Scientific Program

Conference Series Ltd invites all the participants across the globe to attend 5th World Congress on Neurology and Therapeutics London, UK.

Day 3 :

  • General Neurology and Neuropharmacology
Speaker

Chair

Safa Shehab

UAE University, United Arab Emirates

Speaker

Co-Chair

Hui-Chieh Lee

Branch of Kaohsiung Armed Forces General Hospital, Taiwan

Biography:

Safa Shehab has completed his PhD in Sheffield University. He served in several universities in UK including UMIST, Sheffield, Glasgow and Aberdeen before he joined UAE University. He investigates the neuronal circuitry in the dorsal horn of the spinal cord and the neuronal pathways that are likely to be critical in the production and maintenance of the neuropathic pain after peripheral nerve injury. He is also investigating the mechanism of Deep Brain Stimulation. He has published 48 papers in reputed journals.

Abstract:

Rats develop hyperalgesia and allodynia in the hind paw following L5 spinal nerve ligation and transection as seen in human neuropathic pain. Since the skin of the hind paw of the rat is mainly innervated by L4 and L5 nerves, it is assumed that uninjured L4 nerve would be involved in the development of neuropathic pain. Anatomically, we showed that the unmyelinated primary afferents of L5 spinal nerve did not only terminate in the corresponding L5 spinal segment and rather extended to two spinal segments rostrally and one segment caudally where they intermingle with primary afferents of L4 nerve. Subsequently, we demonstrated up-regulations of NPY, VIP and NK1r and down-regulations of SP, CGRP and IB4 binding following L5 nerve injury not only in the dorsal horn of L5 spinal segment where the injured L5 enters, but also extended from L3-L6 spinal segments. To investigate the potential role of adjacent uninjured L4 nerve in heat hyperalgesia, Phosphorylated Extracellular Regulated Kinase (pERK) was used as a pain marker in response to heat noxious stimuli applied to both hind paws following unilateral L5 nerve injury. The results showed that the number of pERK-immunoreactive neurons was significantly higher in the ipsilateral side of L4 spinal segment, which receives innervation from uninjured L4 nerve, compared with contralateral control side which receives both uninjured L4 and L5 spinal nerves. The data demonstrate the role of uninjured L4 nerve in the development of heat hyperalgesia following L5 nerve injury. Two hypotheses on the production and maintenance of peripheral neuropathic pain will be discussed.

Biography:

David Moore is a Post-doctoral research fellow at the Department of Pain Medicine, St James Hospital, Dublin and the Institute of Neurotherapeutics, Dublin City University.

Abstract:

Neuropathic pain poses a significant burden on the individual and society, because of a lack of effective pharmacological therapies. Interventional pain therapies may be more effective in a select cohort of patients. Neuropathic pain results from a lesion or disease of the somatosensory system. Traditionally neuropathic pain was attributed to dysfunctional activity and hypersensitivity of the neuron. However a maladaptive immune response is increasingly recognized as contributing to the maintenance of chronic neuropathic pain. Glial cell activation and altered peptide biosynthesis are implicated in the maintenance of persistent neuropathic pain. Human data suggests that NGF, VEGF and BDNF play a role here. This neuroimmune process is maintained by cellular and neuropeptide biosynthetic responses which become pathological. Intra-thecal opioids and steroids are associated with alterations in cell signaling and the levels of inflammatory mediators at the neuroimmune interface in humans in vivo. Markers of glial and immune cell activity, up-regulated in neuropathic pain states, are down-regulated in spinal cord stimulator patients. Pulsed radiofrequency of the dorsal root ganglion in patients with radicular pain alters CSF lymphocyte subsets and peptide concentrations

Hui-Chieh Lee

Kaohsiung Armed Forces General Hospital, Taiwan

Title: Brown-séquard syndrome: A rare manifestation of decompression sickness
Biography:

Hui-Chieh Lee completed his MD from the National Defense Medical University in 1978 and Undersea Medical Officer Training in Groton USA, in 1979. He had served as the Chief , Dept. of Diving Medicine, Zuoying Naval General Hospital, Taiwan for 10 years and became the President of Hyperbaric and Undersea Medical Association, R.O.C. from 2008 to 2012. Currently, he is the Executive Director of Asian-Pacific Undersea and Hyperbaric Medical Society. He has published 30 papers in the Chinese and International Journal.

Abstract:

Neurological decompression sickness (DCS) is a rare condition that commonly leads to spinal cord injury. We report the case of a 30-year-old man who developed left-sided weakness and numbness after diving to a maximum depth of 15 m with a total dive time of 205 min (10 repetitive dives). To the best of our knowledge, only six cases diagnosed as Brown-Séquard syndrome caused by DCS have been reported in the literature. Divers should be aware of the risk factors of DCS before diving and clinicians should make the diagnosis of spinal cord DCS based primarily on clinical symptoms, not on magnetic resonance imaging findings.

