Shang Fei-Fei, as a PhD candidate of the West China Hospital, has committed to discover the mechanism and treatment with CNS injuries. During his graduate studies, hewas committed to find, through scientific studies, the mechanism of spontaneous functional recovery after spinal cord injury (SCI). His background and expertise ensured the successful completion of some key protein’s molecular mechanism in SCI rats. Some of these results have been published in international journals.

Spinal cord injury (SCI) is a leading cause of injury-related physical disability in human. Although there are no fully restorative treatments, SCI is frequently accompanied by spontaneous functional recovery.Clarifying the mechanisms of this phenomenon could provide a crucial way to treatment the SCI. By using two-dimensional electrophoresis, we found 20 proteins expressed differentially in the caudal cord from SCT (spinal cord transection) 14dpo and 28dpo rats(functional recovery period). Real time PCR and western blotting were performed to further verification foran interesting protein, known as Rho GDI-α. Then lentiviral vectors were used to regulate Rho GDI-αexpression. Compared with normal neurons, Rho GDI-αincreased the neurons’ soma area,neurite length and survival in vitro.In vivo, up-regulated Rho GDI-αshowed a significant rescue for the hindlimb motor function.And the number of regeneration-associated protein neurofilament (NF) was corresponding to Rho GDIαoverexpression and interference. In order to know the mechanism of Rho GDI-α up-regulation, the bioinformaticsand dual luciferase reporterassay confirmed microRNA 124a targeted the mRNA of Rho GDI-α. And real-time PCR also showedmicroRNA 124a was down-regulated in SCT rats’caudal cord. Moreover,regulatedmicroRNA 124a in vitro and vivo results in similar changes to Rho GDIα regulation.These data showed targeting the microRNA 124a might provide a new strategy for improving locomotor functions after spinal cord injury.

Kinga K Borowicz has completed her Ph.D. at the age of 25 years from Medical University of Lublin and received the title of Full Professor of Medicine at the age of 35 years. Her specialties are pharmacology, pathophysiology and internal diseases. She has published 195 papers in reputed journals (IF=191.273). At present, she is the Director of Unit of Experimental Neuropathophysiology, Medical University of Lublin, Poland.

Epilepsy and cardiac arrhythmia were proved to have common molecular background. Furthermore, seizures can dysregulate central autonomic control centers leading to short- and long-term alterations of cardiac rhythm. Sudden unexpected death in epilepsy (SUDEP) has most likely a cardiac mechanism. Common elements of pathogenesis create a basis for the assumption that antiarrhythmic drugs may affect seizure phenomena and interact with antiepileptic drugs. A question arises whether some antiarrhythmic drugs can be effective in adjunctive therapy of epilepsy. The main aim of this study was to evaluate interactions between two antiarrhythmic drugs, presenting different mechanisms of action, and classic antiepileptic drugs in maximal electroshock-induced seizures in mice, the basic screening model of epilepsy. Neurological adverse effects and brain concentrations of antiepileptics were also assessed. Propafenone exhibited biphasic effect on the electroconvulsive threshold. The antidepressant increased the threshold at doses 10-30 mg/kg and 60-90 mg/kg. Additionally, propafenone at doses 2.5-50 mg/kg enhanced the anticonvulsant action of carbamazepine. Effects of valproate, phenobarbital and phenytoin were potentiated by propafenone at higher doses: 40-50 mg/kg, 30-50 mg/kg and 50 mg/kg, respectively. On the other hand, mexiletine behaved as an independent antiepileptic drug with ED50 (50% effective dose) of 11.9 mg/kg. Isobolographic analysis of data showed that mexiletine interacts synergistically with valproate, while additively with carbamazepine, phenobarbital and phenytoin. All revealed interactions seemed to be pharmacodynamic. In conclusion, as far as experimental data can be extrapolated to clinical conditions, propafenone and mexiletine may be considered as potential drugs in adjunctive treatment of epilepsy co-existing with arrhythmias.

Guey-Jen Lee-Chen is a Professor at the Department of Life Science, NTNU, Taiwan since 1999. She has considerable experience in molecular genetic analysis of human genetic disease, including mutation screen and characterization, case-control study of at risk polymorphism and/or cell model studies in spinocerebellar ataxias, Parkinson’s disease and Alzheimer’s disease.

