerebellar infarction. The paroxysms of intense symptoms lasting less than a minute are defining, as is positional provocation. Meniere’s disease is suspected in the patient who presents with simultaneous vertigo and cochlear complaints. Episodes commonly last a few hours, although they can range from 20 minutes to a few days. Formal diagnosis requires hearing loss documented on audiologic examination on at least one occasion and patients may have normal audiologic examination between episodes. The migrainous vertigo appears to be like an aura that lasts for a few minutes (18%), but for others the vertigo lasts for longer than 24 hours (27%). Physical examination should reveal a normal neurologic examination. Formal diagnostic criteria for migrainous vertigo have been proposed: 1) recurrent episodes of vertigo; 2) a formal migraine diagnosis by I.H.S. criteria; 3) a migraine symptom during the attack (headache, photophobia, or aura) and 4) the exclusion of other causes. Vestibular neuritis is characterized by the acute vestibular syndrome, caused by decreased vestibular tone on one side and reveals a gradual onset. The cerebellar stroke tends to present with the sudden onset of symptoms, usually reaching maximal intensity at once. Vascular risk factors raise the prior probability of disease and the severe ataxia is considered a sign of central vertigo. The direction-changing nystagmus is an important sign of cerebellar stroke.

 

Keynote Forum

Walter Bini

Healthpoint Hospital Abu Dhabi, UAE

Keynote: TBA
Conference Series Brain Disorders 2017 International Conference Keynote Speaker Walter Bini photo
Biography:

Walter Bini has completed his diploma from Westminster School, Simsbury Conn. U.S.A. and got postgraduate degree from Universidad de Zaragoza , Facultad de Medicina, Zaragoza-Spain. Presently since 2014, Middle East Chairman of ISLASS. Active Member and Board Member of numerous international societies , among these : SAS, German Neurosurgical Society, AANS and the Skull Base Study Group. He was Head of Neurosurgery, Sheikh Khalifa General Hospital , UAQ-UAE from 2014-2016. Currently he is Consultant Neurosurgeon, Orthopedic Department, spine section of Lanzo Hospital COF, Lanzo d’Intelvi in Italy and also Visiting Consultant Neurosurgeon, Orthopedic Department of Healthpoint Hospital in Abu Dhabi – UAE

Abstract:

  • Brain Disorders | Neurobiology | Novel Treatment Strategies| Neurodegeneration and Aging Disorders | Analysis, Assessment and Diagnosis
Location: Picasso
Speaker

Chair

Eyad Faizo

BG Unfallklinik Murnau, Germany

Session Introduction

Khin Maung Bo

Northern Lincolnshire and Goole NHS Foundation Trust, UK

Title: Multiple Sclerosis, corpus callosum and bedside test

Time : 11:50-12:20

Speaker
Biography:

Khin Maung Bo is involved in neurorehabilitation for over 20 years. He is a Lecturer (Hon) in Hull York Medical School teaching 4th year medical students in CNS and musculoskeletal blocks. He is doing botulinum toxin injection in spasticity, dystonia and involuntary movement disorders for over 15 years and has done poster and oral presentations in international neurorehabilitation conferences. He is also involved in using functional electrical stimulation (FES) over 10 years and presented regularly in international FES conferences. He is working on developing hypertonic hand monitoring scale.

Abstract:

Demyelination affects highly myelinated structures like corpus callosum (CC). CC is unique in function that it connects right and left hemisphere and it synchronises bimanual or bipedal activities. Affecting CC can disturb synchrony between the two hemispheres and will affect bimanual and bipedal tasks. The aim is to see if speed of clapping (bimanual activity) can reflect the involvement of CC in multiple sclerosis. Consecutive 70 multiple sclerosis patients from outpatient clinics and home visits were tests for bimanual hand function (clapping). Exclusion criteria are upper limb power <3/5 MRC scale, pain, visual impairment, intentional tremors, stroke or cognitive impairment. Study period started from 01.09.2016. Comparison of speed between rapid supination/pronation of left and right hand separately and then clapping of both hands (supination/pronation of each hands alternatively) were conducted. Patients had to do as fast as they could and noticeable slowing of clapping comparing to single hand supination/pronation was taken as a sign slowing down of conduction through CC. 31 patients were excluded, 34 patients showed no noticeable difference, 2 patients were difficult to make conclusions and 3 patients showed definite slowing down in clapping. Positive patients will have difficulties in doing bimanual activities like using two sticks for mobility, typing using keyboard, pushing wheel chair bimanually etc. It is possible to detect CC involvement by doing above bedside test and can be used in rehabilitation setting. Sample size is not large enough and larger studies need to follow to validate the finding.

