4^th World Congress on Epilepsy and Treatment November 16-17, 2018 | Radisson Narita | Tokyo, Japan

Biography:

Abstract:

Diagnosis of dementia remains probabilistic and difficult to retain. Noninvasive and inexpensive tools are needed for guiding the diagnosis. Use of electroencephalogram (EEG) in dementia has been the subject of several studies. We selected controls and patients with cognitive impairment. Clinical examination and neuropsychological evaluation was made for all subjects. A cerebral Magnetic resonance imaging (MRI) and biological investigations were also made.  Additionally, all subjects had a wake EEG with visual analyses and scores calculating. Ninety two patients were included (66 patients and 26 controls). After Clinical, neuropsychological, biological and radiological data collection, we classified patients: 16 with mild cognitive impairment, 50 with dementia classified as follows: 24 with Alzheimer disease, 9 with vascular dementia, 5 with dementia with lewy bodies, 5 with fronto-temporal dementia, 5 with mixt dementia and 2 with Parkinson disease. A Grand total score inferior to 5 was in favor of psychiatric cause. A score superior to 5 was in favor of an objective cognitive impairment. Appreciation of reactivity by score 3 allowed to make difference between mild cognitive impairment and dementia.

Biography:

Muneeb Iqbal is a PhD student working in institute of neurobiology, under supervision of Prof. Liu yong. This lab is working on aberrant hippocampal neurogenesis in status epilepticus animal models under supervision of Prof. Jianxin Liu. Muneeb Iqbal has his expertise in evaluating the effect of exercises on epileptic animal models and their behavioral testing. . He has already published a “Systematic review and meta-analysis of the efficacy of different exercise programs in pilocarpine induced status epilepticus models”.  He is further working of evaluating the effect of complementary therapies in the prognosis of SE.

Abstract:

Statement of the Problem: Increased neurogenesis acutely after status epilepticus (SE) is a well-known fact. These increased newly born neurons contribute to the aberrant rewiring of the hippocampus and are hypothesized to promote epileptogenesis. Physical training (PT), which has been recognized as an effective complementary therapy to treat epilepsy, was also reported to cause more increase in neurogenesis acutely after SE by various studies. Fate and role of these extra newly-born neurons due to PT has remained elusive, whether they integrate in normal circuits or increase aberrant integrations is yet to be determined. Answer to this question will reveal the basic mechanisms by which PT effect epilepsy. Methodology: We evaluated the effect of four weeks moderate intensity treadmill running PT on adult male Kunming Mice after pilocarpine induced SE. Dividing progenitors were labelled by BrdU at acute stage (1-week after SE) and histological examinations of hippocampal sections were performed for aberrant hippocampal neurogenesis after spontaneous recurrent seizures’ monitoring. Changes in genetic methylation of BDNF gene and its level in hippocampus through Western blot analysis was measured at acute stage (2-weeks) after SE to explore underlying pathways which cause increased neurogenesis. Findings: Although PT increased proliferation in sub-granular zone of dentate gyrus of hippocampus at acute stage after SE but these newly born neurons not only shown more survival (surviving Brdu+ cells) and maturation (BrdU+NeuN stained cells) but they also integrated into normal circuits and shown reduced aberrant hippocampal neurogenesis assessed through decrease in number of ectopic granular cells, hilar basal dendrites and mossy fiber sprouting as compared to non-exercised SE group. Although SE decreased the %age methylation of CpGs of BDNF gene’ promoters, PT increased BDNF level through some  pathways other than demethylating BDNF CpGs. Normalized integrations of newly born neurons might resulted in decreased spontaneous recurrent seizures and increased spatial memory assessed through Morris water maze test.   Conclusion & Significance: PT increases hippocampal neurogenesis through increasing BDNF levels by some pathways other than demethylating BDNF CpGs and causes post SE newly born neurons to integrate into normal circuits thus resulting in decreased spontaneous recurrent seizures and enhanced spatial memory.

Biography:

Nadia ben Ali  has her expertise in neurology especially on epileptology  and passion in improving the health and wellbeing. Her open and contextual evaluation model based on novel therapy and  creates new pathways for improving healthcare. She has built this model after 10  years of  clinical research   both in hospital and education institutions.

Abstract:

The aim of the study to identify risk factors for recurrence of seizures after withdrawal and  propose recommendations. We recruited 55 patients treated for EGI in whom the withdrawal of antiepileptic treatment was attempted after a remission of at least 24 months. We have specified their status  after therapeutic weaning (remission or relapse) as well as their different demographic, clinical, electrical and therapeutic characteristics. A multivariate statistical study was applied in search of prognostic factors of remission or relapse in order to establish a prognostic score and a strategy of withdrawal of antiepiletics.Our cohort was heterogeneous. The remission rate was 54.5%, with 90% of relapses occurring during the first 24 months after weaning from the AEMs. We established a prognostic score with  clinical and paraclinical parameters that seem to be only the "tip of the iceberg" of epilepsy and epileptogenesis. The question that arises is that it is not neurobiological and genetic factors that would rather determine individual epileptogenesis.