In spinocerebellar ataxia type 17 (SCA17), the expansion of translated CAG repeat in the TATA box binding protein (TBP) gene results in long polyglutamine (polyQ) tract in the TBP protein, leading to intracellular accumulation of aggregated TBP and cell death. The molecular chaperones act in preventing protein aggregation to ameliorate downstream harmful events. In this study, the author used Tet-On SH-SY5Y cells with inducible SCA17 TBP/Q79-GFP expression to test indole and synthetic derivative NC001-8 for neuroprotection. Indole and NC001-8 up-regulated chaperone expression was found to reduce polyQ aggregation in neuronal differentiated TBP/Q79 cells. The effect in promoting neurite outgrowth and reduction of aggregation on Purkinje cells were also confirmed with cerebellar primary and slice cultures of SCA17 transgenic mice. Results demonstrate how indole and derivative NC001-8 reduce polyQ aggregation to support their therapeutic potentials in SCA17 treatment.

Dan Neftalie Juangco is Assistant professor at Institute for Neurosciences St. Luke's Medical Center Quezon City Philippines. His research interests includes stroke and vascular neurology.

Background: Depression following stroke has often been overlooked and is associated with decreased functional recovery and increased mortality. Data regarding its prevention is conflicting. Objective: The objective of the study is to determine if selective serotonin reuptake inhibitors (SSRIs) are effective and safe in preventing post-stroke depression (PSD). Methods: We searched for articles evaluating the efficacy of any SSRI for prevention of PSD. The pooled relative risk (RR) and 95% confidence intervals were calculated. Frequency of side effects was also calculated. Results: A total of 4 articles and 405 patients were included in this study. Our meta-analysis has demonstrated that SSRIs reduced the incidence of PSD (RR = 0.36, 95% CI 0.22-0.60) without significant heterogeneity. Also, the occurrence of adverse effects was not significantly different from that of the control group. Conclusion: SSRIs are beneficial for the prevention of PSD and in doing so, it may increase functional recovery and decrease mortality.

I am the last year medical student at Rafsanjan University of Medical Sciences. I am working for about 4 year at the physiology and pharmacology research center of my university and my main research field was at brain ischemia in rat and new therapeutic methods such as post-conditioning and hypothermia.

Introduction: Both hypothermia and decompressive craniectomy (DC) have been shown to reduce ischemic injury in experimental middle cerebral artery occlusion (MCAO). This study was designed to evaluate the effect of combined DC and direct hypothermia on infarct size and neurological outcome and blood brain barrier (BBB) disruption in a rat model of stroke. Methods: MCAO was performed in 40 Wistar rats assigned to 4 groups. In group A, direct hypothermia (4°C) was induced 6 hour after MCAO for 15 minutes without DC. In group B, DC alone was performed 6 hours after MCAO. Combined DC and hypothermia were performed in group C. No therapy was performed in group D (control). Contralateral temporalis muscle probe was used to monitor the temperature after 15 minutes after direct hypothermia.Infarct size and neurological performance and BBB disruption after 48 hours were used as study end points (groups A through D).BBB disruption in cortex was measured by Evans blue dye leakage. Results: In group A the temperature was 34.2±0.5 and in group C was 32.8±0.5. In group B&D the temperature was not decreased significantly compared to normal temperature. Compared with controls (group D), infarction size was significantly reduced in each three other groups.Neurological performance was significantly improved in group C animals (P<0.05).BBB disruption in DC group was significantly reduced compared to control group (P< 0.05) and also in hypothermia group and combined group (P< 0.01). Conclusions: DC and Temporary direct hypothermia significantly reduces infarction size and decreased BBB disruption in MCAO rats. Combined hypothermia and DC yield significant additional benefits.

Shima Kianifard is PhD student from Rafsanjan University of Medical Science, Iran. As a part of her academic work she researched on common bilateral carotid artery in post conditions of embolic stroke.

