ライフサイエンスコーパス: epileptic

1 y but that long-term IGF-1 treatment was pro-epileptic.

2 observed, including confusion (3 patients), epileptic (1 patient), amnestic (1 patient), and a sever

3 observed, including confusion (12 patients), epileptic (1 patient), amnestic (3 patients), and fulmin

4 in the subiculum, a key structure generating epileptic activities.

5 important to explain the slow propagation of epileptic activity and other normal propagations at simi

6 iation has therapeutic implications, because epileptic activity can occur at early disease stages and

7 al lobe and fusiform gyrus may be related to epileptic activity in IGE patients with absence seizures

8 sights into the mechanisms that may suppress epileptic activity in the NMM.

9 Here we asked whether epileptic activity induces plastic changes that can be r

10 Epileptic activity is frequently associated with Alzheim

11 s released in hourly pulses, whose effect on epileptic activity is unknown.

12 also found that IGF-1 - mediated increase in epileptic activity led to neurotoxicity.

13 hey may thus promote or cause development of epileptic activity or inhibit it.

14 Epileptic activity, frequently occurring in glioma patie

15 ivation of MAPK/CREB signalling, a marker of epileptic activity, in superficial layers.

16 hat could be used to suppress high-amplitude epileptic activity.

17 -type closed-loop controller for suppressing epileptic activity.

18 normal physiological function to paroxysmal epileptic activity.

19 mission, and this defect is thought to cause epileptic activity.

20 nisms that could both amplify and counteract epileptic activity.

21 ngly recognized as potential contributors to epileptic activity.

22 tribution to the emergence or maintenance of epileptic activity.

23 be required for astrocytes to contribute to epileptic activity.

24 g analysis in a mouse model of TLE using 100 epileptic and 100 control hippocampi shows the proconvul

25 d from marijuana (Cannabis sativa) with anti-epileptic and anti-inflammatory properties.

26 ng the clinical-genetic spectrum of combined epileptic and dyskinetic syndromes.

27 (EMG) for differentiation between convulsive epileptic and psychogenic nonepileptic seizures (PNESs).

28 human astrocytes along with astrocytes from epileptic and tumor foci and compared these to human neu

29 ts often do not respond well to classic anti-epileptics and many remain refractory to treatment.

30 and rescue behavioral deficits in a chronic epileptic animal model more than 6 months after treatmen

31 ticus, late electrocorticography to identify epileptic animals and post-mortem immunohistochemistry t

32 r previously reported impaired inhibition in epileptic animals at basket cell-to-granule cell (BC-->G

33 Furthermore, activating granule cells in non-epileptic animals evoked acute seizures of increasing se

34 -mediated seizure enhancement in chronically epileptic animals.

35 l activation in both control and chronically epileptic animals.

36 oing presence of dysplasia has dramatic anti-epileptic benefit.

37 on revealed consistent downregulation in the epileptic brain in heterogeneous forms of epilepsy inclu

38 ctal epileptiform discharges (IEDs) identify epileptic brain regions and can impair memory, but the m

39 ifically target adult-born DGCs arise in the epileptic brain, whereas axons of interneurons and pyram

40 tribute to the molecular architecture of the epileptic brain.

41 ctural features of this projection system in epileptic brain.

42 Much of the prior study of >120 Hz EEG is in epileptic brains.

43 nduced decrease of neuron recruitment during epileptic bursts can lead to an increase in burst freque

44 significantly differentially edited between epileptic cases and controls.

45 opportunity for long-lasting modification of epileptic circuits.

46 ilepsy-aphasia syndrome (EAS), a spectrum of epileptic, cognitive and language disorders.

47 d, epileptiform spikes were more frequent in epileptic compared with nonepileptic rodents; however, t

48 presents a refractory severe post-infectious epileptic condition in previously normal children.

49 s for therapeutic neuromodulation in similar epileptic conditions associated with deep lesions.

50 ic database, we may find that apart from the epileptic conditions, Intermittent Head Drops have been

51 as well as pharmacological interventions and epileptic conditions.

52 alas and hippocampi were conducted in 50 non-epileptic controls (age 7-79 years) and 50 patients with

53 the perforant path input-output operation in epileptic dentate granule cells.

