ライフサイエンスコーパス: epilepsy

1 owing traumatic brain injury (post-traumatic epilepsy).

2 experimental models of chronic temporal lobe epilepsy.

3 and seizure-like hallmarks characteristic of epilepsy.

4 mmon than in other causes of childhood onset epilepsy.

5 of the most catastrophic forms of pediatric epilepsy.

6 riants can lead to various forms of neonatal epilepsy.

7 Risk of childhood epilepsy.

8 associated with autism spectrum disorder and epilepsy.

9 l circuits leading to non-convulsive absence epilepsy.

10 h as cystic fibrosis, Bartter's syndrome and epilepsy.

11 trategy to reduce the incidence of childhood epilepsy.

12 monotherapy for adults with newly diagnosed epilepsy.

13 dentifying the variants and genes underlying epilepsy.

14 encephalography from canines and humans with epilepsy.

15 dhood, Rapid-onset Dystonia Parkinsonism, or epilepsy.

16 itations and future applications of LITT for epilepsy.

17 comorbid memory impairments associated with epilepsy.

18 recessive mutations in SLC45A1 cause ID and epilepsy.

19 emerging role for synaptic dysregulation in epilepsy.

20 ibility variants associated with generalized epilepsy.

21 spontaneous seizures from four patients with epilepsy.

22 izures in a mouse model of pharmacoresistant epilepsy.

23 of mutations in children with SCN2A-related epilepsy.

24 an effective treatment for refractory focal epilepsy.

25 ted with higher odds of an individual having epilepsy.

26 n activity-dependent long non-coding RNA and epilepsy.

27 , months and years play an important role in epilepsy.

28 yhydramnios, megalencephaly, and symptomatic epilepsy.

29 in spatial navigation, memory, dementia and epilepsy.

30 mental epileptogenesis and observed in human epilepsy.

31 cognitive impairment, movement disorder, or epilepsy.

32 eonatal complications and risks of childhood epilepsy.

33 f life and improved safety for patients with epilepsy.

34 s been linked to intellectual disability and epilepsy.

35 es, including behavioral symptoms of ASD and epilepsy.

36 human participants with medically refractory epilepsy.

37 -third of patients with mesial temporal lobe epilepsy.

38 ly behaving genetic rodent models of absence epilepsy.

39 at 2,048 Hz in people with refractory focal epilepsy.

40 results in ASD, intellectual disability, and epilepsy.

41 is no existing animal model of postmalarial epilepsy.

42 ntribute to the development of temporal lobe epilepsy.

43 in many human diseases, including cancer and epilepsy.

44 ents undergoing treatment for drug-resistant epilepsy.

45 s and a long history of drug-resistant focal epilepsy.

46 non-pharmacological treatment for refractory epilepsy.

47 proposed as a natural animal model for human epilepsy.

48 n patients with both idiopathic and acquired epilepsy.

49 help to predict whether someone will develop epilepsy.

50 ched for genes with a genetic association to epilepsy.

51 tive seizures in patients with temporal lobe epilepsy.

52 ure activity in patients with photosensitive epilepsy.

53 and pharmaco!dynamics biomarker for acquired epilepsy.

54 7D is associated with idiopathic generalized epilepsy.

55 mpal sclerosis and seizure burden in chronic epilepsy.

56 diseases such as autism spectrum disorder or epilepsy.

57 fiber axons, both hallmarks of temporal lobe epilepsy.

58 eloped depression and 97177 (0.9%) developed epilepsy.

59 stic yield of genetic testing for early-life epilepsies.

60 in remodeling protein mutated to cause human epilepsies.

61 romising alternative to treat drug-resistant epilepsies.

62 tial anticonvulsant compounds for refractory epilepsies.

63 of LITT for a variety of extratemporal lobe epilepsies.

64 and atypical), and myoclonic and generalized epilepsies.

65 compared with the offspring of women without epilepsy (2.51% in 2154 pregnancies).

