{"title":"Epilepsy in Children with ADHD","authors":"K. Hung","doi":"10.4172/2472-0895.1000E114","DOIUrl":"https://doi.org/10.4172/2472-0895.1000E114","url":null,"abstract":"Epilepsy is increasingly recognized as an important association with Attention Deficit/Hyperactivity Disorder (ADHD) in children. Previous studies reported the seizure occurrence in children with ADHD as 2~7% Epilepsy in children with ADHD appears to be earlier in age onset and more difficult in seizure control than those without. The genetic and clinical information might refer to a common neurobiological basis for epilepsy and ADHD.","PeriodicalId":81656,"journal":{"name":"Journal of epilepsy","volume":"2016 1","pages":"1-1"},"PeriodicalIF":0.0,"publicationDate":"2016-11-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70317466","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}
J. Xiang, K. Leiken, C. Wu, X. Wang, Y. Fan, L. Qi, H. Qiao
{"title":"High Frequency Neuromagnetic Signals: A New Biomarker for Localizing Epileptic Areas Running Title: High-Frequency Neuromagnetic Signals in Epilepsy","authors":"J. Xiang, K. Leiken, C. Wu, X. Wang, Y. Fan, L. Qi, H. Qiao","doi":"10.4172/2472-0895.1000E113","DOIUrl":"https://doi.org/10.4172/2472-0895.1000E113","url":null,"abstract":"Xiang J1* , Leiken K1, Wu C2, Wang X2, Fan Y3, Qi L4 and Qiao H4 1MEG Center, Division of Neurology, Cincinnati Children’s Hospital Medical Center, Cincinnati, OH, USA 2Department of Neurology, Nanjing Brain Hospital, Nanjing, People’s Republic China 3Department of Pediatric, Shengjing Hospital, Shenyang, People’s Republic China 4MEG Laboratory, Tiantan Hospital, Beijing, People’s Republic of China *Corresponding author: Xiang J, Division of Neurology, Cincinnati Children’s Hospital Medical Center 3333, Burnet Avenue, Cincinnati, OH, 45220, USA, Tel: 1-513-636-6303, Fax: 1-513-636-1888; E-mail: Jing.xiang@cchmc.org","PeriodicalId":81656,"journal":{"name":"Journal of epilepsy","volume":"2016 1","pages":"1-3"},"PeriodicalIF":0.0,"publicationDate":"2016-10-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70317423","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}
R. Andrade-Machado, P. Aguledo-Flórez, L. Salazar-Peláez
{"title":"Dysplasia Type Ia, Ib and Hippocampal Sclerosis: Is Reelin the Missing Link?","authors":"R. Andrade-Machado, P. Aguledo-Flórez, L. Salazar-Peláez","doi":"10.4172/2472-0895.1000115","DOIUrl":"https://doi.org/10.4172/2472-0895.1000115","url":null,"abstract":"Abnormal radial and/or tangential cortical lamination in the temporal lobe cortex associated to Hippocampal Sclerosis (HS) is now classified as focal cortical dysplasia (FCD) type IIIa in the current ILAE FCD classification. In these cases, the temporal cortex may show architectural abnormalities or hypertrophic neurons outside layer V. Five variants of FCD type IIIa have been recognized: HS with architectural abnormalities in the temporal lobe; HS with Temporal Lobe Sclerosis (TLS), HS with TLS and heterotopic neurons in subcortical white matter, HS with TLS and small “lentiform” heterotopias in subcortical white matter; and HS without TLS but with small “lentiform” subcortical heterotopias [1]. One of these types of histological features is frequently found in specimens of patients with temporal lobe epilepsy.","PeriodicalId":81656,"journal":{"name":"Journal of epilepsy","volume":"2 1","pages":"1-4"},"PeriodicalIF":0.0,"publicationDate":"2016-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4172/2472-0895.1000115","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70316811","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":"Neonatal Seizures Characteristics and Prognosis","authors":"M. Knežević-Pogančev","doi":"10.4172/2472-0895.1000114","DOIUrl":"https://doi.org/10.4172/2472-0895.1000114","url":null,"abstract":"Seizures are the most common neurological emergency in the neonatal period. Neonatal seizures are very often named neonatal convulsions even they do not present as convulsions. They are one of the most important diagnostic and therapeutic clinical challenges. They occur during neonatal period, from birth to the end of 28th day of life [1]. Seizures are more common in the neonatal period than at any other time during life. They appear mostly during the first 1-2 days, but usually during first week from birth. Neonatal brain is uniquely vulnerable to seizures. Usually they signify serious damage to the developing immature brain. There is also clear evidence that seizure can damage the brain and exacerbate pre-existing injury. Therefore it is very imperative to identify neonatal seizures and treat them as soon as possible.","PeriodicalId":81656,"journal":{"name":"Journal of epilepsy","volume":"2 