54 gest that only limited subsets of neurons in epileptic depth regions initiate the seizure-onset and t

55 gain-of-function) seizures and corresponding epileptic discharges with prominent sleep activation in

56 2 channel and hnRNP U are strongly linked to epileptic disorders and intellectual disability.

57 linked to developmental defects in mice and epileptic disorders in humans, little is known about its

58 sociated with a wide spectrum of early-onset epileptic disorders ranging from benign familial neonata

59 ther neuronal hyperexcitation, a hallmark of epileptic disorders, could accelerate this conversion.

60 made in understanding the pathophysiology of epileptic disorders, seizures remain poorly controlled i

61 Here we show that the novel anti-epileptic drug retigabine (RTG) modulates channel functi

62 ons with levetiracetam, an FDA-approved anti-epileptic drug, enhanced survival of chemotherapy drug-t

63 research is to reconcile the effects of anti-epileptic drugs (AEDs) on individual neurons with their

64 reduced following ingestion of typical anti-epileptic drugs (AEDs;).

65 Local anaesthetics and anti-epileptic drugs can suppress hyperexcitability; however,

66 y.SIGNIFICANCE STATEMENT The effects of anti-epileptic drugs on individual neurons are difficult to s

67 n of status epilepticus and efficacy of anti-epileptic drugs will be important to improve outcomes.

68 r than additional trials of second-line anti-epileptic drugs, to avoid neuronal injury and pharmaco-r

69 Pro-epileptic effects of IGF-1 were mediated by Akt-mTOR sig

70 east 10 years of age (7367 artefact-free non-epileptic electrodes), whereas a younger group included

71 e beta1 subunit gene GABRB1 in children with epileptic encephalopathies (EEs) Lennox-Gastaut syndrome

72 tations in the etiology of developmental and epileptic encephalopathies (EEs), highlighting their gen

73 2 channels are also strongly associated with epileptic encephalopathies and intellectual disability i

74 v7.3 (R230C) recently found in patients with epileptic encephalopathies and/or intellectual disabilit

75 The epileptic encephalopathies are a clinically and aetiolog

76 Epileptic encephalopathies are a devastating group of se

77 Epileptic encephalopathies are a phenotypically and gene

78 s (IS) and Lennox-Gastaut syndrome (LGS) are epileptic encephalopathies characterized by early onset,

79 de novo CHD2 mutations, but is also seen in epileptic encephalopathies due to other gene mutations.

80 known monogenic determinants underlying the epileptic encephalopathies has grown rapidly.

81 Many epileptic encephalopathies have a genetic aetiology and

82 argeted resequencing of 644 individuals with epileptic encephalopathies led to the identification of

83 Epileptic encephalopathies of infancy and childhood comp

84 ht to identify genetic causes of early onset epileptic encephalopathies with burst suppression (Ohtah

85 basis for how these mutations contribute to epileptic encephalopathies, we compared the effects of t

86 g group of genes associated with early-onset epileptic encephalopathies.

87 d to cause a new molecular entity within the epileptic encephalopathies.

88 benign familial neonatal seizures to severe epileptic encephalopathies.

89 pathogenesis of genetic epilepsies including epileptic encephalopathies.

90 Developmental and epileptic encephalopathy (DEE) is a group of conditions

91 Patients with early infantile epileptic encephalopathy (EIEE) are at increased risk fo

92 Patients with early infantile epileptic encephalopathy (EIEE) experience severe seizur

93 nd epileptic phenotypes, including infantile epileptic encephalopathy (EIEE), suggestive of a gain of

94 Early infantile epileptic encephalopathy (EIEE)-associated mutations in

95 RB3) identified in patients with early-onset epileptic encephalopathy (EOEE) and profound development

96 Early-onset epileptic encephalopathy (EOEE) represents a heterogeneo

97 nt publication described a distinct neonatal epileptic encephalopathy (MIM 615905) caused by autosoma

98 rane-fusion machinery, cause infantile early epileptic encephalopathy (Ohtahara syndrome), but it is

99 channel KV1.2, in six isolated patients with epileptic encephalopathy (one mutation recurred three ti