66 omen, and 84791 [37%] were men; P < .001) or epilepsy (54419 [56%] were women, and 42758 [44%] were m

67 In the Scn2a(Q54) mouse model of epilepsy, a focal epilepsy phenotype is caused by transg

68 and Charlson Comorbidity Index with incident epilepsy, accounting for 4.6%, 7.1%, and 20.6% of the to

69 utcome defined as presence of one or more of epilepsy (active or in remission), motor disability, int

70 tcome and Measures: The hazard of developing epilepsy after incident depression and vice versa was ca

71 Epilepsy after pediatric traumatic brain injury (TBI) is

72 In photosensitive epilepsy, alpha-related blood oxygen level-dependent sig

73 loss of function leads to such disorders as epilepsy, Alzheimer's disease, and autism.

74 exclusively seen in patients with late onset epilepsies and lack of response to sodium channel blocke

75 1.2, have been associated with a spectrum of epilepsies and neurodevelopmental disorders.

76 al evaluation of newly presenting early-life epilepsies and not just reserved for those with severe p

77 parallels between human medial temporal lobe epilepsy and a naturally occurring condition in wild sea

78 rapeutic target for treatment of progressive epilepsy and a potential biomarker for epilepsy progress

79 to investigate the familial coaggregation of epilepsy and ADHD and to estimate the contribution of ge

80 Our findings suggest that epilepsy and ADHD may share less genetic risk as compare

81 gression to estimate the association between epilepsy and ADHD within individual and across relatives

82 To evaluate the effects of epilepsy and antiepileptic drugs (AEDs) used during preg

83 is, deficits in the activity of KCC2 lead to epilepsy and are also implicated in neurodevelopmental d

84 highly associated with medication-resistant epilepsy and are the most common cause of neocortical ep

85 Epilepsy and attention-deficit/hyperactivity disorder (A

86 preclinical evidence supporting treatment of epilepsy and autistic-like behaviors linked to DS with C

87 ate intellectual disability, with or without epilepsy and behavioural disorders, and 14 patients with

88 ved in representing space, memory formation, epilepsy and dementia.

89 phenotypes, occasionally with neonatal onset epilepsy and developmental impairment, as well as genera

90 y mass index (BMI) and the risk of childhood epilepsy and examine associations between obesity-relate

91 y implicate PPP3CA in early-onset refractory epilepsy and further support the emerging role for synap

92 es are implicated in synaptic dysfunction in epilepsy and in an array of degenerative and autoimmune

93 143 adults with unexplained childhood-onset epilepsy and intellectual disability who were recruited

94 le candidate CNVs and genes in patients with epilepsy and intellectual disability.

95 s in adults with unexplained childhood-onset epilepsy and intellectual disability.

96 otocadherin-19 (Pcdh19) cause female-limited epilepsy and mental retardation in humans.

97 es to human neurological disorders including epilepsy and neuropathic pain.

98 ew pharmacological and dietary therapies for epilepsy and other disorders.

99 ing inherited neurological diseases, such as epilepsy and pain.

100 mine the effect of depression on the risk of epilepsy and seizure outcomes.

101 behavior changes modeling bipolar disorder, epilepsy and sudden death.

102 l research into mechanisms and prevention of epilepsy and SUDEP.

103 illation at rest is different in people with epilepsy and visual sensitivity.

104 observed only in patients with temporal lobe epilepsy and were recorded exclusively from mesiotempora

105 intellectual disability with absent speech, epilepsy, and hypotonia was observed in all affected ind

106 lfide HMGB1 in patients with newly diagnosed epilepsy, and its persistence was associated with subseq

107 pses, genic intolerance, membrane transport, epilepsy, and mental disorders.

108 between depression severity and the risk of epilepsy, and the degree to which depression mediates th

109 An antibody prevalence in epilepsy (APE) score based on clinical characteristics w

110 Childhood epilepsies are frequently severe, presenting in infancy

111 The causes of epilepsy are poorly understood and, in more than 60% of

112 on people worldwide currently suffering with epilepsy are resistant to antiepileptic drugs (AEDs).

113 The diagnosis of epilepsy as well as obesity-related pregnancy and neonat

114 ll patients free of prevalent depression and epilepsy at 18-90 years of age who were active after the

115 , including schizophrenia, bipolar disorder, epilepsy, autism, Alzheimer's disease, and Parkinson's d

116 ed electroencephalographic recordings) as an epilepsy biomarker in brain injury patients.