Biography:

Mirjana Djukic has completed her PhD in 2001 at the Faculty of Pharmacy at the University of Belgrade. She became a full Professor of Toxicology in 2012. Her research interest has focused on free radicals-mediated mechanism pathways of drugs/poisonings. Accordingly, on oxidative stress-related topics she introduced an optional subject in the faculty study program (2008); wrote (author and editor) two books; published/presented cc 190 papers and has been reviewing articles to reputable journals. She spent two years in the Center for Free Radical and Antioxidant Health (Prof. Valerian Kagan lab) at the University Pittsburgh, USA (2002/3, 2010/11).

Abstract:

Paraquat (PQ) neurotoxicity has not thoroughly investigated. Redox metabolism of PQ2+, results in superoxide anion radical (O2•ï€­) formation. Consequent free radical reactions escalate due to stable resonance radical structure (PQ•+). The OS/NS-associated neurotoxic pathways of PQ were investigated in striatum of Wistar rats after single intra-striatal administration of PQ+ and applied pretreatments, including: N-nitro-L-arginine-methyl ester (L-NAME); 2-amino-5-phosphonovaleric acid (APV); glutathione reductase (GR) and naloxone. Reversible Parkinson’s disease symptoms were observed in PQ group. Contrary to PQ, APV+PQ and GR+PQ groups, initially high O2•ï€­ reached the normal values in L-name+PQ and naloxone+PQ groups, on 7thday. Superoxide dismutase (SOD) activity declined in L-name+PQ, naloxone+PQ and APV+PQ groups. Initially low SOD activity reached normal values on 7th day in Pq and GR+PQ groups. Lipid peroxidation was the highest in PQ, L-name+PQ and GR+PQ groups. Glutathione (GSH) depletion was considerable in L-name, APV and naloxone pretreated rats across the time. Increased GSH values were achieved in PQ and GR+PQ group on the 7th day. Glutathione peroxidase (GPx) activity was inhibited by GR (within 24 hours) and naloxone; elevated GPx activity declined with the time in APV+PQ and L-name+PQ; while it was high in PQ group until the 7th day. In conclusion, inhibitors of NO-synthase, N-methyl-D-aspartate (NMDA) and opioid receptors, reduced SOD and GPx activities and depleted GSH. Rise of O2•ï€­ occurred in APV and GR pretreated groups (twice higher than in PQ group), on 7th day, although APV did not influence LPO.

Biography:

Abstract:

Dietary omega-3 fatty acids have been recognized to improve brain cognitive function. Deficiency leads to dysfunctional zinc metabolism associated with learning and memory impairment. The objective of this study is to explore the effect of short-term dietary omega-3 fatty acids on hippocampus gene expression at the molecular level in relation to spatial recognition memory in mice. A total of 24 male BALB/c mice were randomly divided into four groups and fed a standard pellet as a control group (CTL, n=6), standard pellet added with 10% (w/w) fish oil (FO, n=6), 10% (w/w) soybean oil (SO, n=6) and 10% (w/w) butter (BT, n=6). After 3 weeks on the treatment diets, spatial-recognition memory was tested on a Y-maze. The hippocampus gene expression was determined using a real-time PCR. The results showed that 3 weeks of dietary omega-3 fatty acid supplementation improved cognitive performance along with the up-regulation of α-synuclein, calmodulin and transthyretin genes expression. In addition, dietary omega-3 fatty acid deficiency increased the level of ZnT3 gene and subsequently reduced cognitive performance in mice. These results indicate that the increased the ZnT3 levels caused by the deficiency of omega-3 fatty acids produced an abnormal zinc metabolism that in turn impaired the brain cognitive performance in mice.

Biography:

Abstract:

Dietary omega-3 fatty acids have been recognized to improve brain cognitive function. Deficiency leads to dysfunctional zinc metabolism associated with learning and memory impairment. The objective of this study is to explore the effect of short-term dietary omega-3 fatty acids on hippocampus gene expression at the molecular level in relation to spatial recognition memory in mice. A total of 24 male BALB/c mice were randomly divided into four groups and fed a standard pellet as a control group (CTL, n=6), standard pellet added with 10% (w/w) fish oil (FO, n=6), 10% (w/w) soybean oil (SO, n=6) and 10% (w/w) butter (BT, n=6). After 3 weeks on the treatment diets, spatial-recognition memory was tested on a Y-maze. The hippocampus gene expression was determined using a real-time PCR. The results showed that 3 weeks of dietary omega-3 fatty acid supplementation improved cognitive performance along with the up-regulation of α-synuclein, calmodulin and transthyretin genes expression. In addition, dietary omega-3 fatty acid deficiency increased the level of ZnT3 gene and subsequently reduced cognitive performance in mice. These results indicate that the increased the ZnT3 levels caused by the deficiency of omega-3 fatty acids produced an abnormal zinc metabolism that in turn impaired the brain cognitive performance in mice.