100 SCN8A encephalopathy, or early infantile epileptic encephalopathy 13 (EIEE13), is caused predomin

101 Dravet syndrome, an epileptic encephalopathy affecting children, largely res

102 ynonymous de novo mutations in patients with epileptic encephalopathy and for common susceptibility v

103 RHOBTB2 as causative for a developmental and epileptic encephalopathy and have elucidated the role of

104 We apply the method to prioritize epileptic encephalopathy candidate genes.

105 3 patients (eight previously described) with epileptic encephalopathy carrying either novel or known

106 /Q390X) KI mice are associated with a severe epileptic encephalopathy due to a dominant negative effe

107 Photosensitivity is prominent in a very rare epileptic encephalopathy due to de novo CHD2 mutations,

108 e generally, and intellectual disability and epileptic encephalopathy in particular.

109 s presented with a different and more severe epileptic encephalopathy phenotype.

110 on sequencing on patients with a spectrum of epileptic encephalopathy phenotypes, and we identified f

111 G2 variants may be major contributors to the epileptic encephalopathy phenotypes.

112 spasms are seizures associated with a severe epileptic encephalopathy presenting in the first 2 years

113 ssense mutation p.Asn1768Asp in a child with epileptic encephalopathy that included seizures, ataxia,

114 Scn8a(N1768D) mutant mice provide a model of epileptic encephalopathy that will be valuable for study

115 lepsy was common, with severity ranging from epileptic encephalopathy to well-controlled seizures.

116 ibed here, however, cause a severe infantile epileptic encephalopathy with a central myelin defect an

117 ON: We characterize the genetic landscape of epileptic encephalopathy with burst suppression, without

118 d epilepsy syndrome (FIRES) is a devastating epileptic encephalopathy with limited treatment options

119 Dravet syndrome is an infant-onset epileptic encephalopathy with multiple seizure types tha

120 nd there is an overlap with 'early infantile epileptic encephalopathy'.

121 unrelated individual) with severe infantile epileptic encephalopathy, clubfoot, absent deep tendon r

122 y, generalized tonic clonic seizures and the epileptic encephalopathy, Dravet syndrome.

123 hiatric disorders: autism spectrum disorder, epileptic encephalopathy, intellectual disability and sc

124 al disorders, and 14 patients with infantile epileptic encephalopathy, of which 13 had severe neurode

125 hiatric disorders: autism spectrum disorder, epileptic encephalopathy, schizophrenia, and severe inte

126 y leads to potentially fatal early infantile epileptic encephalopathy, severe developmental delay, an

127 developed a model of a severe human genetic epileptic encephalopathy, the Gabrg2(+/Q390X) knock-in m

128 Among a cohort of 57 individuals with epileptic encephalopathy, we ascertained two unrelated a

129 have recently been recognized as a cause of epileptic encephalopathy, which is characterized by refr

130 deficiency as a cause of autosomal recessive epileptic encephalopathy.

131 el sequencing in two unrelated children with epileptic encephalopathy.

132 tism spectrum disorders, and early infantile epileptic encephalopathy.

133 ng neuronal excitability in this early-onset epileptic encephalopathy.

134 neonatal respiratory-distress syndrome, and epileptic encephalopathy.

135 ognitive impairments characteristic for this epileptic encephalopathy.

136 in function, as KCNQ2 variants could lead to epileptic encephalopathy.

137 to three real exome sequencing data sets of epileptic encephalophathies and intellectual disability

138 pically, the term has mainly been related to epileptic episodes, but the spectrum of clinical conditi

139 ay identify features more consistent with an epileptic event and laboratory studies and brain imaging

140 an essential component in the onset of ictal epileptic events.

141 res (encephalopathy, psychiatric, cognitive, epileptic, extrapyramidal and inflammatory cerebrospinal

142 ing can be used to infer the localisation of epileptic foci and assist in the design of intracranial

143 increased tryptophan uptake and trapping in epileptic foci and brain tumors, but the short half-life

144 ve astrocytes are commonly found in putative epileptic foci and have been hypothesized to be disease

145 itability, with many distinctive features of epileptic foci, including high-frequency oscillations wi

146 ic activity (i.e. synaptic noise) within the epileptic focus is one endogenous method of ictogenesis.

