ライフサイエンスコーパス: epileptogenic

1 prise brain regions that are not necessarily epileptogenic.

2 nodes with a short transition time as highly epileptogenic.

3 y, raising the possibility that IGF-1 may be epileptogenic.

4 oup I mGluRs to elicit translation-dependent epileptogenic activities.

5 Both epileptogenic activity and atrophy spread appear to foll

6 s a simple consequence of the propagation of epileptogenic activity in one model, and as a progressiv

7 stimulation might be used to alter spread of epileptogenic activity, accelerate learning or enhance c

8 tereotyped origination and spread pattern of epileptogenic activity, which is reflected in stereotype

9 stimulation of hippocampal neurons using the epileptogenic agent kainic acid (KA) increased the numbe

10 Comparing to a well-known epileptogenic agent kainic acid (KA), CTZ affects neuron

11 HHs are intrinsically epileptogenic, although the basic cellular mechanisms re

12 ewly generated dentate granule cells are pro-epileptogenic and contribute to the occurrence of seizur

13 es and neurons for a fuller understanding of epileptogenic and epileptic mechanisms in the brain netw

14 ons of which only 1 or 2 are suspected to be epileptogenic and if electroencephalogram changes are eq

15 tic epilepsy comprises a rapid assay of anti-epileptogenic and neuroprotective activities and, in thi

16 ses to intracerebral electric stimulation in epileptogenic and nonepileptogenic areas.

17 l and human hippocampus, was similar between epileptogenic and nonepileptogenic temporal lobe, wherea

18 e a powerful tool in differentiating between epileptogenic and nonepileptogenic tubers in patients wi

19 r, by including two neuron subpopulations of epileptogenic and nonepileptogenic type, making it capab

20 ordering hypometabolic regions can be highly epileptogenic and should be carefully assessed in presur

21 energy substrates glucose and lactate in the epileptogenic and the nonepileptogenic cortex and hippoc

22 crodialysis probes were used to identify the epileptogenic and the nonepileptogenic sites.

23 ately demonstrate perfusion increases in the epileptogenic area but often requires dedicated personne

24 he analysis was of piriform cortex, a highly epileptogenic area of cerebral cortex, where pyramidal c

25 ccurrence were significantly associated with epileptogenic areas.

26 ificant, because HFOs may be good markers of epileptogenic areas.

27 e-like symptoms that occur in the absence of epileptogenic brain activity.

28 00 Hz) frequency range, may be signatures of epileptogenic brain and involved in the generation of se

29 s generated in the weeks before and after an epileptogenic brain injury can integrate abnormally into

30 us, the insult most commonly used to produce epileptogenic brain injury, is too severe and necessaril

31 inhibiting granule cell production before an epileptogenic brain insult can mitigate epileptogenesis.

32 urrent clinical practice for localization of epileptogenic brain largely ignores fundamental oscillat

33 T pathway mutations as an important cause of epileptogenic brain malformations and establish megalenc

34 pathology, and accurate localisation of the epileptogenic brain region by various clinical, neuroima

35 s in noninvasive presurgical localization of epileptogenic brain regions in intractable-seizure patie

36 ism is often applied for the localization of epileptogenic brain regions, but hypometabolic areas are

37 eizure activity analogous to recordings from epileptogenic brain tissue.

38 ly recognized as potential biomarkers of the epileptogenic brain.

39 ental oscillations that are signatures of an epileptogenic brain.

40 t neurophysiological processes in normal and epileptogenic brain.

41 This has been proposed to be epileptogenic by a variety of different mechanisms.

42 structural disorganization exists in occult epileptogenic cerebral lesions.

43 Spectral analyses of non-epileptogenic cerebral sites stimulated directly with hi

44 Treatment of TG neurons with epileptogenic compound-PTZ led to a marked increase in a

45 us reduction of NMDAR redox sites under this epileptogenic condition.

46 Accurate estimation of the epileptogenic cortex and its removal requires the estima

47 c structural abnormalities, and can identify epileptogenic cortex and predict surgical outcome, espec

48 The epileptogenic cortex had only marginally increased gluta

49 olic areas are often larger than or can miss epileptogenic cortex in nonlesional neocortical epilepsy

50 To accurately estimate the epileptogenic cortex or to make inferences about cogniti

51 ssion of brain damage markers in nonlesional epileptogenic cortex studied in postsurgical tissue from

52 ly seen in only one patient recorded outside epileptogenic cortex.