Gary Sinoff

University of Haifa, Israel

Title: Anxiety and cognitive decline: What precedes what in this intricate model?

Time : 12:20-12:50

Speaker
Biography:

Gary Sinoff is a geriatrician with expertise in psychogeriatrics. He is Clinical Assistant Professor in the Faculty of Medicine, Technion- Israel’s Institute of Technology and senior lecturer in the Department of Gerontology, Faculty of Social Welfare and Health Studies, University of Haifa. His research and teaching are in the areas of geriatric assessment, cognitive impairment, anxiety, depression, research ethics, and death anxiety. He has published, and presented his research both locally and internationally. He is involved in educating students of gerontology, physicians, nursing students, occupational therapists and administrative directors of long-term care institutes. The impact of his work has been recognized both locally and internationally.

Abstract:

Anxiety as a separate disorder was reintroduced into the DSM manuals in 1980 but is now widely recognized as probably the most common mood disorder in the elderly, with a prevalence ranging between 10% to 20%, greater than for depression. The elderly may not meet the full requirements for an anxiety disorder, yet they still experience enough symptoms which can disrupt their daily lives. During the last years, the interaction between neuropsychiatric syndromes and cognition has been widely researched in view of the fact that these symptoms have been reported to accompany memory loss especially in the initial stages of cognitive decline. In fact, anxiety/depression have been reported to not only be a reaction to cognitive decline, but also possible predictors of future cognitive decline. The debate is intensified by studies showing that anxiety and not only cognitive decline have shown an increase in Aβ in the amygdala as well as in the hippocampus. Since cognitive decline now has become a major burden to society, if one could delay the decline by initiating treatment as early as possible, the savings, for both the individual and society, would be significant. Some studies have shown that anxiety is more prevalent in early mild cognitive impairment and subjective cognitive impairment, and may have a predictive value for the future cognitive decline, but the predictive value in the late mild cognitive impairment is still debatable. Anxiety is inter-related and inseparable with loss of memory and has sometimes been shown to be a predictor for the future cognitive decline, shown in studies published by some years ago. Theoretically, this may be explained by Braak and Braak’s staging with changes initially in the entorhinal cortex, spreading to the hippocampus and amygdala and finally to the cortex. This lecture will relate to anxiety in the elderly, its high prevalence, the problems in its detection and especially its interaction with cognitive decline.

Break: Lunch Break 12:50-13:50 @ Nature Restaurant
Speaker
Biography:

Ghazi Daradkeh is a clinical dietitian supervisor in Nutrition & Dietetics department - Al Khor Hospital – Hamad Medical Corporation – Qatar and clinical preceptor of human nutrition program at Qatar University ACEND. He completed his Ph.D. in clinical nutrition and dietetics specifically in traumatic brain injury nutritional status at sultan Qaboos University, Oman, in October 2016. He received his Master’s degree in maternal and child nutrition from faculty of medicine-public health department at Jordan University of Science and Technology Jordan, in 1995 and his Bachelor degree in human nutrition from same university, in 1990. He is a reviewer and editorial board member of the International Journal of Nutrition, Pharmacology, Neurological Diseases (USA), reviewer for British Journal of Medicine and Medical Research (UK) and a member of an International Neuro Society (INS), Australia, Linnaean Society (FLS) UK, and International Society of Antioxidants in Nutrition & Health (INSAH), Diabetes Association (QDA), Qatar and Environmental Friend Center (QEFC), Qatar.

Abstract:

Objective: The aim of this study were to assess the nutritional status and macronutrients adequacy of traumatic brain injury (TBI) patients and controls, attending treatment from a specialized unit in Qatar.

Research Design and Methods: This study was conducted among male (TBI) in-patients admitted in Rumailah Hospital Rehabilitation Unit, Hamad Medical Corporation-Doha, Qatar from August 2014 to June 2015 (21 cases and 21 healthy volunteers). The attendees were consecutive patients with TBI. Demographic variables were solicited via medical records or directly from the attendees with TBI. Anthropometric measurements and dietary intake (24- hour recall) were collected and assessed by the super tracker.