147 ll, among all patients with AE and a defined epileptic focus, 7 had predominant increased volume ipsi

148 dominant increased volume ipsilateral to the epileptic focus.

149 biological pathways are dysregulated in the epileptic focus.

150 me, differentially connected pathways in the epileptic focus.

151 deviations in brain metabolites characterize epileptic hippocampi.

152 is preserved across-species, specific to the epileptic hippocampus and upregulated in chronic epileps

153 ipple-like oscillations (150-250Hz) in human epileptic hippocampus are associated with 2 distinct pop

154 gest a potential role for RNA editing in the epileptic hippocampus in the occurrence and severity of

155 ility to sustain recurrent excitation in the epileptic hippocampus, which raises questions about the

156 ells to hippocampal hyperexcitability in the epileptic hippocampus.SIGNIFICANCE STATEMENT In the hipp

157 We review the use of LITT for epileptic indications in the context of its application

158 fects of both the KD and KB in spontaneously epileptic Kcna1-null mice using a combination of behavio

159 al role for noise results from disruption of epileptic-like network states.

160 lthough carbamazepine (CBZ) has a known anti-epileptic mechanism, paradoxically, it has also been rep

161 we show that feeding levetiracetam, an anti-epileptic medication, to Abeta-expressing flies suppress

162 ippocampal slices at 270 DAT, was reduced in epileptic mice but restored to naive levels in epileptic

163 The degree of differential RNA editing in epileptic mice correlated with frequency of seizures, an

164 ranscribing P2rx7 in hippocampal slices from epileptic mice displayed enhanced agonist-evoked P2X7 re

165 eduction in seizure activity was observed in epileptic mice receiving intrahippocampal CGE progenitor

166 ileptic mice but restored to naive levels in epileptic mice receiving MGE transplants.

167 enitors transplanted into the hippocampus of epileptic mice rescued handling and open field deficits

168 apillary constrictions in the hippocampus of epileptic mice than in that of normal mice, in addition

169 A 5 d treatment of epileptic mice with systemic injections of the centrally

170 In epileptic mice, sparse granule cell activation could be

171 stereological analyses in several models of epileptic mice.

172 d epilepsy progression relative to untreated epileptic mice; the latter showing a significant and dra

173 m to selectively ablate these cells from the epileptic mouse brain.

174 to include not only normal (n = 22) but also epileptic (n = 22) samples.

175 method to identify cellular changes in human epileptic neocortex using transcriptional clustering.

176 s of activations, as expected for periods of epileptic network dominance.

177 The epileptic network is characterized by pathologic, seizur

178 ronization in a validated model of the human epileptic network.

179 role is to synchronize or desynchronize the epileptic network.

180 gions that facilitate synchronization in the epileptic network.

181 dom, but represent an electrically connected epileptic network.

182 nchronous relationships from the surrounding epileptic network.

183 In vivo genetic deconstruction of epileptic networks, ex vivo validation of variant profil

184 ly temporally precise cross-area analyses of epileptic neuronal networks and find a feed-forward prop

185 ible for transforming a normal brain into an epileptic one remain largely unknown.

186 amplitude and HCN1 surface expression under epileptic or normal physiological conditions are poorly

187 The negative feedback promotes epileptic oscillations whereas the striatal feedforward

188 We demonstrate the capacity to predict the epileptic outcome in five different models of PIE, highl

189 esulted in a 90% clinical improvement in non-epileptic paroxysmal manifestations and a normalised bra

190 ents with GLUT1-DS (7-47 years old) with non-epileptic paroxysmal manifestations.

191 actors in complex network phenomena, such as epileptic pathology.

192 inhibitory function is an important facet of epileptic pathology.

193 CTA" was significantly less frequent in male epileptic patients (0.173) than in normal males (0.305).

194 econd, we tested 20 refractory temporal lobe epileptic patients (11 women) with unilateral hippocampa

195 es implanted in the VOTC of a large group of epileptic patients (n = 28).

196 In a speeded detection task, human epileptic patients (N = 3) responded to unisensory (audi

197 roduce dentate hyperexcitability are seen in epileptic patients and animal models.