117 mbination significantly delayed the onset of epilepsy, blocked disease progression between 2 and 5 mo

118 des not only a candidate for human myoclonic epilepsy but also insights into the disease etiology, wh

119 bring seizure remission in people with focal epilepsy but requires careful selection of candidates.

120 children and adolescents with drug-resistant epilepsy, but additional data are needed from randomized

121 Childhood absence epilepsy (CAE) is the most common paediatric epilepsy sy

122 Approximately one-third of newly diagnosed epilepsy cases fail to become seizure-free in response t

123 Seizure patterns identified in focal epilepsies caused by diverse etiologies are likely due t

124 y abnormal brain development and intractable epilepsy, caused similar defects in Golgi localization a

125 show that epilepsy eQTLs are enriched within epilepsy-causing genes: an epilepsy cis-gene is signific

126 yhydramnios, megalencephaly, and symptomatic epilepsy, characterized by abnormal brain development an

127 e enriched within epilepsy-causing genes: an epilepsy cis-gene is significantly more likely to be a c

128 epsy; mean (SD) age at first delivery of the epilepsy cohort was 30.54 (5.18) years.

129 mans and in different animal models of focal epilepsy correlates with reduction of neuronal firing an

130 ward chloride transport had no effect during epilepsy development, and significantly increased granul

131 t on granule cell activation earlier, during epilepsy development.

132 loss-of-function mutations; (ii) more severe epilepsy, developmental problems and ataxia, and atrophy

133 However, a limited understanding of how epilepsy develops, particularly in the immature brain, l

134 factors play a major role in the etiology of epilepsy disorders.

135 endent predictors of seizure recurrence were epilepsy duration before remission, seizure-free interva

136 seizures in the last year of follow-up were epilepsy duration before remission, seizure-free interva

137 asive, potentially lifelong TES treatment of epilepsy either alone or as a complement to drug treatme

138 In conclusion, an epilepsy-eQTL analysis is superior to normal hippocampal

139 We also show that epilepsy eQTLs are enriched within epilepsy-causing gene

140 S) GWAS are significantly more enriched with epilepsy-eQTLs than with normal hippocampal eQTLs from t

141 ched with normal hippocampal eQTLs than with epilepsy-eQTLs.

142 her adults with a history of childhood-onset epilepsy exhibit increased brain amyloid accumulation, p

143 TraP analysis of 843 exomes from epilepsy family trios identifies synonymous variants in

144 echanisms may explain the risk of developing epilepsy following incident depression.

145 rios identifies synonymous variants in known epilepsy genes, thus pinpointing risk factors of disease

146 Both epilepsy groups had bilateral atrophy of the dorsal cing

147 ephalopathies with infantile/childhood onset epilepsies (>/=3 months of age) occur almost as often as

148 ate that disease-associated variants from an epilepsy GWAS meta-analysis and a febrile seizures (FS)

149 he influence of independent risk factors for epilepsy, has yet to be examined.

150 People with epilepsy have greatly increased probability of premature

151 us work in monogenic mouse models of absence epilepsy have shown that the interictal EEG displays aug

152 tiepileptic drug withdrawal, age at onset of epilepsy, history of febrile seizures, number of seizure

153 the treatment regimen and the course of the epilepsy in 66 patients for which well-documented medica

154 s study aimed to characterize post-traumatic epilepsy in a mouse model of pediatric brain injury, and

155 otherapy are needed to treat newly diagnosed epilepsy in adults.

156 average seizure duration or the incidence of epilepsy in animals.

157 EEG were performed in people with suspected epilepsy in Bhutan (2014-2015), and recordings were inte

158 The overall incidence of epilepsy in children aged 28 days to 16 years was 6.79 p

159 The elevated risk of epilepsy in children of overweight or obese mothers was

160 and are the most common cause of neocortical epilepsy in children.