Biography:

I am a postgraduate neurology trainee 1st year in china with MRCP UK  London ,Diploma in emergency Medicine and critical care (Royal college UK)  ,Diploma in clinical neuropsychology (UK),Pediatric Neurology certification  BPNA (UK, ongoing) ,Neuroscience and neuroimaging course john Hopkins university(on going).I have recently submitted a meta analyses of  vit D and its association with PD in frontiers of neuroscience under review plus submitted this above mentioned abstract in Movement disorders under review , working on WD with secondary PKD ,Face of Giant Panda in WD ,PARK 2 neuropathy ,EA 2 with novel mutation , DYT -27 etc

Abstract:

Anti-Ma2 antibody -associated encephalitis, which usually occurs in young men with  germ cell tumors of  the testis with features of encephalitis ,it can also present in elderly females with basal ganglia disorder features like Parkinsonism and  cerebellar ataxia in absence of limbic or brainstem or diencephalic encephalitis . Patients may not present with any form or symptoms  of encephalitis but the treatment response rate with steroids , IVIG , plasmapharesis to control the initial symptoms is very high and after resection of the tumor all the symptoms  can be totally cured .So ,even there is no evidence of tumor on basic contrast CT /MRI scans ,other special imaging  like FDG -PET or highly advanced tumor searching imaging plus serum tumor markers of different tumors should be considered as the tumor spectrum associated with anti ma 2 antibody encephalitis is huge and resection of the tumor can totally cure the patient .A 68-year-old female presented to our department with resting tremor of right hand for 2 years . After 6 months, resting tremor gradually involved her right leg. Antiparkinsonian drugs were initiated but her symptoms worsened gradually. Since last 3 months, she developed features of imbalance with occasional falls and a weight loss of 10 kg. Neurological examination showed features of Parkinsonism. Brisk DTR right side more than left with abnormal cerebellar signs. CE MRI mild atrophy of cerebellum. Anti-Ma2 antibodies in serum and CSF positive .Serum cancer antigen 72-4was elevated. A sigmoid colon mass was discovered by colonofiberoscopy and adenocarcinoma was diagnosed via tissue biopsy. Steroids, IVIG and resection of the tumor completely cured the disease.

Biography:

Carol Ireland:CEO and Managing Director of Epilepsy Action Australia (EAA), Carol has an extensive background spanning 35 years in the not-for-profit human services sector, holding a variety of executive positions. She has been at the forefront of the medical cannabis movement in Australia. 

Lisa Todd:Lisa Todd is a Clinical Nurse Consultant in Epilepsy and Clinical Governance Manager for Epilepsy Action Australia. She is a Registered Nurse with a Post Graduate Certificate in Neuroscience Nursing and Masters of Education.

Abstract:

Epilepsy Action Australia (EAA) sought to understand the attitudes toward and lived experiences of adults and parents of children living with epilepsy of cannabinoid-based therapies in an ever-changing climate of public opinion, government legislation and clinical trials in Australia. Two studies were undertaken with the first informing the second study. A nationwide online survey was conducted assessing demographics, clinical factors, including diagnosis and seizure types, and experiences with and opinions towards cannabis use in epilepsy. The second study (PELICAN) focused on experiences of 61 families of children with epilepsy under the age of 16 years who desired, were currently or had previously administered cannabinoid-based therapies to their children to manage seizures. Semi-structured interviews were conducted; samples collected with subsequent laboratory analysis. 976 responses met the inclusion criteria of the initial survey. 15% of adults with epilepsy and 13% of parents/guardians of children with epilepsy were currently using, or had previously used, cannabinoid-based products to treat epilepsy. Of those with a history of cannabis product use, 90% of adults and 71% of parents reported success in reducing seizure frequency. Forty-one of the sixty-five families participating in the second study (PELICAN) were currently or had previously administered cannabinoid-based therapies to their children. Analysis of the products highlighted a wide variability of cannabinoid content and low concentration of Cannabidiol (CBD) while Δ9-tetrahydrocannabinol (THCΔ9) was present in nearly every sample.