Objective(s): It has been reported that ischemic post conditioning, conducted by a series of brief occlusion and release of the bilateral common carotid arteries, confers neuro-protection in permanent or transient models of stroke. However, consequences of post conditioning on embolic stroke have not yet been investigated. Materials and Methods: In the present study, rats were subjected to embolic stroke (n=30) or sham stroke (n=5). Stroke animals were divided into control (n=10) or three different patterns of post conditioning treatments (n=20). In the first pattern of post conditioning (PC10, n=10), the common carotid arteries (CCA) were occluded and reopened 10 and 30 sec, respectively for 5 cycles. Both occluding and releasing times in pattern 2 (PC30, n=5) and 3 (PC60, N=5) of post conditionings, were five cycles of 30 or 60 sec, re¬spectively. Post conditioning was induced at 30 min following the stroke. Subsequently, cerebral blood flow (CBF) was measured from 5 min before to 60 min following to stroke induction. Infarct size, brain edema and neurological deficits and reactive oxygen spe¬cies (ROS) level was measured two days later. Results: While PC10 (P<0.001), PC30 and PC60 (P<0.05) significantly decreased infarct volume, only PC10 decreased brain edema and neurological deficits (P<0.05). Corre¬spondingly, PC10 prevented the hyperemia of brain at 35, 40, 50 and 60 min after the embolic stroke (P<0.005). No significant difference in ROS level was observed between PC10 and control group. Conclusion: Ischemic post conditioning reduces infarct volume and brain edema, de-creases hyperemia following to injury and improves neurological functions after the embolic model of stroke.

Dr. Sidharth Mehan, (Ph.D, M.Pharm, CFN) is an Associate Professor of Pharmacology at Rajendra Institute of Technology & Sciences, Sirsa, Haryana, India. He is a editorial board member and reviewer of various Pharmaceutical and Therapeutic Committee nationally and internationally like ARDSI (Alzheimer’s and Related Disorders Society of India) of various national and international journals and magazines. He is young neuropharmacologist, published various research, review and conference papers extensively and lectured worldwide. He did major contributions to describe the course of neurodegenerative disorders liken Alzheimer’s, Huntington’s, Parkinson’s and the effect of medical conditions on the course of neuropathy pain, renovascular diseases as well as to explore the novel therapeutic strategies and phytochemicals in the development and drug discovery in the field of molecular pharmacology.

