Y. Kawakami, Kenichi Saito, Asami Baba, Shinya Koizumi, K. Kuwabara, T. Fujita, O. Fujino
{"title":"Measures to Counteract Oseltamivir Phosphate-Induced Changes on Electroencephalograms of Epilepsy-Prone El Mice","authors":"Y. Kawakami, Kenichi Saito, Asami Baba, Shinya Koizumi, K. Kuwabara, T. Fujita, O. Fujino","doi":"10.3805/EANDS.5.20","DOIUrl":"https://doi.org/10.3805/EANDS.5.20","url":null,"abstract":"Oseltamivir phosphate has been reported to change spike discharges on electroencephalograms (EEGs) of epilepsy-prone El mice. The present study shows that two anti-epileptic drugs (sodium valproate and diazepam) counteract such alterations. Our observations sug-gest that short-term supplemental administration of sodium valproate or diazepam may be considered as an option when patients with epileptic tendencies but are not on a regular course of anti-epileptic drugs are taking oseltamivir phosphate. Abstract","PeriodicalId":39430,"journal":{"name":"Epilepsy and Seizure","volume":"22 1","pages":"20-27"},"PeriodicalIF":0.0,"publicationDate":"2012-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70082956","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}
G. Imataka, R. Kuribayashi, Keiko Tsukada, T. Tsuboi, H. Yamanouchi, O. Arisaka
{"title":"Pyridoxine-dependent status epilepticus diagnosed during infancy","authors":"G. Imataka, R. Kuribayashi, Keiko Tsukada, T. Tsuboi, H. Yamanouchi, O. Arisaka","doi":"10.3805/EANDS.4.1","DOIUrl":"https://doi.org/10.3805/EANDS.4.1","url":null,"abstract":"Pyridoxine dependence is a very rare inborn error of metabolism. The disorder develops mainly during the early neonatal period, and cases diagnosed in infants are even rarer. We herein report a case of a 77-day-old boy with status epilepticus diagnosed with pyridoxine dependence. On day 2 after birth, the boy required respiratory management after entering a partial convulsive state. The convulsions did not respond to phenobarbitals and were temporarily controlled by continuous intravenous administration of midazolam. Subsequently, partial seizures occurred frequently, and the patient was observed under treatment with oral phenobarbital and phenytoin, and intravenous midazolam. However, at 65 days of age, partial convulsions of the right upper and lower limbs lasting for one minute occurred episodically in clusters every few to ten minutes. A high dose of phenobarbital was administered and the blood concentration increased to 42 μg/ml, but convulsions were not controlled. At 77 days of age, when 100 mg of pyridoxine was slowly injected intravenously during electroencephalography, the background activity flattened and spikes disappeared. Pyridoxine dependence was diagnosed and all antiepileptic agents were discontinued. Oral administration of pyridoxine at 10 mg/kg/day was started and seizures no longer occurred. Pyridoxine dependence is a treatable inborn error of metabolism. To obtain a diagnosis of pyridoxine dependence, trial administration of pyridoxine is essential, and the pyridoxine test for a definitive diagnosis should also be conducted in cases of status epilepticus during infancy.","PeriodicalId":39430,"journal":{"name":"Epilepsy and Seizure","volume":"4 1","pages":"1-6"},"PeriodicalIF":0.0,"publicationDate":"2011-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70082823","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":"Usefulness of 123I-iomazenil SPECT for childhood focal epilepsies","authors":"Kentaro Okamoto, H. Oguni, Y. Hirano, M. Ōsawa","doi":"10.3805/EANDS.4.15","DOIUrl":"https://doi.org/10.3805/EANDS.4.15","url":null,"abstract":"Purpose: We investigated the usefulness of 123I-iomazenil (IMZ-) SPECT to detect epileptic foci in children with symptomatic focal epilepsy (SFE).Subjects: 21 children with SFE who underwent IMZ-SPECT to identify the epileptic focus were studied.Methods: We retrospectively compared the localization and lateralization of epileptic foci obtained from visualization of IMZ-SPECT images and those speculated based on a combination of clinical manifestations, EEG findings, and brain MRI. We then verified the concordance of the results between the two methods.Results: There was concordance in both lateralization and localization in 9⁄12 patients with temporal lobe epilepsy (75%), in 2⁄5 patients with frontal lobe epilepsy (40%), and in 2⁄4 patients with parieto-occipital lobe epilepsy (50%). Overall, the epileptic foci detected by IMZ-SPECT was consistent with those speculated based on other findings at least in 13 of 21 patients (62%) with SFE.Discussion: As IMZ-SPECT is a potentially useful method for detecting epileptic foci, we should accumulate cases to verify the limitations and appropriate application of this method in the diagnosis of childhood SFE.","PeriodicalId":39430,"journal":{"name":"Epilepsy and Seizure","volume":"4 1","pages":"15-25"},"PeriodicalIF":0.0,"publicationDate":"2011-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3805/EANDS.4.15","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70082851","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}
