Journal of epilepsy最新文献

{"title":"Epilepsy Comorbidity of Autism in Children","authors":"K. Hung","doi":"10.4172/2472-0895.1000E111","DOIUrl":"https://doi.org/10.4172/2472-0895.1000E111","url":null,"abstract":"Autism Spectrum Disorder (ASD) is a group of developmental disorder in children characterized by social interaction difficulties, verbal/nonverbal communication disturbance and stereotyped behaviors. ASD can be found in most countries all over the world, while the prevalence differs among areas. The association between autism and epilepsy has been recognized for a long time, yet the basis of association is little understood [1]. One of the main reasons comes from the fact that various diagnostic subtypes exist in many reports of epilepsy with ASD [2].","PeriodicalId":81656,"journal":{"name":"Journal of epilepsy","volume":"2 1","pages":"1-2"},"PeriodicalIF":0.0,"publicationDate":"2016-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4172/2472-0895.1000E111","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70317134","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Can Ictal F18-FDG PET/CT Drawing Epileptogenic Zone in Refractory Focal Epilepsy? Histopathological and Outcome Correlation","authors":"D. Dl, M. Campos, F. Solari, L. Ríos, G. Kuester, M. Gálvez, F. Otayza","doi":"10.4172/2472-0895.1000109","DOIUrl":"https://doi.org/10.4172/2472-0895.1000109","url":null,"abstract":"Unlike interictal Positron Emission Tomography (PET), ictal PET is not regularly used in the study of refractory focal epilepsy, and its usefulness in presurgical evaluations, and prognosis value have not been established. The aim is to present six patients with epilepsy whose PET/CT brain scans showed focal hypermetabolism, and analyze their correlation with the histopathological findings and clinical results. We reviewed 146 18F-FDG PET/CT scans performed on patients with refractory focal epilepsy. Only those cases with hypermetabolic foci which were subsequently surgically resected were selected. The epidemiological and clinical data were reviewed in addition to the brain MRI, Electroencephalography (EEG), video-EEG monitoring, intraoperative Electrocorticography (ECoG), histopathology, and postsurgical outcome. The PET findings were correlated with the clinical characteristics of the seizures, the EEG, brain MRI, ECoG, and histopathology. Seven PET/CT scans carried out on six patients showed well-defined hypermetabolic foci (three temporal, four extratemporal). There was a high correlation between the clinical lateralization, EEG/ECoG findings, and hypermetabolic foci located by PET. An MRI correctly identified the resected histopathological lesion in five cases and it was negative in two. Three patients had Focal Cortical Dysplasia (FCD), one had FCD with areas of polymicrogyria, one had temporal lobe cavernoma associated with hippocampal sclerosis, and one had a focal subcortical heterotopia. Mean postsurgical follow-up was 29.1 months (range: 16-24 months) and all patients were seizure free during this period. This small series of patients who underwent surgery for intractable focal epilepsy have shown good correlation between the ictal F18-FDG PET/CT scan and the electroclinical and pathological findings. These results suggest that hypermetabolic foci showed in PET/CT provides a reliable estimation of epileptogenic zone. Focus size underestimation in one case suggest the need of doing an interictal PET before surgery.","PeriodicalId":81656,"journal":{"name":"Journal of epilepsy","volume":"21 1","pages":"1-6"},"PeriodicalIF":0.0,"publicationDate":"2016-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4172/2472-0895.1000109","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70316601","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Understanding Hyper Motor Seizures","authors":"R. Andrade-Machado","doi":"10.4172/2472-0895.1000108","DOIUrl":"https://doi.org/10.4172/2472-0895.1000108","url":null,"abstract":"Introduction: Hyper Motor Seizures [HMS] are characterized by complex high amplitude movements involving proximal segments of the body resulting violent and inappropriate to the context. \u0000Objective: To review the possible ictal onset zones related to HMS and the cortical areas that would be covered if invasive recording are needed. \u0000Development: Semiology can predict the localization of ictal onset zone. Two subtypes of HMS [type 1 and 2] have been described. HMS1 is associated with an epileptogenic zone on