Huntington’s disease (HD) is an autosomal dominantly inherited progressive neurodegenerative disorder, characterized by progressively worsening chorea, psychiatric disturbances, cognitive impairment and weight loss. The degenerative process primarily involves medium spiny striatal neurons (MSN) and to a lesser extent cortical neurons. Importantly, γ-amino butyric acid (GABA) ergic projection neurons of the striatum, which make up roughly 90% of the striatal neurons are the most vulnerable in HD and their early dysfunction is responsible for the development of chorea. Growing body of evidences suggest the involvement of impaired energy metabolism, excitotoxicity, microglial activation and production of pro-inflammatory cytokines leading to neuronal death, by both necrosis and apoptosis. These events of neurodegeneration are relevant to the striatal cell loss seen in HD.Fruits of G. mangostanaare the most treasuredpart of this plant and are famous for the remarkablypleasant flavour. Therefore, mangosteenis even namedas the ‘queen of tropical fruits’. The fruit hull of G. mangostanahas beenused for hundreds of years around the world, mostlyin Southeast Asia, as a medicine for a great variety ofmedical conditions. Over the past decades, it is shown that mangosteen contains high amounts of xanthones,a class of polyphenolic compounds which are shownto have significant biological activities in in-vitro systems.Dried and powdered fruit hull isused as antimicrobial agents and for the anti-parasitictreatments in dysentery as well as externally for healing wounds,suppurations and chronic ulcers. Mangosteen leaves and barkare recognized to have strong anti-inflammatory propertiesand therefore an ointment derived from them is usedfor treating eczema, hyperkeratosis and other skindisorders such as psoriasis. A tea made from mangosteenfruits is used widely as a tonic for fatigue and lowenergy states. Moreover, the antioxidant activitiesof selected xanthones. 1,2-Dihydro-1,8,10-trihydroxy-2-(2-hydroxypropan-2-yl)-9-(3-methylbut-2-enyl)furo[3,2-a] xanthen-11-one, 6-deoxy-7-demethylmangostanin,1,3,7-trihydroxy-2,8-di-(3-methylbut-2-enyl)-xanthoneand mangostanin induced quinonereductase in theHepa 1c1c7 cell line in an in vitro screening assay (IC50,0.68-2.2 μg/mL) whereas γ-mangostin exhibited hydroxylradical-scavenging activity (IC50, 0.20 μg/mL). Antioxidantactivities are also shown for 8-hydroxycudraxanthone,gartanin, α-mangostin, γ-mangostin and smeathxanthoneA using authentic and morpholinosydnonimine-derivedperoxynitrite methods. An extractof G. mangostanais reported to have very goodantioxidant action in the 2,2-diphenyl-1-picrylhydrazylradical (DPPH) assay. Theextract inhibited 50% of free radicals at a concentrationof 6.13 μg/mL. In addition, this extract showedhigh inhibition on TNF-α production generated fromperipheral blood mononuclear cells (PBMC) stimulatedwith Propionibacterum acnes. Therefore this plant isclaimed to have a remarkable antiinflammatory effectand to reduce cell damage. A vast number of studies have demonstrated the anti-inflammatory properties of mangosteen. In a clinical study, mangosteen juice exhibited potential anti-inflammatory potential. Further research exploring the role of mangosteen in-vitro demonstrates that mangosteen inhibits key features that are critical for inflammatory cytokine production in WAT. Primary human adipocytes treated with xanthones, the major bioactive compounds found in mangosteen, demonstrated reduced LPS-induced expression of pro-inflammatory genes (i.e. TNF-α, IL-6, IFN-γ and IL-10). In RAW264.7 macrophage cells, mangosteen extract, α-mangostin and γ-mangostin demonstrated a clear ability to inhibit NO and PGE2 release, along with the gene encoding iNOS and COX-2.Anti-inflammatory mechanism of γ-Mangostinvia inhibitionof spontaneouslyPGE(2) releasein a concentration-dependent manner as well as inhibit of lipopolysaccharide (LPS)-inducedexpression of COX-2 protein and its mRNA. γ-Mangostinalso inhibits cyclooxygenase and prostaglandinE2 synthesis. Where, both α-Mangostin&γ-Mangostinshowed anti-inflammatory activity by inhibition ofinducible NO synthase.α-Mangostin and its derivatesalso exhibits CNS depression like actions like (ptosis, sedation, decreasedmotor activity, potentiation of pentobarbitalsleeping time, ether anaesthesia) in mice and rats.Despite substantial research into neuroprotection, treatment options for HD are still limited to supportive care and the management of complications. Currently available drugs provide symptomatic relief but do not stop progression of disease. Thus, the development of new therapeutic strategies remains an unmet medical need. Failure of current drug therapy may be due to their action at only one of many neurotransmitters involved or their inability to upregulatesignaling messengers reported to have important role in neuronal functioning, neurotransmitter biosynthesis and release neuronal growth and differentiation, synaptic plasticity and cognitive functioning. Therefore, as already mentioned above, one of the alternatives to restore the anti-oxidant defence mechanism as well to inhibit inflammatory cytokines which are mainly involved in the preogression of Huntington’s diseases.Based on important and versatile role of Mangosteenin prevention of oxidation and inflammation, it may be possible protective strategies of Mangosteen: Garciniamangostana in Huntington’s diseaseand to find out if both complications are equally implicated in the disease pathogenesis or progression.

Lavanya Yaidikar is Professor in the Institute of Pharmaceutical Technology, Sri Padmavati Mahila Visvavidyalayam (Women's University), Tirupati, Andhra Pradesh, India. His research interests includes stroke, neurology.

Background: Cerebral ischemia is a chief cause of death worldwide. After cerebral ischemia/reperfusion, the reactive oxygen species production is dramatically increased and overwhelms endogenous antioxidant systems, leading to oxidative stress. The brain is particularly vulnerable to oxidative stress injury due to its high consumption of oxygen, abundant polyunsaturated fatty acids and low levels of endogenous antioxidants. Many antioxidants are described to block reactive oxygen species-mediated reactions and rescue neurons from ischemia/reperfusion-induced injury in experimental transient middle cerebral artery occlusion models. Aims: Arjunolic acid (AA), (triterpenoidal saponin of Terminalia arjuna) is a potent antioxidant and neuroprotective in nature. Our study was conducted to investigate its antioxidant potential against cerebral ischemia/reperfusion (I/R) neuronal injury in middle cerebral artery occlusion (MCAO) rat model. Methods: Arjunolic acid (AA) at a doses of 5 mg/kg and 10 mg/kg were administered orally for 7 days. After 1 hr of drug administration on the 7th day, rats were anaesthetized with chloral hydrate and subjected to MCAO for 2 h and reperfusion for 22 h. Behavioural parameters like neurological deficit, grip strength, adhesive removal test, infarct volume, brain water content, histological changes and oxidative stress markers like superoxide dismutase (SOD), catalase, malondialdehyde (MDA), carbonyl content, mitochondria generated reactive oxygen species, reduced glutathione (GSH), glutathione peroxidase (GSH-Px) were evaluated after 22 h of reperfusion. Results: In comparision with MCAO group, treatment with Arjunolic acid (AA) significantly reduced the altered behavioural and neurochemical changes associated with I/R neuronal injury. Conclusion: Taken together, these results suggested that Arjunolic acid showed neuroprotection against I/R induced neuronal injury through its antioxidant action.