Biography:

Cheryl Shoubridge is an Associate Professor of Human Genetics with a research focus on investigating the molecular pathogenesis underpinning genetic causes of intellectual disability and seizures. Her research utilizes numerous experimental models relevant to the associated clinical phenotypes, including rodent models, primary neurons in culture through to clinical specimens.  Currently, A/Prof Shoubridge is working in the pre-clinical setting on identifying and validating treatments to improve disease outcomes. Her expertise in genetics, neuroscience and molecular biology underpin her more recent focus on investigating the pathogenic mechanisms contributing to disease outcomes of intellectual disability and seizures due to deficits in synaptic plasticity.

Abstract:

The IQ motif and SEC7 domain-containing protein 2 (IQSEC2) is an X-chromosome gene mutated in both males and females leading to intellectual disability (ID) and severe early-onset seizures. The pathogenesis underpinning these mutations remains unknown. Utilising CRISPR/Cas9 targeted editing (Prof PQ Thomas, SA Genome Editing Facility, University of Adelaide) we have generated an Iqsec2 KO mouse model to investigate the molecular and cellular deficits in this gene resulting in disease outcomes; a fundamental step towards the design and implementation of potential treatment options. We confirmed the loss of Iqsec2 mRNA expression and the lack of Iqsec2 protein detected within the brain of founder and progeny mice. Recapitulating the human setting, both male (48%) and female (45%) Iqsec2 KO mice present with frequent and recurrent seizures. There was an increased occurrence of seizures, reabsorption and unsuccessful nurturing of live young in breeding females. Developmentally, the KO mice exhibit significantly increased hyperactivity, altered anxiety and fear responses, decreased social interactions, delayed learning capacity and decreased memory retention/novel recognition; recapitulating the psychiatric issues, autistic-like features and cognitive deficits present in patients with loss-of-function IQSEC2 mutations. Interestingly, the loss of Iqsec2 function not only causes severe ID and seizures in KO male mice, but in agreement with the patient setting, similar severity is also noted in females despite being in a heterozygous state for this X-chromosome gene. We contend this newly generated mouse model provides a highly relevant biological tool required to interrogate IQSEC2/Iqsec2 function in the brain.

Biography:

Yung-Feng Liao has completed his PhD in Biochemistry and Molecular Biology from University of Georgia and Postdoctoral studies from Harvard Medical School/Massachusetts General Hospital/Brigham and Women’s Hospital. He is the Principal Investigator of the Laboratory of Molecular Neurobiology in the Institute of Cellular and Organismic Biology, Academia Sinica, Taiwan. He has published more than 50 papers in reputed journals and has been serving as an Editorial Board Member and as a Peer Reviewer of prestigious journals.

Abstract:

γË—Secretase catalyzed production of Amyloid-β (Aβ) underlies the pathogenesis of Alzheimer’s Disease (AD). The aim is to identify genetic modifiers that can selectively affect γ-secretase cleavage of Alzheimer's disease amyloid protein precursor i while sparing Notch cleavage, we generated cell-based assays employing Bioluminescence Resonance Energy Transfer (BRET) technology to monitor the protein-protein interactions between PS1 and two γ-secretase substrates, Alzheimer's disease amyloid protein precursor i C-terminal fragment (C99) and extracellular domain truncated Notch (N∆E). An RNAi screen identified 14 candidate genes whose downregulation resulted in a selective decrease in the interaction between PS1 and C99. Among those 14 candidate genes, an ErbB2-centered interaction network was found to preferentially govern the proteostasis of APP-C99. We further demonstrated that overexpression of ErbB2 upregulates the levels of C99 and AICD effectively. The knockdown of ErbB2 selectively decreased the protein levels of C99, AICD, and secreted Aβ40 but not those of N∆E and NICD. Selective suppression of ErbB2 expression by CL-387,785, an ErbB1/2-selective irreversible tyrosine kinase inhibitor can preferentially attenuate the levels of C99 and AICD, resulting in a significant reduction in Aβ production. Down-regulation of ErbB2 by CL-387,785 also resulted in a significant decrease in the levels of C99 and secreted Aβ in both zebrafish and mouse models of AD, through the activation of autophagy. Oral administration of CL-387,785 for 3 weeks significantly improves the cognitive functions of APP/presenilin-1 (PS1) transgenic mice. These findings unveil a noncanonical function of ErbB2 in modulating autophagy and established ErbB2 as a novel therapeutic target for AD.

Biography:

Archana A is currently pursuing her PhD in Stress Physiology in Department of Physiology, University of Madras, Tamil Nadu. She has published two papers in sleep deprivation and unpredictable acute and chronic stress. She is currently researching noise stress on hippocampus and Alzheimer’s disease.

Abstract:

Background: In our modern lifestyle exposure to noise stress/pollution not only affects the auditory system but rather extend to the central nervous system.

Objective: The aim of the study is to investigate the effect of acute noise stress on cognitive functions in male Wistar albino rats.