the ventromedial frontal cortex and HMS2 has been associated with a more dorsal epileptogenic zone than those resulting in HSM1. However, HMS can also be originated in temporal lobe [mesial, neocortical or in the pole], in insular cortex or even in parietal lobe. The origin of HMS can be suspected by the associated signs. Thus, HMS originating in the insula–operculum regions can be associated with various somatosensory auras; in parietal seizures, propioceptive sensations may precede hyper motor behavior [HM], whereas autonomic and emotional auras prompt to think in the temporal lobe origin. \u0000Conclusion: Except in cases of lesional temporal lobe epilepsy with concordant prersurgical results, all patients with HMS should be evaluated through intracranial recordings. The auras, the HMS subtype, the hypometabolic areas showed by PET study, and the localization and lesion type seeing on MRI can help to decide what structures should be covered with depth electrodes during invasive recordings.","PeriodicalId":81656,"journal":{"name":"Journal of epilepsy","volume":"2 1","pages":"1-4"},"PeriodicalIF":0.0,"publicationDate":"2016-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4172/2472-0895.1000108","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70316554","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Epilepsy and Psychiatric Disorders: Is There a Common Genetic Susceptibility?","authors":"A. Chentouf","doi":"10.4172/2472-0895.1000E109","DOIUrl":"https://doi.org/10.4172/2472-0895.1000E109","url":null,"abstract":"According to epidemiological data, 25-48% of PWE suffer from mood disorders, and 14-31% from anxiety [2]. Moreover, depression represents one of the most common psychiatric disorders in PWE, with a point prevalence ranging from 12-37% in community settings [3]. In clinical studies, depressive symptoms in epilepsy have been associated with several variables such as poor seizure control, duration of epilepsy, having complex partial seizures or temporal lobe epilepsy, unemployment and the use of antiepileptic polytherapy.","PeriodicalId":81656,"journal":{"name":"Journal of epilepsy","volume":"2 1","pages":"1-1"},"PeriodicalIF":0.0,"publicationDate":"2016-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4172/2472-0895.1000E109","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70317449","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Muscle-eye-brain Disease and Drug-resistant Seizures: Unravelling the Phenotypic Heterogeneity of Congenital Muscular Dystrophies","authors":"D. Menon, Joseph Samuel, S. Satish, R. Menon, B. Thomas, A. Radhakrishnan","doi":"10.4172/2472-0895.1000107","DOIUrl":"https://doi.org/10.4172/2472-0895.1000107","url":null,"abstract":"Muscle-Eye-Brain Disease (MEB) constitutes part of a spectrum of closely overlapping Congenital Muscular Dystrophies (CMD) and neuronal migration disorders. Here, we present a child with MEB presenting with refractory epilepsy, a rare disease and all the more, a rare presenting manifestation. We hereby highlight the rarity of the syndrome per say, its presentation as refractory seizures to an Epileptologist and the radiological characteristics which help diagnosing MEB accurately obviating the need for an invasive procedure like muscle biopsy and molecular genetic studies in centres with limited infrastructure.","PeriodicalId":81656,"journal":{"name":"Journal of epilepsy","volume":"2 1","pages":"1-2"},"PeriodicalIF":0.0,"publicationDate":"2016-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4172/2472-0895.1000107","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70317014","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Nav1.7 Sodium Channel Isoform is Expressed in Growth Cones of Hippocampal Neurons in Culture","authors":"V. Bonetti, J. Carballo, L. García, Elizabeth Gómez, M. Longart","doi":"10.4172/2472-0895.1000106","DOIUrl":"https://doi.org/10.4172/2472-0895.1000106","url":null,"abstract":"Voltage Dependent Sodium Channels (VDSC) is fundamental for neuronal excitability and action potential propagation. There is a differential expression of the VDSC isoforms in different regions within the Central (CNS) and Peripheral Nervous System (PNS). The different isoforms (Nav1.1–Nav1.9) are widely expressed within the nervous system during specific developmental stages; however, the precise subcellular distribution for some isoforms is still incomplete. VDSC are important therapeutic targets for a wide variety of pathophysiological