161 ed significantly to evaluate the etiology of epilepsy in clinic and lay the foundation to develop mol

162 tions in KCC2 are a known cause of infantile epilepsy in humans and KCC2 dysfunction is present in pa

163 Genetically inherited absence epilepsy in humans is typically characterized by brief (

164 heritable absence epilepsy or post-traumatic epilepsy in humans, and may instead reflect typical rode

165 rkers for epileptogenesis and drug-resistant epilepsy in humans, necessitating evaluation in larger-s

166 d cohort of individuals with childhood-onset epilepsy in southwestern Finland, together with 46 match

167 One of the largest single sources of epilepsy in the world is produced as a neurological sequ

168 ched for functional terms highly relevant to epilepsy, including "neuron projection" and "seizures."

169 The rates of childhood epilepsy increased with maternal overweight or obesity i

170 x-matched controls underwent a comprehensive epilepsy interview.

171 Focal epilepsy involves excessive cortical activity that propa

172 ppocampal cholinergic system in experimental epilepsy, involving fiber sprouting into the dentate mol

173 eizure susceptibility.SIGNIFICANCE STATEMENT Epilepsy is a common cause of morbidity after traumatic

174 Epilepsy is a common neurological disease, manifested in

175 Epilepsy is a common neurological disorder occurring in

176 Epilepsy is a serious and common neurological disorder.

177 s seizures.SIGNIFICANCE STATEMENT Postinjury epilepsy is an unpreventable and devastating disorder th

178 It is now established that epilepsy is characterized by periodic dynamics that incr

179 Temporal lobe epilepsy is common and can be difficult to treat effecti

180 Epilepsy is common in Rett syndrome, an X-linked dominan

181 Surgical treatment in epilepsy is effective if the epileptogenic zone (EZ) can

182 for seizures in patients with photosensitive epilepsy is engagement of the circuitry that produces ga

183 orial model of white matter atrophy in focal epilepsy is proposed.

184 It demonstrates that the epilepsy lesions can be detected, located and treated th

185 , such as Fragile X syndrome, Rett syndrome, epilepsy, major depressive disorder, and autism spectrum

186 sodium channel (VGSC) mutations cause severe epilepsies marked by intermittent, pathological hypersyn

187 ons that cause neurological diseases such as epilepsy may affect a surprising range of connection typ

188 sample, 5373 births were in 3586 women with epilepsy; mean (SD) age at first delivery of the epileps

189 ice with epilepsy (pilocarpine-temporal lobe epilepsy model) and 100 healthy control hippocampi, we i

190 uous EEG for clinical indications, excluding epilepsy monitoring unit admissions.

191 altered in experimental mesial temporal lobe epilepsy (mTLE) and whether their integration differs fr

192 The cause of mesial temporal lobe epilepsy (MTLE) is often unknown.

193 s vigabatrin spectroscopy studies in healthy epilepsy-naive subjects.

194 l morbidity, but primarily in those who have epilepsy, neurological abnormalities, or both before the

195 nal membrane contribute to the generation of epilepsy, neuropathic pain, and autism spectrum disorder

196 However, neither the longitudinal course of epilepsy nor the patterns of seizure onset and remission

197 re withdrawal, female sex, family history of epilepsy, number of seizures before remission, focal sei

198 nd parasite strain combinations, so that the epilepsy observed retained universality with respect to

199 Epilepsy occurs in one of 26 people.

200 er at CSE was the only predictor of incident epilepsy (odds ratio [OR] 7.5, 95% CI 2.25-25.1).

201 good seizure outcome than were patients with epilepsy of unknown etiology (15 of 23 [65.2%] vs 24 of

202 Among adult patients with epilepsy of unknown etiology, a significant minority had

203 seizure control, in cases of drug-resistant epilepsy, often requires neurosurgical intervention targ

204 In trying to understand a patient's epilepsy, one should consider the contribution of all hy

205 form progressively increased in blood before epilepsy onset and prospectively identified animals that

206 of Pafah1b1(+/-) mice that may contribute to epilepsy or cognitive impairments associated with lissen

207 nd, non-inferiority trial, patients from 185 epilepsy or general neurology centres in Europe, North A

208 nomena do not always model heritable absence epilepsy or post-traumatic epilepsy in humans, and may i

209 recruited from the Toronto Western Hospital epilepsy outpatient clinic from January 1, 2012, through

210 Yields were greater for epilepsy panels (28 of 96 [29.2%]; P < .001) and whole e

211 Adults with childhood-onset epilepsy, particularly APOE epsilon4 carriers, have an i

212 ed electric potentials intracranially in ten epilepsy patients and estimated electric fields across t

213 e analyzed iEEG recordings obtained from 215 epilepsy patients as they performed a free recall task.