Results: Half of the participants (52.4%) were of age 30 -38 years range. Approximately 23.8% of cases were classified as having ‘mild TBI’ while 28.6% and 47.6% were classified as moderate and severe TBI respectively. In terms of nutritional parameters, three fourth (76.2%) of the cases were at high or moderate risk of malnutrition, 23.8% of cases were underweight, while 66.7% in the normal range and 9.5% were overweight. TBI patients were noted to have a deficiency in energy (30.2%), carbohydrate (43.0%), protein (24.8%), and fiber (54.1%) intake.

Conclusion: Despite the high prevalence of TBI in emerging economies such as Qatar, to our knowledge, there is a dearth of studies examining the nutritional status and its correlates among the TBI population. This study indicates that TBI patients in Qatar are at a high risk of developing malnutrition, and macronutrients deficiency. Therefore, nutritional assessment, intervention, and support are highly essential to improve TBI patient’s health status beyond the brain injury.

Ashutosh Tiwari

Spine & Multispeciality Clinic, India

Title: Nutrition in neurological conditions

Time : 14:20-14:50

Speaker
Biography:

Abstract:

Speaker
Biography:

Maria Silvia Lopez Alonso is a Pre-doctoral researcher at the UCV, 3rd year. Thesis title is Study of Valencia for the practice of Physical Education of the Elderly according to the Vancouver Protocol and obtained Degree in Religious Sciences UCV, Master in Marriage and Family UNAV1, Master’s Degree Education and Rehabilitation of Addictive Behaviors UCV, 2nd course in Psychology at the UCV. Own trademark: “Active Aging for 50 by Silvia López”.

Abstract:

The following study aims to publicise the neurological research work of Jordi Cervós Navarro through some of his conferences, speeches and talks.When Jordi Cervós Navarro - born in Barcelona (Spain) in 1930 - finished his degree in medicine, (1952) he travelled to Austria and Germany to work as a doctor in neurology clinics. Since 1954 he has been an associate lecturer and since 1961, a lecturer in neuropathology at the Free University of Berlin (Germany). From 1968 until 1998 he was a professor of neuropathology at this same university. Cervós, when embarking on his career in Austria, devoted himself to psychiatry, but over time he edged towards neuropathology. As a neurologist, his studies focused on the Metabolic and Degenerative Diseases of the Central Nervous System, of the Cerebellum, Brain Stem, and Spinal Cord (Spinocerebellar Degenerations), disorders of Lipid, Pigment, Protein or Mineral Metabolism or blood-Spinal Cord and Brain Barriers in Health and Disease for example. Cervós has had a prolific career of research and exhibition of his works that has taken him around the world for almost 50 years.

Speaker
Biography:

Mzia Zhvania is a Doctor of Science, Professor at Ilia State University and head of the Department of Brain Ultrastructure and Nanoarchitecture, I. Beritashvii Center of Experimental Biomedicine, Tbilisi, Georgia. She is an author of more than 80 scientific articles, published in reputed journals and the participant of numerous international scientific conferences. Mzia Zhvania permanently organizes international scientific mini-symposiums, concerning different aspects of neuroplasticity, Mzia Zhvania is a board member of two international scientific journals.

Abstract:

The ability of chronic motor deficit to produce alterations on the functioning of the central nervous system has been studied extensively. However, many questions still demand further investigation. Thus, the consequences of such limitation on the brain structure have been described only in a few studies. Moreover, the biggest part of research has been focused on restraint stress, while the effect of mild motor deficit are not well elucidated. In the present comparative electron microscopic study, we examine the effects of 40-day restraint stress and moderate motor deficit on the ultrastructure of limbic, extrapyramidal and neocortical regions of rat brain – the central and lateral nuclei of amygdale, the CA and CA3 hippocampal areas, caudate nucleus and neocortical motor area. Both types of motor deficit produce ultrastructural modifications, however the effects of diverse motor experiences are not the same. Chronic restraint stress produces much more significant pathologies, which are mainly concentrated in the central amygdale nucleus – brain region, which is actively involved in the organization of stress-response. Mild motor deficit produces mainly moderate modifications. They are concentrated mostly in the caudate nucleus, which is actively participates in motor and cognitive functions. In both cases the motor cortex retains almost normal ultrastructure. Therefore, we suggest that chronic motor deficit itself does not alter significantly the architecture of brain. More substantial modifications should produce stress, which often accompanies some forms of motor deficit.