Niramom Ungtrakul is a PhD student of Khon Kaen University, Thailand. Niramom did his research on evaluation of risk on OSA in stroke and sleepiness scale persons. Niramom completed his PhD in 2014 in the neurology and health sciences.

Background: The aim of the study was to develop a Thai-language Berlin Questionnaire (Thai BQ) to evaluate the risk for OSA in stroke patients. We also aimed to assess content validity, construct validity and the agreement of the Thai BQ with the Thai Epworth Sleepiness Scale (Thai ESS). Methods: 100 patients with stroke enrolled in the study. The BQ was first translated into Thai and then translated back to English using the forward-backward translation method. Evaluation of content validity was performed by 4 health care professionals. Evaluation of construct validity of the questionnaire was done by factor analysis. Internal consistency of the Thai BQ and the Thai ESS were evaluated using Cronbach’s alpha coefficient. Test-retest reliability and the agreement of the Thai BQ and the Thai ESS were evaluated using Cohen’s kappa coefficient. Results: Factor analysis identified 4 main factors. Cronbach´s Alpha coefficient was 0.74 and a Cohen’s kappa coefficient was 0.86 in the Thai BQ. The internal consistency of the Thai ESS evaluated by Cronbach’s Alpha was 0.59 and the test-retest reliability (Cohen’s kappa coefficient) was 0.81. The agreement of the Thai ESS and the Thai BQ was fair (Cohen’s kappa coefficient=0.29). Conclusions: The Thai BQ has been developed and shown to be a more valid and reliable tool than the Thai ESS in stroke patients. However, as factor analysis revealed 4 factors which are different from the 3 factors in the original BQ, modification of the Thai BQ may be required before the administration in Thai stroke patients.

Indireddy Theja is PhD student of Jawaharlal Nehru Technological University, India. Theja did research as a part of academic on investigation of Neuro –Protective Effect hydroalcoholic extract of Tinospora cordifolia in partial sciatic nerve transection induced neuropathic pain model in rats. Theja completed her PhD in 2013 from Jawaharlal Nehru Technological University, India.

Our study investigated the neuroprotective effect of hydroalcoholic extract of Tinospora cordifolia in partial sciatic nerve transection induced neuropathic pain model in rats. Adult male albino rats weighing 200 ± 40 gms were used for the study, and were divided into five groups with 8 animals in each group. Group I – Control group (Vehicle), Group II – Pain induced group (vehicle), Group III – Extract treatment (200 mg/kg/p.o), Group IV – Extract treatment (400 mg/kg/p.o), Group V – Gabapentin (50 mg/kg/p.o). Animals were treated with the respective drugs/vehicle/extract for 21 days after partial sciatic nerve transaction surgery. Behavioural parameters like Tail cold-hyperalgesia, motor co-ordination, foot deformity, neurological deficit were assessed on 0th day, 7th day, 14th day and 21st day in order to evaluate the extent of neuropathic pain. On 21st day after behavioural assessment, rats were sacrificed by cervical decapitation. The sciatic nerve was isolated and 5% homogenate was prepared to estimate Superoxide dismutase (SOD), catalase (CAT), and lipid peroxide (MDA), Calcium, reduced glutathione (GSH), nitric oxide and treatment with the extract 400 mg/kg and standard drug showed the restoration of oxidative stress and pain as compared with normal and pain induces rats suggesting the significant traditional use of Tinospora cordifolia in neuropathic pain

Daihua Yu has completed his PhD at the age of 35 years from the Fourth Military MedicalUniversity. He is the associate director of department of anesthesiology, Tangdu Hospital. He has published more than 30 papers in reputed journals and has been serving as an editorial board member of repute.His studies mainly focus on using preconditioning and postconditioning for treatment of human brain ischemic disease, via mechanisms of immunomodulation, neural cell repopulation and neuroregeneration.