53 ts with intracranial recordings can identify epileptogenic cortex.

54 at of structural brain lesions surrounded by epileptogenic cortex.

55 patient-specific dynamical network models of epileptogenic cortex.

56 (TSC) and focal cortical dysplasia (FCD) are epileptogenic cortical malformations caused by pathogeni

57 lation between glucose PET abnormalities and epileptogenic cortical regions.

58 he expression of microglial proinflammatory, epileptogenic cytokines, suggesting its contribution to

59 s that might predispose the dentate gyrus to epileptogenic damage, we evaluated recurrent excitation

60 sult from decreased influences of interictal epileptogenic discharges on brain areas involved in card

61 The epileptogenic effect of CTZ is probably due to its enhan

62 This epileptogenic effect of GABA(A)R antagonists has rarely

63 seizure susceptibility and showed that these epileptogenic effects are selectively blocked by the alp

64 shown previously that the acute and chronic epileptogenic effects of hypoxia are age-dependent and r

65 mice also were protected against the effects epileptogenic effects of KA compared to Igf2(+/+) mice s

66 ility of the network to the oscillogenic and epileptogenic effects of kainate, whereas lack of GluR6

67 yramidal cells underlie the oscillogenic and epileptogenic effects of kainate.

68 pathway is particularly important in the pro-epileptogenic effects of the neurotrophins.

69 table seizures are a common feature of FCDs, epileptogenic electrophysiological properties are also o

70 o be generated by variable and widely spread epileptogenic foci acting upon a temporarily hyperexcita

71 focal cortical lesions that correlated with epileptogenic foci and that showed massive neuronal loss

72 nflammatory mediators overexpressed in human epileptogenic foci are known to promote seizures in anim

73 uctural associations and the varied sites of epileptogenic foci, considered together, suggest that th

74 hich recordings were obtained were distal to epileptogenic foci, making it likely that we recorded fr

75 ide an additional method for localization of epileptogenic foci.

76 l slice model of focal epilepsy in which the epileptogenic focus can be identified and the role of Pv

77 l epilepsy in whom surgical resection of the epileptogenic focus fails or was not feasible in the fir

78 inflammation and development of a secondary epileptogenic focus in the brain.

79 in ictal brain SPECT for localization of an epileptogenic focus is obtaining a timely injection of a

80 critical period of postnatal development the epileptogenic focus is thought to be of cortical origin.

81 So far, resection of the epileptogenic focus represents the only curative therapy

82 Our data suggest that the hypometabolic epileptogenic focus seen in [18F]FDG-PET studies is also

83 recording location (e.g., inside/outside an epileptogenic focus) in high-resolution studies, even in

84 In epilepsy, ASL can be used to assess the epileptogenic focus, both in peri- and interictal period

85 time in hippocampi that are not the primary epileptogenic focus, the wide variety of structural asso

86 as and eventually contribute to the cortical epileptogenic focus.

87 ther than by underlying aetiology or site of epileptogenic focus.

88 stant epilepsy involves the resection of the epileptogenic focus.

89 atomical connectivity and clinically defined epileptogenic heatmaps.

90 ) C]ABP688 BP(ND) was focally reduced in the epileptogenic hippocampal head and amygdala (p < 0.001).

91 that interictal energetic deficiency in the epileptogenic hippocampus could contribute to impaired g

92 The epileptogenic hippocampus had surprisingly high basal gl

93 ized overexpression of P-glycoprotein in the epileptogenic hippocampus of patients with drug-resistan

94 olume effect, [11C]FMZ Vd in the body of the epileptogenic hippocampus was reduced by a mean of 42.1%

95 lite deviations consistently lateralized the epileptogenic hippocampus.

96 s in the hippocampal dentate gyrus may cause epileptogenic hyperexcitability by triggering the format

97 gy in typical absence seizures that may have epileptogenic importance and highlight potential therape

98 Whereas IL-6 is epileptogenic in C57BL/6 mice, its upregulation by TGF-b

99 lian target of rapamycin (mTOR) signaling is epileptogenic in genetic epilepsy.

100 in the brain stem and cerebellum can become epileptogenic in pediatric patients.

101 MDA receptor in epileptic DGC may trigger an epileptogenic increase of intracellular free calcium, an

102 These findings suggest that after epileptogenic injuries the layer II entorhinal cortical

103 key initiator of neuroinflammation following epileptogenic injuries, and its activation contributes t

104 After epileptogenic injuries, dentate granule cell axons (moss

105 nule cell axon (mossy fiber) sprouting after epileptogenic injuries, including pilocarpine-induced st

106 susceptibility of the human dentate gyrus to epileptogenic injuries.