M. Oguni, N. Inoue, Kyoya Takahata, Masamichi Koseki
{"title":"Is Modified Atkins Diet Therapy Applicable for Adults with Intractable Epilepsy Patients? - A Short Trial in Adult Volunteers","authors":"M. Oguni, N. Inoue, Kyoya Takahata, Masamichi Koseki","doi":"10.3805/EANDS.4.7","DOIUrl":"https://doi.org/10.3805/EANDS.4.7","url":null,"abstract":"Background: The Atkins diet modified for epilepsy patients (modified Atkins diet: MAD) was reported to be a substitute for the classical ketogenic diet. Recently, it has been shown that this diet is effective not only for intractable childhood epilepsy but also for intractable adulthood epilepsy and Glut 1 deficiency syndrome. In Japan, this diet is difficult to promote, because the menu and the taste are not suitable for Japanese and side effects of this unbalanced diet remain unclear.Methods: To promote this therapy in Japan, the recipes of MAD were modified to adapt to the Japanese population, and evaluated in 10 healthy adult volunteers for 1 week. Subjects' evaluation for taste and hunger, as well as urinary and blood laboratory examinations were analyzed.Results: All volunteers evaluated the diet menu as sufficiently palatable, and continued the diet without difficulty for 1 week. However, they felt uneasy with the fatty menu and complained of constipation that was within tolerable levels. As for urinary ketone bodies measured by ketostick, four and six volunteers were 2 to 4+ and 1 to 2+, respectively at the end of the trial. Side effects including variable degrees of weight loss, hypoglycemia, hypercholesterolemia, and hyperuricemia were observed in all subjects.Conclusion: MAD can be used more comfortably as a substitute for the classical ketogenic diet, if the recipes are adapted for Japanese population. The diet would result in a sufficient level of ketosis since our adult volunteers developed mild to moderate ketosis despite only one-week trial without starvation. The long-term side effects should be carefully monitored because even the short-term trial results in some metabolic changes.","PeriodicalId":39430,"journal":{"name":"Epilepsy and Seizure","volume":"4 1","pages":"7-14"},"PeriodicalIF":0.0,"publicationDate":"2011-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3805/EANDS.4.7","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70082907","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. Tanaka, T. Ohto, Takashi Saito, N. Iwasaki, R. Sumazaki
{"title":"Ethosuximide completely suppressed epileptic negative myoclonus in childhood localization-related epilepsy","authors":"R. Tanaka, T. Ohto, Takashi Saito, N. Iwasaki, R. Sumazaki","doi":"10.3805/EANDS.3.1","DOIUrl":"https://doi.org/10.3805/EANDS.3.1","url":null,"abstract":"We report two cases of localization-related epilepsy manifesting frequent brief atonia. The patients were assumed to have epileptic negative myoclonus (ENM), and were successfully treated with ethosuximide (ESM). Both exhibited hemi-orofacial twitches during sleep, and interictal electroencephalography (EEG) showed paroxysms over the contralateral posterior-temporal and centroparietal regions. Incessant atonia appeared at nine and 10 years of age accompanied by motor paresis. Ictal EEG showed irregular high-voltage spike-waves predominantly over bilateral centroparietal regions. Carbamazepine and zonisamide were ineffective in controlling, or even aggravated ENM. The addition of ESM resulted in immediate and complete disappearance of ENM and partial motor seizures along with an improvement of motor paresis. The first case was assumed to have idiopathic etiology because of normal development before the onset of epilepsy, while the second case was considered to have cryptogenic etiology based on a pre-existing intellectual disability. Hence, we recommend that ESM should be considered for the treatment of ENM that develops during the course of localization-related epilepsy, regardless