We aim to explore whether erythropoietin (EPO) preconditioning protects against rat cerebral ischemia-reperfusion injury and affects the expression of glutamate transporter 1 (GLT-1) and glutamate aspartate transporter (GLAST).One hundred and forty Sprague Dawley rats were randomly divided into four groups: DMSO-sham, EPO-sham, DMSO-MCAO and EPO-MCAO. Neurological function scores were obtained 24 h after reperfusion. Cerebral infarction volume and the number of apoptotic neural cells of each group were measured. The mRNA levels of GLT-1 and GLAST were determined by reverse transcription-polymerase chain reaction (RT-PCR), while the protein levels of GLT-1 and GLAST were determined by Western blot assay. The cerebral infarction volume was significantly greater in DMSO-MCAO group compared with DMSO-sham group (P<0.01). The infarction volume of EPO-DMSO group, however, was significantly smaller than that of DMSO-MCAO group (P<0.01). Compared with DMSO-sham group, there were more apoptotic cells in DMSO-MCAO group (P<0.01). But the number of apoptotic cells in EPO-MCAO group was significantly less than that in DMSO-MCAO group (P<0.01). The mRNA and protein levels of GLT-1 and GLAST decreased significantly 24 h after the cerebral ischemia-reperfusion (P<0.01) compared with the DMSO-sham group, whereas their levels increased significantly in the EPO-MCAO group (P<0.01). EPO preconditioning protected against cerebral ischemia-reperfusion injury and up-regulated the expression of GLT-1 and GLAST.

Rasha Elshafey is radiologist in the Radiodiagnosis Department, Tanta University Hospital, Egypt and also worked as Faculty of Medicine, Tanta University, Elgharbia, Egypt. His research interests incledes neuroradiology and neuclear medicine.

Purpose: studying the sensitivity of diffusion tensor imaging in detecting abnormalities in focal lesions of MS and the extent to which NAWM pathology in the form of variations in MD and FA in different types of MS patients, both during activity and in remission. Material and Methods: The regional ethics committee approved the study and written informed consent were obtained from all participants. diffusion tensor imaging (DTI) was performed in 45 consecutive MS patients, (18 men and 27 women) with a mean age of 47.3±7.9 years, 20 healthy control (4 male and 6 female) referred to Radiodiagnosis Department from neuropsychiatry department from March 2012 to November 2013.Clinical diagnoses of MS were established using McDonald's criteria. Results: mean diffusibility (MD) and the fractional anisotropy (FA) were determined in normal appearing white matter (NAWM) and in different types of focal MS lesions during activity and remission and compared with NAWM of control group, significant increase of the MD and decrease of FA from normal white matter of the controls to normal appearing white matter of the patients to MRI detected active lesions and the least is inactive plaques. Conclusion: DTI –MRI quantitative parameters have been found to show tissue damage not only in MRI-defined lesions but also in NAWM as a result of Wallerian degeneration and helpful not only as diagnostic elements, but also as prognostic factors.

Mohmmadreza Zarisfi is PhD student of Rafsanjan University of Medical Sciences, Iran. He did his research work on ischemic injury in experimental middle cerebral artery occlusion (MCAO)in Both hypothermia and decompressive craniectomy (DC).

Introduction: Increased levels of proinflammatory cytokines have been recorded after the onset of transient or permanent brain ischemia and are usually associated with exacerbation of ischemic injury. Embolic stroke model is more relevant to the pathophysiological situation in such patients, because the majority of ischemic injuries in humans are induced by old thrombi that originate from the heart and carotid arteries. Therefore, the aim of the present study was to investigate changes of inflammatory cytokines after embolic stroke. Material and methods: Rats were subjected to embolic stroke, induced by a natural old clot which was injected in Middle Cerebral Artery (MCA), or sham stroke, which the same volume of saline was injected into the MCA. At 48 h after stroke induction, the levels of 5 cytokines (IL-1α and β, IL-6, IFN-ɤ and TNF-α) were determined in 500 2g of total protein using the Bio-Plex Rat Cytokine Array (BioRad), according to the manufacturer’s instructions in ischemic and nonischemic cortices. Results: While stroke animals showed infarctions and neurological deficits, we did not observe any cerebral infarction and neurological deficits in sham-operated animals. The levels of IL-1+ (p=0.000) and -, (p =0.004), IL-6 (p =0.008), TNF-+ (p =0.000) and IFN-0 (p =0.044) were significantly increased compared to sham treated animals. Conclusion: The findings of the present study suggest that part of ischemic injury in the embolic stroke may be mediated through the increased levels of inflammatory cytokines.