conditions, including chronic pain, cardiac arrhythmia, and epilepsy. Studies on the genetic basis underlying several striking human phenotypes have revealed the importance of NaV1.7 in pain signalling pathways and as a therapeutic target for treatment of chronic pain. Given that NaV1.7 expression in CNS has not been precisely addressed, and that the determination of its precise location is important to understand its function within neurons, we attempted to study the NaV1.7 subcellular localization in hippocampal neurons in culture by immunofluorescence. On the other hand, we studied the NaV1.2 subcellular localization and compared its expression pattern with NaV1.7. NaV1.2 is a Tetrodotoxin (TTX)-sensitive channel, predominantly expressed in the central nervous system and its subcellular distribution has been widely studied in central neurons. When we compared NaV1.2 and NaV1.7 we observed a distinctive subcellular localization for these two isoforms. Additionally, using a PanNaV antibody, which recognizes all sodium channel isoforms, we observed that PanNaV signal overlapped NaV1.2 and NaV1.7 specific signals. PanNaV labeled the Axon Initial Segment (AIS), cell bodies and neurites. NaV1.2 specific signal was mainly observed in the AIS, soma, dendrites and Golgi apparatus; while NaV1.7 mainly was present in soma, axons and growth cones. Our findings describing Nav1.7 in growth cones represent a new subcellular localization for this isoform and provide new evidences that suggest additional roles in neuronal functioning within the CNS.","PeriodicalId":81656,"journal":{"name":"Journal of epilepsy","volume":"32 1","pages":"1-7"},"PeriodicalIF":0.0,"publicationDate":"2016-06-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4172/2472-0895.1000106","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70316971","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Calculation of the Need of Multidisciplinary Units of Epilepsy in America","authors":"C. Valencia","doi":"10.4172/2472-0895.1000E108","DOIUrl":"https://doi.org/10.4172/2472-0895.1000E108","url":null,"abstract":"In the year 2011, I published an article related with the Multidisciplinary Epilepsy Units (MEU) [1]. However, in the time passed since this publication have done evident other needs in the treatment of patients, needs that only could cover through the association of different specialists; likewise, have appeared new advances in the treatment as well as in the epidemiological knowledge of different epileptogenic entities that force to a general review of this topic.","PeriodicalId":81656,"journal":{"name":"Journal of epilepsy","volume":"2 1","pages":"1-4"},"PeriodicalIF":0.0,"publicationDate":"2016-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70317436","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Post-operative Delirium after Cardiac Surgery: Can it be Prevented?","authors":"S. Kar","doi":"10.4172/2472-0895.1000E107","DOIUrl":"https://doi.org/10.4172/2472-0895.1000E107","url":null,"abstract":"Studies have found that risk of delirium after open heart surgeries to be higher as compared to other surgeries and twice as much incidence after valve surgeries as compared to CABG. The cause of delirium after cardiac surgery is not very well known. The triggering of this situation points towards inflammation, acute stress responses and disruption of transmission of neurological pathways due to systemic inflammatory response syndrome, caused by the CPB process.","PeriodicalId":81656,"journal":{"name":"Journal of epilepsy","volume":"2016 1","pages":"1-1"},"PeriodicalIF":0.0,"publicationDate":"2016-04-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70317396","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Ketogenic Diet Approach as Metabolic Treatment for a Variety of Diseases","authors":"R. Pilla","doi":"10.4172/2472-0895.1000E110","DOIUrl":"https://doi.org/10.4172/2472-0895.1000E110","url":null,"abstract":"Human brain derives over 60% of its energy from ketones when glucose availability is limited. After prolonged periods of fasting or Ketogenic Diet (KD), the whole body utilizes energy obtained from Free Fatty Acids (FFAs) released from adipose tissue. However, the brain is not capable to obtain significant energy from FFAs, thus hepatic ketogenesis converts them into ketone bodies: βHydroxybutyrate (BHB) and acetoacetate (AcAc), while a percentage of AcAc spontaneously decarboxylates to acetone [1]. To date, it has been broadly demonstrated how