Break: Networking and Refreshments Break 15:50-16:10 @ Foyer

Fiorenza Stagni

University of Bologna, Italy

Title: In the search of safe therapies for Down syndrome

Time : 16:10-16:40

Speaker
Biography:

Fiorenza Stagni obtained her PhD in Biomedical Sciences at University of Bologna, Italy in 2014. She is currently involved as Postdoctoral fellow in an international project aimed at identifying a panel of drugs that may be safely used during pregnancy or in infants in order to counteract the neurodevelopmental defects linked to Down syndrome. In 2016, she was awarded by the Trisomy 21 Research Society for the Best Dissertation in the field of DS defended in 2014-2015. She has published more than 15 papers in the field of preclinical studies for the treatment of cognitive deficits in DS.

Abstract:

No therapies currently exist for intellectual disability in Down syndrome (DS), a relatively high-incidence genetic condition (1:700/1000). Neurogenesis impairment starting from fetal life stages is considered a major determinant of intellectual disability in DS. We have previously shown that perinatal treatment with fluoxetine, an antidepressant, fully restores neurogenesis and cognitive performance in the Ts65Dn mouse model of DS. The finding that these effects were accompanied by an increase in the levels of brain-derived neurotrophic factor (BDNF) suggests that BDNF may be an important determinant of the proneurogenic effect of fluoxetine. This important discovery prompted us to find a therapy that is as effective as fluoxetine but that may pose fewer caveats for clinical application in children with DS. A therapy based on BDNF is impracticable due to its poor blood-brain barrier penetration. However, the naturally-occurring flavone 7,8-DHF is a BDNF mimetic that crosses the blood-brain barrier and binds to the BDNF TrkB receptor. Based on these premises, the goal of our study was to establish whether early treatment with 7,8-DHF can rescue trisomy-linked neurodevelopmental defects, similarly to fluoxetine. We found that neonatal treatment with 7,8-DHF increased neurogenesis and restored neuron maturation in the hippocampus of Ts65Dn mice. Importantly, Ts65Dn mice treated from birth to adolescence exhibited restoration of hippocampus-dependent memory. This study provides novel evidence that treatment with a natural compound 7,8-DHF restores brain development and cognitive performance in a DS mouse model. In view of the safe nature of 7,8-DHF our results, potentially, are readily transferable into clinical practice.

Speaker
Biography:

Farnaz Nikbakht was born in Tehran, Iran, on 8 October 1969. Before obtaining her Ph.D. degree in Human Physiology from Shiraz University in 2007, she received an award from the Iran Ministry of Health and Education and spent six months at Flinders University, Adelaide, Australia for completing her research on degenerative diseases. Now, as the Associate professor of Department of Physiology, in Iran University of Medical Sciences, she has managed several research programs and has conducted the thesis of several Masters and Ph.D. 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 & Purpose: Apigenin, a non-toxic and non-mutagenic flavone, has the potential of free radical scavenging activity. Recent studies revealed the protective effect of apigenin against Aβ neurotoxicity but the underlying mechanism was unclear. The purpose of this study was to reveal the protective effect of apigenin against Aβ 25-35 by inhibition of mitochondrial caspase 9 and cytochrome C release. The ability of apigenin to prevent dynamin-related protein (Drp1) activation and thereby protection against mitochondrial fragmentation and dysfunction was the second goal of this study.

Methods: Aβ 25-35 was microinjected into the left lateral cerebral ventricle. Oral administration of apigenin was started half an hour before the surgery and continued for the following 21 days. After three weeks, the animals were sacrificed and their brains were removed for further histological and molecular processes. Cell death and neurodegeneration was assessed by Nissl and Fluoro Jade B staining in CA1 area of the hippocampus. Cytochrome C and caspase 9 was detected by immunohistochemistry in the same area and Drp1 was detected by western blotting.

Results: The results revealed that oral administration of apigenin protected CA1 neurons from Aβ toxicity (P<0.001 for Nissl and Fluoro Jade B). The protection was associated with a significant decrease in mitochondrial caspase 9 and Cytochrome C release (P<0.01). Drp1 was also significantly decreased in apigenin treated groups (P<0.01).

Conclusion: These data demonstrate that the flavone apigenin protects highly vulnerable CA1 neurons against Aβ toxicity and suggest that it is mediated by amelioration in mitochondrial dysfunction.