198 ha 1 subunit gene, SCN1A, were identified in epileptic patients and confirmed as causative factors of

199 y of numerous antiepileptic drugs, 20-30% of epileptic patients are pharmacoresistant with seizures n

200 Many epileptic patients do not achieve adequate seizure contr

201 vels of these neurochemicals are abnormal in epileptic patients is unknown.

202 C allele was significantly less frequent in epileptic patients than in normal males (OR 0.424).

203 btained from the laser-microdissected GCL of epileptic patients, identifying several miRNAs (miR-21-5

204 the human motor cortex in pharmacoresistant epileptic patients, we report a pattern of electroenceph

205 emorrhage, spine, demyelinating disease, and epileptic patients.

206 t model of TBI as well as in brains of human epileptic patients.

207 outing and recurrent seizures in the chronic epileptic phase.

208 tency, first spontaneous seizure and chronic epileptic phase.

209 inished M-current to the previously reported epileptic phenotype of BACE1-deficient mice.

210 this molecular structure contributes to the epileptic phenotype of Fmr1(-/y).

211 us mutations cause developmental defects and epileptic phenotypes, including infantile epileptic ence

212 ve been identified in patients with distinct epileptic phenotypes.

213 lts in the exacerbation of hyperactivity and epileptic phenotypes.

214 transmission failures at BC-->GC synapses in epileptic pilocarpine-treated rats are not attributable

215 Compared with controls, epileptic pilocarpine-treated rats displayed boutons wit

216 es using slices from healthy and chronically epileptic rats and find that epileptiform activity is as

217 Larger active zones in epileptic rats are consistent with previous reports of l

218 oximal locations, i.e., closer to CA3; while epileptic rats exhibited stronger interactions at distal

219 Consistent with QT prolongation, epileptic rats had longer ventricular action potential d

220 impaired transmission at BC-->GC synapses in epileptic rats is attributable to later steps in exocyto

221 The epileptic rats showed circulating levels of Hsp60 higher

222 graded in this condition, we used normal and epileptic rats to examine theta activity accompanying ac

223 cholinergic fiber varicosities was higher in epileptic rats versus control rats in the inner and oute

224 This opposing trend in epileptic rats was associated with the reorganization of

225 henotype and their density were increased in epileptic rats when compared to control rats.

226 In pilocarpine-treated chronically epileptic rats, we describe a novel mechanism that cause

227 but not for ChAT, have enlarged perikarya in epileptic rats.

228 ds of the dorsal hippocampus was impaired in epileptic rats.

229 pil and hippocampus proper (CA3, CA1) of the epileptic rats.

230 re-established theta coordination of LFPs in epileptic rats.

231 her addition of cannabidiol to existing anti-epileptic regimens would be safe, tolerated, and efficac

232 of p39 and p35 in synaptic Cdk5 function and epileptic responses, arguing that cooperation between Cd

233 sal cavity and poor water solubility of anti-epileptics restrict absorption, leading to insufficient

234 monstrate the spontaneous transition between epileptic seizure and spreading depression states as the

235 d neurosurgeons using simulated and recorded epileptic seizure data to demonstrate our system's effec

236 Epileptic seizure emergencies are life-threatening condi

237 the entire network, which is reminiscent of epileptic seizure propagation in the brain.

238 ulti-unit computational neural mass model of epileptic seizure termination and postictal recovery was

239 tor cells causes mice to develop progressive epileptic seizure, and dramatically reduces basal synapt

240 thology and die 30-60 days postnatal from an epileptic seizure.

241 out (AE3(-/-) ) mice are more susceptible to epileptic seizure.

242 Psychogenic non-epileptic seizures (PNES) are classified with other func

243 Epileptic seizures also repress Cbln1 and are found to e

244 t clinically lie in the "borderland" between epileptic seizures and physiological deja vu.

245 Spontaneous epileptic seizures and the integrity of the blood-brain

246 gy and explosive dynamical transitions as in epileptic seizures and their propagations in the brain.