107 hysiology of slices from rats 3-7 d after an epileptogenic injury (pilocarpine-induced status epilept

108 These findings suggest that an epileptogenic injury reduces inhibition of layer II neur

109 echniques at varying times (1-60 d) after an epileptogenic injury, pilocarpine-induced status epilept

110 pression of KCC2 persists for weeks after an epileptogenic injury, reducing inhibitory efficacy and e

111 were then eliminated beginning 3 d after the epileptogenic injury.

112 a VD3 metabolites reflect the severity of an epileptogenic insult and that a panel of plasma VD3 meta

113 The majority of newborn cells exposed to an epileptogenic insult exhibited reductions in dendritic s

114 tial hippocampal circuit remodeling after an epileptogenic insult that generates prominent excitatory

115 of blocking new neurons generated after the epileptogenic insult to alleviate the development of chr

116 by ablating newly generated cells after the epileptogenic insult using a conditional, inducible diph

117 As epileptogenic insult, a status epilepticus (SE) was indu

118 neuronal integration can be disrupted by an epileptogenic insult.

119 at a clinically relevant time point after an epileptogenic insult.

120 Epileptogenic insults may often involve prolonged excita

121 ts that restore normal DGC development after epileptogenic insults may therefore ameliorate epileptog

122 uggests that neuroinflammation, triggered by epileptogenic insults, contributes to seizure developmen

123 al stimulation is used to produce controlled epileptogenic insults.

124 ippocampal dentate gyrus and increases after epileptogenic insults.

125 considered for patients exposed to potential epileptogenic insults.

126 elevance of the proposed biomarker, two anti-epileptogenic interventions were used; isoflurane anaest

127 s in which MR imaging failed to identify any epileptogenic lesion (61% [33/54]), SISCOM or (18)F-FDG

128 ts indicated that the MR study localized the epileptogenic lesion correctly in 8 of 8 cases.

129 lectroencephalographic studies localized the epileptogenic lesion in 5 of 8 cases; positron emission

130 When an epileptogenic lesion is present, antiepileptic drugs alo

131 between functionally important areas and the epileptogenic lesion must be assessed before surgery.

132 ich MR imaging findings were abnormal but no epileptogenic lesion was identified.

133 incomplete resection (59.1%) of the putative epileptogenic lesion.

134 mputed the connectivity of institutional non-epileptogenic lesions (NEL_INST), calculating voxel-wise

135 l cerebral deficits secondary to potentially epileptogenic lesions and epilepsy surgery, underlining

136 h was also applied to an external dataset of epileptogenic lesions identified from the literature (EL

137 heric shift of language despite having major epileptogenic lesions in close proximity to eloquent cor

138 ary objective analytic method in identifying epileptogenic lobar regions by (18)F-FDG PET in children

139 thyl tryptophan shows promise for localizing epileptogenic malformations of cortical development.

140 ing them as networks consistently engaged by epileptogenic mass lesions.

141 ing NMDA-R-mediated transmission and a novel epileptogenic mechanism for human CAE.

142 The discovery of this novel epileptogenic mechanism hopefully will facilitate the de

143 differential increase of NR2B constitutes an epileptogenic mechanism in humans.

144 One potential epileptogenic mechanism is loss of GABAergic interneuron

145 To shed light on the Posttraumatic Epileptogenic mechanisms and on the generation of bilate

146 ed the identification of clinically relevant epileptogenic mechanisms and the development of effectiv

147 facilitate efforts to characterize relevant epileptogenic mechanisms and to identify clinically effe

148 ss and mossy fiber sprouting are not primary epileptogenic mechanisms in this animal model.

149 lepticus has been used to identify secondary epileptogenic mechanisms under the assumption that a sei

150 rt- and long-range functional convergence of epileptogenic molecular pathways, reducing the broad spe

151 (+) channel, which is also a major target of epileptogenic mutations and is particularly important fo

152 glutamate content that may contribute to the epileptogenic nature of hippocampal sclerosis.

153 ngly, previously described folding-defective epileptogenic NaV1.1 mutants show loss of function also

154 al-resolution MR images enables detection of epileptogenic neocortical lesions, some of which are occ

155 homeostatic gain control, but also dampened epileptogenic network activity.