Methods: Adult albino rats were randomly divided into two groups. Each group contains six animals. Rats exposed to acute noise stress (100 dB/4 hour) were compared with control animal and assessed for cognition by using T-maze, hole board test, open field test, marble burying test, and social interaction behavior.

Results: The rats exposed to acute noise stress shown the significance (p<0.05) of behavioral alterations such as impaired learning and memory, memory retention, increased fear and anxiety, obsessive-compulsive behavior, social avoidance and decreased social interaction.

Conclusion: The results report that acute noise stress affects the cognition and it became chronic may confer the increased risk of neurodegenerative disorders.

Biography:

Abstract:

Antiepileptic drug (AED) therapy in  epileptic children can be optimized via an anticipation of AED efficacy during early stages of therapy. We hypothesize that the comprehensive EEG evaluation can determine AED efficacy in epileptic children. Thus, this study aimed to investigate the alteration of characteristics of interictal EEG during AED therapy.  Forty-three children aged 3-9 were investigated.  EEGs were recorded three times: prior to Valproic Acid-Depakin (Dep) monotherapy and twice under Dep therapy (at three and six/eight months). Baseline EEG was analyzed for quantitative characteristics of interictal EEG such as absolute values of the power (AVP) spectra and EEG topography/Brain Mapping. The study involved epileptiform EEG and clinical condition assessments. Dep decreased AVP spectra in a low-frequency range, suppressed spontaneous epileptic discharge, and spike-wave complex 3/s. Dep partially decreased spikes-polyspikes, sharp waves, and generalized paroxysmal bursts during functional trials. Dep did not diminish rhythmic monomorphic theta-waves (RMT) of tempo-parietal localization observed by Brain Mapping. The presence of RMT correlated with the reocurrence of seizures if Dep was withdrawn.

Biography:

Nadia ben Ali  has her expertise in neurology especially on epileptology  and passion in improving the health and wellbeing. Her open and contextual evaluation model based on novel therapy and  creates new pathways for improving healthcare. She has built this model after 10  years of  clinical research   both in hospital and education institutions.

Abstract:

Vagus nerve stimulation (VNS) is a new therapeutic approach of drug-resistant epilepsy, when surgery is not indicated. Though effective, few data from developing countries exist. The aim of this work is to draw out the Tunisian experience in VNS, concerning its efficacy in patients with different intractable epileptic syndromes. We retrospectively reviewed 6 patients with different epileptic syndromes who underwent VNS therapy.  All patients have a neurological exam, EEG recording, MRI and neuropsychological tests. The mean duration of the follow-up was 48 60 months. Demographic data, epileptic syndrome, the different stimulation parameters, seizure frequency as well as clinical response after implantation and side effects were described. The mean age was 19.6 year.  Output current, pulse duration, frequency, and off time changed significantly between the 3- and 48 month long-term follow-ups. The global mean decrease in seizure frequency at last follow-up was over than 50 %. Some seizure types responded better than others did: complex partial seizures with secondary generalization and atonic seizures. Improvements in memory, mood, alertness and postictal recovery period were observed in all patients.

Biography:

I am a postgraduate neurology trainee 1st year in china with MRCP UK  London ,Diploma in emergency Medicine and critical care (Royal college UK)  ,Diploma in clinical neuropsychology (UK),Pediatric Neurology certification  BPNA (UK, ongoing) ,Neuroscience and neuroimaging course john Hopkins university(on going).I have recently submitted a meta analyses of  vit D and its association with PD in frontiers of neuroscience under review plus submitted this above mentioned abstract in Movement disorders under review , working on WD with secondary PKD ,Face of Giant Panda in WD ,PARK 2 neuropathy ,EA 2 with novel mutation , DYT -27 etc.

Abstract:

A 45 year old working lady presented to us with bradykinesia  for  six months, accompanied with difficulty in walking for  four months. Six months ago, the patient started feeling clumsy while doing house hold work and her movements became slower as time passed by.Four months ago, she started to have difficulty in walking which gradually aggravated. Since onset, she was depressed,  and  experienced sleep related behavioral issues but never lost weight.Her Mother had similar symptoms but was on antiparkinsonian drugs.P/E: increased muscle tone in all 4 limbs ,right >> left with reduced right arm swing, with masked type facies . In view of positive family history ,parkinsonism symptoms, depression/apathy patient was diagnosed with definite PS(Perry syndrome) supported by international diagnostic criteria.To confirm PSG showed airflow restriction and hypoventilation using apnea hypopnea index with no respiratory acidosis  in ABG  .Genetic test was performed which confirmed novel point  DCTN 1 gene mutation.Patient was started on Antiparkinsonian agents,antidepressants , and clonazepam and her symptoms got somewhat better.