247 Epileptic seizures are generally unpredictable and arise

248 igate the brain amino acid metabolism during epileptic seizures by (18)F-FET PET and to elucidate the

249 Recurrent high-frequency epileptic seizures cause progressive hippocampal scleros

250 e and fertile, and they did not manifest the epileptic seizures characteristic of the Alpl(-/-) model

251 Understanding how epileptic seizures develop or identifying diagnostic ind

252 in the development of hyperexcitability and epileptic seizures following traumatic brain injury (TBI

253 he galanin neuropeptide in the regulation of epileptic seizures has been established in animal models

254 RY ON THIS ARTICLE : Accurate forecasting of epileptic seizures has the potential to transform clinic

255 Epileptic seizures potently modulate hippocampal adult n

256 Epileptic seizures represent altered neuronal network dy

257 Epileptic seizures represent dysfunctional neural networ

258 euronal death induced by proneurotrophins or epileptic seizures was assessed and compared with respon

259 ailable antagonist, JNJ-47965567, suppressed epileptic seizures well beyond the time of treatment and

260 pomas, higher incidence of pharmacoresistant epileptic seizures, and more severe neuropsychiatric dis

261 fected tissues, and in plasma in response to epileptic seizures, and point to it as biomarker of hipp

262 ing to severe neurological symptoms, such as epileptic seizures, but no specific treatment is availab

263 id 10 significantly reduced the incidence of epileptic seizures, cortical amyloid burden, and neuroin

264 At high levels, generating sustained epileptic seizures, however, we find that rNSCs divide s

265 e comprising severe retardation, early onset epileptic seizures, optic nerve/cerebellar atrophy, peda

266 neurodevelopmental disorder characterized by epileptic seizures, severe intellectual disability, and

267 nd manifests in an altered susceptibility to epileptic seizures, underscoring the importance of FGF-d

268 e a possible mechanism for the recurrence of epileptic seizures, which are known to be the results of

269 in mice lowers the threshold for triggering epileptic seizures.

270 uronal death induced by proneurotrophins and epileptic seizures.

271 column (DCS) of the spinal cord to suppress epileptic seizures.

272 central to the initiation and progression of epileptic seizures.

273 (median follow-up 23.6 years) had unprovoked epileptic seizures.

274 , a disrupted blood-brain barrier (BBB), and epileptic seizures.

275 ting, on-demand CN stimulation could disrupt epileptic seizures.

276 enetic activation has been reported to block epileptic seizures.

277 is that astrogliosis is sufficient to induce epileptic seizures.

278 hippocampal neuronal injury during prolonged epileptic seizures.

279 ippocampus in the occurrence and severity of epileptic seizures.

280 ng the evaluation of gustatory and olfactory epileptic seizures.

281 cation, and thereby reduce susceptibility to epileptic seizures.

282 n that docosahexaenoic acid (DHA) attenuates epileptic seizures; however, the molecular mechanism by

283 eizures, with 9 patients (36%) starting with epileptic spasms between 3 and 18 months of age.

284 re score (P = 0.003), and a higher number of epileptic 'spike' events (P = 0.023) than the control mi

285 f high seizure likelihood the probability of epileptic spiking also increased.

286 ion contribute to seizure generation and the epileptic state.

287 tients tend to transit from non-epileptic to epileptic states more often than controls in the model.

288 BAergic drugs both on gamma oscillations and epileptic states.

289 Treatment requires rapid delivery of anti-epileptics such as benzodiazepines to the brain.

290 h mild to severe ID, long-lasting hypotonia, epileptic susceptibility, frontal bossing, mild hypertel

291 equencing in Finnish individuals with severe epileptic syndromes, we identified pathogenic compound h

292 er a promising new avenue for effective anti-epileptic therapy for intractable pediatric epilepsy pat

293 galanin have antiepileptic actions in human epileptic tissue as well, we applied these neuropeptides

294 gical therapeutic approach, whereby resected epileptic tissue from temporal lobes of pharmacoresistan

295 iomarkers of the transformation of normal to epileptic tissue would help to stratify patients at risk

296 that were up-regulated in both human and rat epileptic tissue.

297 at, first, patients tend to transit from non-epileptic to epileptic states more often than controls i

298 ect implications for the development of anti-epileptic treatment.

299 de transcriptomic analysis to date comparing epileptic with normal human hippocampi.

300 and electrophysiological characterization of epileptic zebrafish.