214 Approximately 30% of epilepsy patients do not respond to antiepileptic drugs,

215 wever, the molecular basis for a majority of epilepsy patients remains elusive, and furthermore, most

216 s in the amygdala and hippocampus from human epilepsy patients to examine oscillatory activity during

217 Using recordings from neurosurgical epilepsy patients with intracranially implanted electrod

218 onnectivity with the visual thalamus only in epilepsy patients with photosensitivity.

219 Scn2a(Q54) mouse model of epilepsy, a focal epilepsy phenotype is caused by transgenic expression of

220 t (Scn1a (+/-)) mice recapitulate the severe epilepsy phenotype of Dravet syndrome and are an accepte

221 s study, we evaluated activity of SGE-516 on epilepsy phenotypes in the Scn1a (+/-) mouse model that

222 Postinjury epilepsy (PIE) is a devastating sequela of various brain

223 cing data from 100 hippocampi from mice with epilepsy (pilocarpine-temporal lobe epilepsy model) and

224 apsin II (SynII) leads to the development of epilepsy, probably due to impairments in inhibitory syna

225 ely collected from the Calgary Comprehensive Epilepsy Programme).

226 this disinhibition diverge significantly as epilepsy progresses.

227 ssive epilepsy and a potential biomarker for epilepsy progression in CD.

228 Ablation halted epilepsy progression relative to untreated epileptic mic

229 d 2), a metazoan-specific protein mutated in epilepsy, recruits a fraction of mammalian GATOR1 and GA

230 gnostic yields in newly diagnosed early-life epilepsies regardless of key clinical features.

231 We hypothesize that epilepsy-related neuroplasticity of septohippocampal cho

232 In patients with drug-resistant focal epilepsy requiring surgery, hippocampal sclerosis was th

233 A major challenge in experimental epilepsy research is to reconcile the effects of anti-ep

234 reas seizures have been the central focus of epilepsy research, they are commonly accompanied by cogn

235 sment using the International League Against Epilepsy seizure outcome scale.

236 h a similar phenotype, including early-onset epilepsy, severe intellectual disability, postnatal micr

237 and molecular correlates of strain-dependent epilepsy severity in this model.

238 peutic target to treat seizure disorders and epilepsy.SIGNIFICANCE STATEMENT We recently reported tha

239 variety of neurological illnesses, including epilepsy, stroke, and neurodegenerative disease.

240 enrolled in the Turku Adult Childhood Onset Epilepsy study at the mean (SD) age of 5.1 (4.5) years (

241 mortality due to sudden unexpected death in epilepsy (SUDEP).

242 elevated risk of sudden unexpected death in epilepsy (SUDEP).

243 the potential for sudden unexpected death in epilepsy (SUDEP).

244 ncreased risk for sudden unexpected death in epilepsy (SUDEP).

245 zure outcome of 693 adults who had resective epilepsy surgery between 1990 and 2010 and used survival

246 n specimens from 9523 patients who underwent epilepsy surgery for drug-resistant seizures in 36 cente

247 Individuals with auras only after epilepsy surgery had a higher COSY than those who were s

248 th drug-resistant epilepsy who had undergone epilepsy surgery had a significantly higher rate of free

249 Our data support the early consideration of epilepsy surgery in this patient group.

250 Epilepsy surgery is an effective treatment for refractor

251 aded on the The International League against Epilepsy surgery outcome scale.

252 METHOD: We calculated COSY in 819 epilepsy surgery patients with up to 25 years follow-up.

253 se comprising 16 patients who have undergone epilepsy surgery, revealing rich-club structures within

254 not deter from exploring the possibility of epilepsy surgery.