SwapnaPokkula has completed MPharmacy (Pharmacology) in 2010 from Sri Padmavathi Mahila Visvavidyalayam, Tirupati. She worked as an Assistant Professor in Max Institute of pharmaceutical sciences, Khammam, A.P, India. Currently, she is pursuing PhD in the field of pharmacology under the guidance of Professor T Santh Rani with in the same university. She has published 2 research papers in reputed journals and presented various Posters and oral presentations in many conferences.

Neuropathic pain associated with peripheral nerve injury and is characterized by the sensory abnormalities such as unpleasant abnormal sensation, an increased response to painful stimuli and pain in response to a stimulus that does not normally provoke pain. Neuropathic activity can be screened by both in vitro and in vivo methods. In vivo assays classifiedin to different models. A number of synthetic neuroprotective agents (NPA) including amitrptyline, carbamazepine and gabapentine have been developed but they are far away from an ideal agent for neuropathic pain. Therefore, many researchers are trying to find new, potent and safe NPA from natural sources. Few naturally occurring compounds have been reported to have NP activity. The present review attempts to highlight plant extracts and phytochemicals with potential NP activity. It also summarizes the structure of compounds which have proven NP activity. Phytochemicals such as 24-hydroxytormentic acid and Guttiferone A are found to have most promising NP activity. The exhaustive literature presented in this article clearly indicates the role of plant extracts and phytochemicals as potential neuroprotectants for the management of neuropathic pain.

Felipe Augusto dos Santos Mendes is Ph. D student at University of Brasília, Brazil. His research interests includes Parkinson’s disease and movement disorders.

Objectives: To evaluate the learning, retention and transfer of performance improvements after Nintendo Wii FitTM training in patients with Parkinson’s disease and healthy elderly people. Design: Longitudinal, controlled clinical study. Methods: Participants: Sixteen patients with early-stage Parkinson’s disease and 11 healthy elderly people. Interventions: Warm-up exercises and Wii Fit training that involved training motor (shifts centre of gravity and step alternation) and cognitive skills. A follow-up evaluative Wii Fit session was held 60 days after the end of training. Participants performed a functional reach test before and after training as a measure of learning transfer. Main outcome measures: Learning and retention were determined based on the scores of 10 Wii Fit games over eight sessions. Transfer of learning was assessed after training using the functional reach test. Results: Patients with Parkinson’s disease showed no deficit in learning or retention on seven of the 10 games, despite showing poorer performance on five games compared with the healthy elderly group. Patients with Parkinson’s disease showed marked learning deficits on three other games, independent of poorer initial performance. This deficit appears to be associated with cognitive demands of the games which require decision-making, response inhibition, divided attention and working memory. Finally, patients with Parkinson’s disease were able to transfer motor ability trained on the games to a similar untrained task. Conclusions: The ability of patients with Parkinson’s disease to learn, retain and transfer performance improvements after training on the NintendoWii Fit depends largely on the demands, particularly cognitive demands, of the games involved, reiterating the importance of game selection for rehabilitation purposes.

Abdalla Bowirrat is assiatant professor at Galilee Faculty of Medicine - Bar Ilan University, Zafed, Israel. His research interests includes parkinsons disease and movement disorders.

Purpose: The aim of this manuscript is to shed light and to try to identify the underlying causes of and circumstances surrounding the fall and hip fractures in Parkinson's disease (PD) patients, in order to find prevention strategies and choose appropriate therapy. Methods: We have analyzed, discussed and overviewed the latest updates of the medical literature concerning PD and the orthopedic complications. Conclusions: PD is a chronic neurodegenerative disorder characterized by rest tremor, rigidity, bradykinesia and loss of postural reflexes, leading to immobility and gait disturbance. The usual age of onset is between the sixth and eighth decades. Globally, the percentage of elderly aged 65 years and over was calculated to be 8 percent (521 million) in 2011 and it is expected to be 11 percent (939 million) of the total global population by 2030. Hip fractures are life-threatening and frustrated quandary that is usually seen among elderly people that requires high economic expenses. Plethora of factors contributes to falls and to increased risk of hip fractures in patients with PD. These factors include potential physiological aging changes and medical causes. One should try to identify the underlying causes of and circumstances surrounding the fall and hip fractures in PD patients specifically, in order to find prevention strategies and choose appropriate therapy by taking a multidisciplinary approach interventions that include neurologist, physiatrist, podiatrist, and family or caregivers the thing that will result in optimal outcomes for patients with PD.