Biography:

Abstract:

Deafness is the most frequent sensory deficit in humans. The etiology is genetic in about half of the cases worldwide. The most frequent cause of non-syndromic autosomal recessive deafness is an altered connex in 26-protein, a communicating gap junction protein encoded by the gene GJB2. Previous studies included Sudanese and Kenyan patients suggested other causes for hearing impairment other than GJB2. Two Sudanese patients with a prelingual, profound, sensorineural, bilateral, non-syndromic hearing loss were screened for GJB2 using DNA extracted from blood which was followed by PCR and sequencing. The patients had different frame shift mutations that were unreported before

  • Young Researcher Forum
Biography:

Nkemamaka Okonkwo is a Junior Doctor embarking on her Core Medical Training (CMT) in NHS England. She completed her Foundation Training in various trusts across London's North East Thames Deanery and Wales Deanery. Prior to the this, she led student committee projects in conjunction with the Wales 1000 Lives Campaign and the Institute for Healthcare Improvement (IHI) where she is an accredited leader. She supported and pioneered work on issues related to quality improvement and assurance, patient safety and use of retrospective measurement data, real-time monitoring and patient stories to drive overall healthcare improvement.She obtained her medical degree from Cardiff University, an intercalated BSc from Leicester University and is currently studying for an MSc in International Health Management from Imperial College London, where she chairs the BioPharma and Healthcare society.

Abstract:

Background: Temporal artery biopsies (TAB) are often performed in suspected cases of sight-threatening arteritis. The results of which often do little to change clinical management. While the American College of Rheumatology (ACR) formed a clinical classification criterion in 1990 for diagnosing GCA to ensure early steroid therapy was commences, they acknowledge TAB should aim in establishing a definitive diagnosis Aims: The audit aimed to assess if TABs were performed in accordance with the national ACR guideline and whether their results altered course of treatment in suspected GCA. Method: A retrospective audit of all patients undergoing TAB at a single DGH between 2010 and 2014, identified from the histopathology database. Main outcome measures included clinical profile and biochemical criteria associated with positive histology; proportion of negative histology patients who were commenced on steroid therapy; Length of TAB’ relationship between ACR score and TAB result Results: Forty TABs were performed (male: female 1:2, mean age=70.23 years). Three (7.5%) biopsies were histologically positive and 37 (92.5%) were negative. One biopsy was non-arterial. 62.5% of Tabs were performed within the recommended one week of suspected diagnosis. Only 46% of TABs were >1cm. Preoperative steroid therapy was commenced in 80% of patients and a negative histology changed management in 32%. 67.5% had sufficient clinical features to classify GCA and not warrant TAB. Histologically positive TAB patients had higher average age, higher ESR, longer biopsy length and shorter time interval between diagnosis and procedure compared to histologically negative TABs. Conclusion: Raised ESR and higher age may be the most useful diagnostic adjunct of GCA. Many histologically negative TAB individuals were nevertheless clinically diagnosed and managed as GCA. Sub-optimal specimen length may be contributing to lack of diagnostic accuracy. Alternative techniques may be warranted in the near future.

Biography:

Deepa Rani has been working as community health worker and site investigator in Haryana, India for last 3 years. While working in the community, she joined NMP Medical Research Institute and been heading Institute's program as part of lifting the burden compaign, Global Campaign to reduce the burden of headache disorder. She is certified research associate on a multicenteric research study in northern states of India.

Abstract:

Worldwide, headache disorders are among the most common medical conditions.Many people with headache need not experience further pain if the diagnosis and treatment are correct. Most patients do not have correct diagnosis and treatment. This study tested a model for treatment of people with headache disorders at primary health-care level in rural areas of Haryana, India. METHODS: A quasi experimental study with peer education intervention was conducted in selected primary care health clinics. Threee hundred sixty patinets from randomly selected communities of Kaithal, Haryana were assessed through screening questionnaires conducted in pre- and post-intervention periods. Pertinent data on socio-demographic and headache related factors were collected. The statistical packages used for data entry and analysis were epi-info version 3.5.4 and SPSS version 20.0 respectively. RESULTS: When the pre and post intervention data of each group were compared, comprehensive Knowledge of headache (P-Values =0.004) and willingness to go to neurologist for diagnosis and treatment (Pvalue = 0.001) showed significant differences among intervention group during post intervention period. In 68% of patients who completed 12 months' treatment, headache frequency was decreased by at least 60%, and a third of patients were headache free. Medication was well tolerated and reported adverse events were mild; only 36 patients (1%) discontinued medication because of side-effects. CONCLUSION: This study confirmed that this simple protocol was suitable for the treatment of headache disorders in rural areas of India. Physicians and community workers with basic training could diagnose and refere headache patients, with beneficial effects for most patients with treatment.