of the etiology. However, further studies are still needed to evaluate the effects of ESM in the treatment of ENM.","PeriodicalId":39430,"journal":{"name":"Epilepsy and Seizure","volume":"3 1","pages":"1-9"},"PeriodicalIF":0.0,"publicationDate":"2010-11-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70082195","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":"Genetic susceptibility and pharmacogenomics of severe cutaneous adverse drug reactions","authors":"Yuan-Tsong Chen","doi":"10.3805/EANDS.3.51","DOIUrl":"https://doi.org/10.3805/EANDS.3.51","url":null,"abstract":"Several recent studies have reported strong genetic associations between HLA-B and susceptibility to drug hypersensitivity. The genetic associations are often drug-specific; HLA-B*1502 is associated with carbamazepine-induced Stevens-Johnson syndrome and toxic epidermal necrolysis (SJS⁄TEN), HLA-B*5701 with abacavir hypersensitivity, and HLA-B*5801 with allopurinol-induced severe cutaneous adverse reactions. The genetic association can also be phenotype-specific; B*1502 is associated solely with carbamazepine-SJS⁄TEN, and not with either maculopapular eruption or hypersensitivity syndrome. Furthermore, genetic association can be ethnicity-specific; carbamazepine-SJS⁄TEN associated with B*1502 is seen in Southeast Asians but not in Caucasians or Japanese, which can be explained by the difference in allele frequencies among populations. The strong genetic association suggests a direct involvement of HLA in the pathogenesis of drug hypersensitivity, in which the HLA molecule presents an antigenic drug for T-cell activation. Pharmacogenomic study has identified an unusual form of granulysin secreted by cytotoxic T lymphocytes and natural killer cells responsible for the disseminated keratinocyte death in Stevens-Johnson syndrome and toxic epidermal necrolysis. The high sensitivity⁄specificity of some of these genetic markers provides a plausible basis for developing tests to identify individuals at risk for these life-threatening conditions in some populations. Application of HLA-B*1502 and HLA-B*5701 genotyping as a screening tool for patients taking carbamazepine and abacavir, respectively, has reduced the incidence of these adverse drug reactions.","PeriodicalId":39430,"journal":{"name":"Epilepsy and Seizure","volume":"30 6 1","pages":"51-58"},"PeriodicalIF":0.0,"publicationDate":"2010-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3805/EANDS.3.51","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70082928","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":"Thoracocervicofacial purpura and hypoxemia after generalized tonic-clonic seizure","authors":"Daisuke Matsuoka, T. Hashimoto, T. Kashima","doi":"10.3805/EANDS.3.19","DOIUrl":"https://doi.org/10.3805/EANDS.3.19","url":null,"abstract":"We report a case of a 41-year-old man who showed thoracocervicofacial purpura after generalized tonic-clonic convulsion. The patient also had hypoxemia with chest CT findings of non-homogeneous high density in the posterior areas in both lungs, without signs of infection or heart failure. The purpura suggested that strong valsalva maneuver during airway closure and the resultant increase in systemic arterial and pulmonary vascular pressure may have led to pulmonary congestion.","PeriodicalId":39430,"journal":{"name":"Epilepsy and Seizure","volume":"3 1","pages":"19-23"},"PeriodicalIF":0.0,"publicationDate":"2010-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70082725","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":"Genomics of drug resistance: moving ahead","authors":"S. Sisodiya","doi":"10.3805/EANDS.3.59","DOIUrl":"https://doi.org/10.3805/EANDS.3.59","url":null,"abstract":"Drug resistance is an important clinical problem. Significant efforts have been made recently to improve understanding. Most recently, a Commission of the International League against Epilepsy has produced a document on the definition of drug resistance [1]. This is an important step forward. It must be recognised, however, that the definition of drug resistance may need to be adjusted according to the needs of a particular clinical or research question. Overall, about one in three patients who have epilepsy do not respond to currently available anti-epileptic drugs. Not only is this a significant burden on healthcare systems, but it is also associated with an increased risk of morbidity and premature mortality for patients, as well as a broad range of psycho-social consequences. One