1","pages":"1-2"},"PeriodicalIF":0.0,"publicationDate":"2016-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4172/2472-0895.1000114","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70316745","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":"Conflict Processing and Response Inhibition in Patients with Temporal Lobe Epilepsy: fMRI Study","authors":"J. Alvarez-Alamilla, Velasco Al, Río-Portilla Yd","doi":"10.4172/2472-0895.1000113","DOIUrl":"https://doi.org/10.4172/2472-0895.1000113","url":null,"abstract":"We evaluate the conflict processing and response of inhibition with the Stroop task in patients with intractable temporal lobe epilepsy who underwent depth electrode amygdala-hippocampal recording to determine focus laterality for further lobectomy and control subjects analyzing the cerebral metabolic response by fMRI. Patients showed longer reaction times and more errors in the Stroop task than control subjects. At the conflict processing and response of inhibition, TLE patients presented difficulties in the executive system regulated by the frontal lobe; they showed dominant brain activation in the right hemisphere frontal lobe and right inferior frontal junction, inferior frontal, superior frontal, middle frontal gyri and ACC. Patients did not show left activation, as observed in control subjects.","PeriodicalId":81656,"journal":{"name":"Journal of epilepsy","volume":"2 1","pages":"1-6"},"PeriodicalIF":0.0,"publicationDate":"2016-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4172/2472-0895.1000113","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70316728","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}
Hala A. Shaheen, Sayed S. Sayed, L. Daker, Mostafa Magdy
{"title":"Early Atherosclerotic Changes in the Patients with Idiopathic Epilepsy: Egyptian Preliminary Study","authors":"Hala A. Shaheen, Sayed S. Sayed, L. Daker, Mostafa Magdy","doi":"10.4172/2472-0895.1000112","DOIUrl":"https://doi.org/10.4172/2472-0895.1000112","url":null,"abstract":"Background: Patients with epilepsy are at higher risk for atherosclerosis which may be due to epilepsy or antiepileptic drugs. The frequency of atherosclerosis in patients with epilepsy was not previously studied in Egypt. Objective of this study: This study aimed to detect the frequency of subclinical atherosclerosis and some vascular risk factors in patients with idiopathic epilepsy and to correlate it to clinical and laboratory data. Patients and methods: Ninety patients with idiopathic epilepsy and 30 ages, sex matched healthy controls subjected to neurological examination, extra cranial carotid duplex, lipid profile, uric acid and CRP levels. Results: The level of high density lipoprotein cholesterol was significantly lower in all patients with epilepsy and those treated with enzyme inducer antiepileptic drugs than the control subjects. Level of serum uric acid was statistically significantly higher in all patients with epilepsy including the untreated patients and those treated with non-enzyme inducer and poly antiepileptic drugs than control subjects. The Common Carotid Artery Intima Media Thickness (CCA IMT) was significantly higher in all patients with epilepsy including untreated and treated patients with enzyme inducer or non-inducer than control. There was a significant positive correlation between the CCA IMT and duration of illness as well as duration of the antiepileptic drugs. Conclusion: Frequency of subclinical atherosclerosis in the patients with idiopathic epilepsy was 63.33%. The epilepsy itself could result in subclinical atherosclerotic changes in the patients with epilepsy, which could be exacerbated by the antiepileptic drugs, particularly the enzyme inducer drugs.","PeriodicalId":81656,"journal":{"name":"Journal of epilepsy","volume":"2 1","pages":"1-6"},"PeriodicalIF":0.0,"publicationDate":"2016-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4172/2472-0895.1000112","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70316665","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":"Which are the Molecular Basis of Dysplasia Type IIIa, What Should We Know and Why?","authors":"R. Andrade-Machado","doi":"10.4172/2472-0895.1000E112","DOIUrl":"https://doi.org/10.4172/2472-0895.1000E112","url":null,"abstract":"Many papers are focused in the risk factors associated to temporal lobe epilepsy with HS. Complex febrile seizures, early head traumas, central nervous system infections or mild perinatal hypoxia have been associated with HS [3]. Although not totally elucidated, the molecular basis of HS is better known than the molecular basis of dysplasia type Ia or Ib. Thus, less is known about the complex mechanisms that provoke HS with dysplasia type Ia or Ib (dysplasia type IIIa).","PeriodicalId":81656,"journal":{"name":"Journal of epilepsy","volume":"2 