Saodatkhon Khamidova is Ph.D student at Tashkent Pediatric Medical Institute, Uzbekistan. Her research interests includes stroke, cerebral palsy and pediatric neurology.

Relevance. Current diagnosis of mental development of children and treatment of cerebral palsy (CP) are important tasks of childhood neurology. Along with conventional neuro-physiological research methods (EEG, Echo -ES, etc.) neuro-psychophysiological research methods in pediatric neurological practice are increasingly being used as a local topical diagnosis of brain damage, and in the assessment of non-verbal intelligence. Many patients with cerebral palsy, movement disorders combined with cognitive disabilities that still depend on the form of the disease. Objective: to study cognitive deficits in different forms of cerebral palsy with seizures. Materials and Methods: During a prospective study analyzed cognitive function in 17 children (8 girls, 9 boys) with cerebral palsy with seizures. The age of patients at the time of the analysis of clinical data ranged from 7 to 14 years. Held: EEG, video - EEG monitoring night's sleep, brain MRI, neuropsychological testing (assessment test verbal intelligence (British Picture Vocabulary Scale / BPVS /), which is estimated at 100 mark system test and Raven ( colored version of the test used for children aged 7 to 11 years old, black and white - for children over 11 years) which is estimated as a percentage). Results: intrapartum brain injury - 10 cases; prematurity 28-32 weeks - 7 cases. In all patients at the time of inspection - rough speech retardation and cognitive decline. In the neurological status: cerebral palsy, spastic diplegia - 4 cases, hyperkinetic form – 10, mixed - 3 cases. According to MRI: subatrophy right hippocampus - 1 case, perisylvian polymicrogyria in two cases, periventricular leukomalacia - 5 cases, cortical atrophy fronto- parietal- temporal lobe - 9 cases. When tested by the method identified BPVS following changes; spastic diplegia -63.4 score hyperkinetic form - 68.2 grades, mixed - 69.3 score (at a rate of 100 points). According to test Raven (in percentage): spastic diplegia, 19.1, 26.4 - hyperkinetic form and mixed - 18.6 (normal 75-95 %) Conclusion. When cerebral palsy with seizures in patients receiving anticonvulsants, mainly depakine, cognitive disorders can occur in all forms, but suffers more spastic diplegia.

German Augusto is Junior researcher at Manuela Beltran University, Colombia and his Academic background includes Master / Magister PUBLIC HEALTH INSTITUTE OF MEXIC MASTER OF SCIENCE IN THE AREA HEALTH headings Epidemiology; Specialization Colegio Mayor de Nuestra Señora del Rosario; Specialization in University Teaching; Undergraduate / University Colegio Mayor de Nuestra Señora del Rosario,Physiotherapy.

Introduction: The medular lesions are events with high frequency in the neurological pathologies, and their impacts have important effects in sensitive and motor elements related functional movements affecting the possibilities of performance of individuals, and levels of quality of life. With large economic costs for rehabilitation processes that are required for those affected, and for this reason is necessary to know the frequency and types of medular lesions that can occur to take a picture which is to plan efficient and effective actions of purpose, its prevention and to improve care processes. Material and Methods: Developed a cross-sectional study with patients treated by neurological and particularly medular lesions in one Physiotherapy Center of a Public Hospital of High Complexity in Bogota, between the months of February to September 2013.The selection mechanism of the population was a census of all elderly subjects, 18 years old treated for neurological and medular lesions, and was calculated to analyze the raw information and specific prevalence’s with a level of standard errors, and to see the relation of gender with the occurrence of medular lesions was calculated. Odds ratio and Chi Square test were used. Results: In the observation period of the study 66 people were treated for diverse neurological pathologies.10.60% (n=7, Standard Error=0.09) of them had medular lesions, 42.85% of them were cases of spinal cord injury (n=3, Standard Error=0.26), 28.57% had myelopathy events (n=2, Standard Error=0.37), 66.6% of those who had spinal cord injury were males (n=2, Standard Error=0.27, X2=0.23, p>0.05, OR=1.81). Conclusions: Medular lesions are a frequent reason for consultation at neurological diseases in Physiotherapy, and they are linked mainly with traumatic nature that surpass infectious, and oncological, primarily affecting people of masculine gender.