the metabolic state of mild ketosis, which can be induced through KD administration, calorie restriction or fasting, represents a valid tool for the metabolic management of epilepsy and a number neurodegenerative diseases [2], Amyotrophic Lateral Sclerosis (ALS) [3], and some types of cancer [4,5]. In addition, nutritional treatments represent an effective alternative where pharmaceutical approaches fail or produce unbearable side effects and costs for public health worldwide. However, before analyzing how benefits from therapeutic ketosis could be exploited, let us mention some pivotal concepts about metabolism. Under normal conditions and mostly in western societies, a healthy brain utilizes glucose as primary energy source, which unbalance can lead to a number of neurodegenerative disorders often associated with mitochondrial impairment and glucose transport-related dysfunctions, such as in epilepsy, Traumatic Brain Injury (TBI), Parkinson’s and Alzheimer’s diseases [6,7]. Ketone bodies and Krebs cycle intermediates represent the best fuels for brain and other organs. In fact, through their utilization, impaired glucose metabolism may be bypassed and their neuroprotective properties may be exploited [8]. However, neuroprotective mechanisms of ketosis are currently object of studies as mechanisms of action are still not sufficiently understood. It has been shown that ketone bodies are neuroprotective as they induce a consistent increase in mitochondrial biogenesis regulating the synaptic function, and also generate ATP increases, thus reducing the reactive oxygen species production in neurological tissues [9,10], and notably inhibit superoxide synthesis in primary rat neuronal cultures exposed to hyperoxia [11]. Moreover, the main reason why the KD has been proven so effective as an anticonvulsant aFpproach is because it significantly reduces the metabolism of glucose [12]. In addition, Ma and colleagues [13] demonstrated that, at physiological concentrations, BHB and AcAc reduce spontaneous discharges of GABAergic neurons in the rat substantia nigra, through ATP-sensitive potassium channels. Also, a reduction of total CNS aspartate levels in association with an increase of glutamate concentrations was found during ketosis, observing a significant increase of decarboxylated glutamate to GABA, the main inhibitory neurotransmitter [14,15]. Moreover, a remarkable increase in mitochondrial transcription enzy","PeriodicalId":81656,"journal":{"name":"Journal of epilepsy","volume":"2 1","pages":"1-3"},"PeriodicalIF":0.0,"publicationDate":"2016-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70317081","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Nuclear Medicine Imaging in Epilepsy","authors":"Jiaqiong Wang, R. Carroll","doi":"10.4172/2472-0895.1000E105","DOIUrl":"https://doi.org/10.4172/2472-0895.1000E105","url":null,"abstract":"For epilepsy patients who are not responding to anticonvulsant medications, surgery is an alternative treatment. A key issue in epilepsy surgery is the accurate localization of the “epileptogenic zone”. To date, pre-surgical evaluation of the epileptogenic network can be carried out by Electroencephalogram (EEG), video-EEG, magnetic resonance imaging, magneto-encephalography, single-photon emission computed tomography (SPECT) and positron emission tomography (PET). The interictal FDG-PET reveals hypometaboism at the epileptic focus, and it has been demonstrated to be much more sensitive than the interictal SPECT, and similarly sensitive to the ictal SPECT for the accurate localization of epileptogenic foci prior to surgical therapy. Visual assessment of 18F-FDG-PET is associated with interobserver and intraobserver variability. We have studied the issues of rigorous quantitation of FDG-PET brain studies and developed self-normalization technique. In addition to FDG-PET imaging, PET receptor imaging has also been demonstrated to provide significant insight into the mechanisms of neurotransmitters in epileptogenesis. In conclusion, we believe that nuclear medicine imaging can facilitate the identification of epileptic foci and investigate novel treatment for epilepsy.","PeriodicalId":81656,"journal":{"name":"Journal of epilepsy","volume":"2 1","pages":"1-2"},"PeriodicalIF":0.0,"publicationDate":"2015-12-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4172/2472-0895.1000E105","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70317331","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}