1","pages":"1-3"},"PeriodicalIF":0.0,"publicationDate":"2016-08-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4172/2472-0895.1000E112","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70317408","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":"Implementation of Ketogenic Diet Therapy in Refractory Epilepsies","authors":"J. Liao, L. Xiong","doi":"10.4172/2472-0895.1000111","DOIUrl":"https://doi.org/10.4172/2472-0895.1000111","url":null,"abstract":"The Ketogenic Diet (KD) has been used in treatment of epilepsy in mainland China since 2004. Clinical indications of KD include: Glucose Transporter Type 1 (GLUT-1) deficiency, Pyruvate Dehydrogenase Deficiency (PDHD, myoclonus-astatic epilepsy (Doose syndrome), tuberous sclerosis complicated with or without epilepsy, Rett syndrome, Dravet syndrome, infantile spasms, and Landau-Kleffner syndrome, Lafora disease, and super-refractory status epilepticus. The contraindications of KD include: Inborn error of lipid metabolism, porphyria, and patients who are unable to cooperate with the KD. There should be standardized clinical consultation and evaluation before starting KD treatment; and special attention should be paid to selection and preparation of food, and to indication of age and geographic area etc. During the KD treatment, the transition time from ordinary diet to KD often takes 1-2 weeks; and a final 2: 1-4: 1 ketogenic diet ratio will normally produce ketosis of clinical therapeutic effect. The KD could be combined with anticonvulsant treatment. A qualified ketogenic diet therapy means: (1) Proper nutrition and growth with normal nutrition biomarkers; (2) Tasty foods: patients are willing to accept the therapeutic diet; (3) Ideal state of ketosis: urine ketone remains above (+++), blood ketone at about 4.0 mmol/L, blood sugar is controlled at 4.0 mmol/L, ratio of blood sugar/blood ketone is about 1: 1-2: 1; (4) Reasonable balanced food composition, defecate daily and naturally without constipation; (5) No remarkable complication(s). It is recommended that KD could be tried at least for three months continuously. Good responders should maintain the KD therapy for 2 yrs. or so. It often needs to take 3-6 months to return back to a regular diet. KD therapy should be monitored with close follow-ups and assessments. Our extensive experience has confirmed that it is safe in clinical practice.","PeriodicalId":81656,"journal":{"name":"Journal of epilepsy","volume":"2 1","pages":"1-5"},"PeriodicalIF":0.0,"publicationDate":"2016-08-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4172/2472-0895.1000111","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70316625","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}
Jose g. Gonzalez, Isabella Rendon, Marisol Vilamizar, J. Campos, L. González
{"title":"A New de novo Mutation Associated with Neurofibromatosis (NF-1)","authors":"Jose g. Gonzalez, Isabella Rendon, Marisol Vilamizar, J. Campos, L. González","doi":"10.4172/2472-0895.1000110","DOIUrl":"https://doi.org/10.4172/2472-0895.1000110","url":null,"abstract":"Neurofibromatrosis type 1 (NF-1) in the most common neurocutaneous disease with a autosomal dominant inheritance pattern and a frequency of 1:3.500 lives births in the general population, regardless of race and sex. NF-1 is a progressive disorder characterized by multiples cafe-au-lait macules, neurofibromas, Lish nodules and others manifestations such as bone abnormalities, short stature, epilepsy, learning disabilities, hyperactivity, with a highly variable and unpredictable expression. Half of its cause comes from different mutations in a gene on chromosome 17, resulting in less or performance neurofibromin having the regulatory domain of tumor activity. The other 50% of the case are caused by de novo mutation. It is an infant 13 months old, no family history of neurofibromatosis, which features six cafe-au lait spots 1 cm of diameter in the legs, chest, auxiliary region a and short stature. The clinical diagnostic criteria of NF-1 were established by The National Institutes Heath Consensus Development Conference in 1987. It has been suggested that pathogenic mutation in the NF-1 gene be added to the list of diagnostic criteria, but not yet accepted. A molecular genetics study showed an alteration in exon 16 c.2540T>G (p.Leu847 Arg). No genetic alterations found in phenotypic parents. After six year of follow-up she was not observed clinical or radiographic abnormalities. The genetic study is mandatory for confirmation of the suspected diagnosis and to monitor de novo mutations that knowledge and phenotypic expression thereof.","PeriodicalId":81656,"journal":{"name":"Journal of epilepsy","volume":"9 1","pages":"1-3"},"PeriodicalIF":0.0,"publicationDate":"2016-08-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4172/2472-0895.1000110","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70316612","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}