can estimate that in the United Kingdom alone, for example, the cost of the first failed anti-epileptic drug is of the order of £20 to £30 million per year. There are of course costs well beyond monetary values. Observational studies have demonstrated that some patients who have not responded to several anti-epileptic drugs in the past, and might therefore be expected to continue to have seizures despite trials of further anti-epileptic drugs [2], might in fact occasionally respond to a new anti-epileptic drug [3, 4].","PeriodicalId":39430,"journal":{"name":"Epilepsy and Seizure","volume":"3 1","pages":"59-64"},"PeriodicalIF":0.0,"publicationDate":"2010-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70082982","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. Saruwatari, T. Ishitsu, Takayuki Seo, Masatsugu Shimomasuda, Yusuke Okada, Shuji Goto, R. Nagata, Ayaka Takashima, Shiho Yoshida, Shuichi Yoshida, N. Yasui‐Furukori, S. Kaneko, K. Nakagawa
{"title":"The clinical impact of cytochrome P450 polymorphisms on anti-epileptic drug therapy","authors":"J. Saruwatari, T. Ishitsu, Takayuki Seo, Masatsugu Shimomasuda, Yusuke Okada, Shuji Goto, R. Nagata, Ayaka Takashima, Shiho Yoshida, Shuichi Yoshida, N. Yasui‐Furukori, S. Kaneko, K. Nakagawa","doi":"10.3805/EANDS.3.34","DOIUrl":"https://doi.org/10.3805/EANDS.3.34","url":null,"abstract":"The goal of pharmacogenetics is to deliver safe and effective drug therapy. Genetic polymorphisms in cytochrome P450 (CYP) enzyme genes are implicated in the inter-individual variability in pharmacokinetics of antiepileptic drugs (AEDs). However, the clinical impact of CYP polymorphisms on AED therapy remains controversial. Previous studies have shown that the defective CYP2C9 alleles affect the required dose of phenytoin and the risk of its toxicity. We have reported that the CYP2C19-deficient genotype is associated with the serum concentration of an active metabolite of clobazam, N-desmethylclobazam, and with the clinical efficacy of clobazam therapy. We determined also the influence of polymorphisms in CYP genes on the population pharmacokinetic parameters of AEDs us-","PeriodicalId":39430,"journal":{"name":"Epilepsy and Seizure","volume":"3 1","pages":"34-50"},"PeriodicalIF":0.0,"publicationDate":"2010-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3805/EANDS.3.34","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70082868","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":"Are drug-resistant and drug-sensitive patients the same?","authors":"M. Brodie","doi":"10.3805/EANDS.3.131","DOIUrl":"https://doi.org/10.3805/EANDS.3.131","url":null,"abstract":"Around 30% of adults with epilepsy remain refractory to antiepileptic drug (AED) therapy despite having similar seizure semiologies and syndromes to drug responsive individuals. How, when and why do they become pharmacoresistant? Observations from the Glasgow database of newly diagnosed patients receiving their first ever AED at the Epilepsy Unit have provided fascinating insights into the natural history of treated epilepsy. Prospective analyses of this expanding cohort were undertaken in 1997 (n=470), 2003 (n=780) and, most recently, in 2008 (n=1098). Overall, around 50% of patients became seizure free on their first ever AED with diminishing numbers responding to subsequent regimens either as monotherapy or in low dose combinations. The overall prognosis has modestly improved over recent years as newer drugs with novel mechanisms of action have become available. However, from the most recent analysis, around 25% of the population never had useful period of seizure freedom despite receiving many AEDS singly and in combination. Interestingly, a similar number never had another seizure after starting treatment. Differences between these clinical phenotypes included higher seizure densities prior to initiation of therapy and concurrent psychiatric comorbidities suggesting greater brain dysfunction. The presence of a family history of epilepsy and⁄or febrile convulsions also predicted refractory epilepsy, implicating a genetic component in drug response. These observations tend to support the suggestion that drug-resistant and drug-sensitive patients are not necessarily the same.","PeriodicalId":39430,"journal":{"name":"Epilepsy and Seizure","volume":"3 1","pages":"131-140"},"PeriodicalIF":0.0,"publicationDate":"2010-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70082050","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}