255 epilepsy (CAE) is the most common paediatric epilepsy syndrome and is characterized by frequent and t

256 e likely to be a causal gene for a Mendelian epilepsy syndrome than to be a causal gene for another M

257 before remission, absence of a self-limiting epilepsy syndrome, developmental delay, and epileptiform

258 ishment might be impaired in a human genetic epilepsy syndrome, polyhydramnios, megalencephaly, and s

259 are bioequivalent when tested in people with epilepsy taking concomitant antiepileptic drugs.

260 Patients who develop post-injury epilepsy tend to have poor functional outcomes.

261 ype was associated with higher prevalence of epilepsy than those with classic Rett syndrome.

262 elatives of HS-TLE subjects who did not have epilepsy themselves (HS-1 degrees Rel; n = 26).

263 For refractory epilepsy, this surgical intervention offers many advanta

264 n available, 7592 (0.5%) were diagnosed with epilepsy through December 31, 2012.

265 Seizures in temporal lobe epilepsy (TLE) disturb brain networks and lead to connec

266 CANCE STATEMENT Development of temporal lobe epilepsy (TLE) generally takes years after an initial in

267 in the DG of individuals with temporal lobe epilepsy (TLE) or AD and correlate with performance on t

268 evance of herpes simplex encephalitis and of epilepsy to AD, the action of IFN, and the possible rele

269 neocortex of rats with chronic temporal lobe epilepsy to demonstrate that subsets of cells discharge

270 udy evaluated a mouse model of temporal lobe epilepsy to test which pathological changes in the denta

271 late onset group, including myoclonic-atonic epilepsy (two patients), Lennox-Gastaut not emerging fro

272 drome, including movement disorders, absence epilepsy (typical and atypical), and myoclonic and gener

273 ailure to thrive, dilated cardiomyopathy and epilepsy, ultimately leading to death in early childhood

274 In women with epilepsy, using AEDs during pregnancy did not increase t

275 n of temporal lobe seizures in temporal lobe epilepsy, using diffusion tensor imaging and automated f

276 The cumulative incidence of epilepsy was 24.7% (95% CI 16.2-35.6), with most (89%) e

277 ected, and cumulative lifetime prevalence of epilepsy was determined using the Kaplan-Meier estimator

278 The cumulative incidence of epilepsy was lower in patients with prolonged febrile se

279 Pre-existing epilepsy was the only predictor of intellectual disabili

280 from rare patients with medically resistant epilepsy, we find that theta oscillations are a distinct

281 nslation of closed-loop TES for treatment of epilepsy, we show here for the first time that unsupervi

282 Risk factors for epilepsy were assessed using Cox proportional hazards mo

283 with intellectual disability, autism, and/or epilepsy were identified: 2p16.1-p15 duplication, 6p25.3

284 The 41 individuals with epilepsy were originally enrolled in the Turku Adult Chi

285 d 16 years or older and with newly diagnosed epilepsy were randomly assigned in a 1:1 ratio, via a co

286 s strongly suggesting an autoimmune cause of epilepsy were seen in 23 patients (20.5%).

287 People with epilepsy who became seizure-free while taking antiepilep

288 erviews with family members of patients with epilepsy who died suddenly without other identifiable ca

289 children and adolescents with drug-resistant epilepsy who had undergone epilepsy surgery had a signif

290 Patients diagnosed with nontractable epilepsy who were implanted with entorhinal cortical ele

291 es had to report on cohorts of patients with epilepsy who were seizure-free and had started withdrawa

292 Fifty adults (>/=18 years) with epilepsy who were taking concomitant antiepileptic drugs

293 atients with pharmacoresistant temporal lobe epilepsy will not be rendered completely seizure-free af

294 from West syndrome (two patients), and focal epilepsies with an electrical status epilepticus during

295 devastating group of severe childhood onset epilepsies with medication-resistant seizures and poor d

296 Monogenic epilepsies with wide-ranging clinical severity have been

297 Autosomal dominant epilepsy with auditory features results from mutations i

298 brile seizures group developed temporal lobe epilepsy with mesial temporal sclerosis.

299 ne associations between exposure to maternal epilepsy with or without antiepileptic drug (AED) therap

300 c features of a canine generalized myoclonic epilepsy with photosensitivity and onset in young Rhodes