156 ileptogenic insults may therefore ameliorate epileptogenic network dysfunction and associated morbidi

157 sed in the context of the construction of an epileptogenic network.

158 icient disconnection of an anterior temporal epileptogenic network.

159 EEG/fMRI can also assess epileptogenic networks and changes in brain state, leadi

160 l utility of these recordings for localizing epileptogenic networks and understanding seizure generat

161 n areas and can help to generate concepts of epileptogenic networks both in individual patients and g

162 for identification of potentially vulnerable epileptogenic networks in mass lesions causing medically

163 latively broadly and bilaterally distributed epileptogenic networks, genetic determinants of psychiat

164 acts, which constitute crucial components of epileptogenic networks, is unknown.

165 locally hyperexcitable node dynamics of the epileptogenic networks, provides a mechanistic explanati

166 ically relevant biomarkers characteristic of epileptogenic networks.

167 they are vulnerable to being recruited into epileptogenic neuronal circuits.

168 leep states differentially modulate abnormal epileptogenic neuronal discharge properties within human

169 ot clear whether mTOR inhibition has an anti-epileptogenic, or merely anticonvulsive effect.

170 Glutamate was also elevated in epileptogenic (p < 0.001) compared to nonepileptogenic h

171 Glutamate levels were elevated in epileptogenic (p = 0.03; n = 7), nonlocalized (p < 0.001

172 concentration of AEDs in the vicinity of the epileptogenic pathology and thereby render the epilepsy

173 Therefore, its value as a biomarker for epileptogenic pathology is not well understood.

174 onitoring the development and progression of epileptogenic pathology, particularly mesial temporal sc

175 as a key component of a genetically complex epileptogenic pathway.

176 uggest that changes in theta band during the epileptogenic period may serve as a diagnostic biomarker

177 This pro-epileptogenic phenotype resulted from Ube3a deletion in

178 del of fragile X syndrome (Fmr1(-/y)) has an epileptogenic phenotype that is triggered by group I met

179 optogenetic strategy can reverse an in vitro epileptogenic phenotype.

180 ondary, propagated activity occurs have less epileptogenic potential and do not need to be excised.

181 liable markers are available to evaluate the epileptogenic potential of a brain injury.

182 ition in neuronal circuits, leading to their epileptogenic potential.

183 In preparing to study this epileptogenic process in genetically altered mice, we de

184 cal recurrent seizures often occurs after an epileptogenic process induced by transient insults to th

185 sorders with the potential to facilitate the epileptogenic process or cortical hyperexcitability in e

186 imental febrile seizures (i.e., early in the epileptogenic process), the preserved and augmented inhi

187 nvulsant that masks the true duration of the epileptogenic process.

188 ysregulation of HCNs might contribute to the epileptogenic process.

189 e could be targeted therapies to prevent the epileptogenic process.

190 lutamatergic network that contributes to the epileptogenic process.

191 he enlarged amygdala could be related to the epileptogenic process.

192 has been hypothesized to participate in the epileptogenic processes.

193 Second, we show long-term monitoring during epileptogenic progression in a scn1lab mutant recapitula

194 immediate postictal SPECT in localizing the epileptogenic region in refractory partial epilepsy.

195 of resection, compared to the homotopic non-epileptogenic region in the contralateral hemisphere.

196 l seizure, and that focal stimulation of the epileptogenic region terminates electrographic seizures

197 Influx (K1*) in the epileptogenic region was reduced in comparison with the

198 on likely underlies burst generation in this epileptogenic region, and may also shape processing of s

199 epileptogenicity, and the delineation of the epileptogenic region.

200 formation that helps to identify the primary epileptogenic region.

201 orrelated highly with phosphorylation in the epileptogenic region.

202 for any rate constants measured outside the epileptogenic region.

203 that the shell of the lesion constituted an epileptogenic region.

204 tion rates (26 +/- 10%) were observed in the epileptogenic region.

205 jacent normal-appearing area included in the epileptogenic region.

206 (ROIs), which included (1) the hypometabolic epileptogenic regions and (2) the homologous regions in

207 thus provide a noninvasive means to localize epileptogenic regions in hippocampus.

208 Identifying epileptogenic regions in the temporal lobe using magneti

209 (2) a locally increased excitability in the epileptogenic regions supporting the mixture of hypercon

210 vasive localizing criterion and can localize epileptogenic regions with accuracy comparable with that

211 tionally, we observed higher excitability in epileptogenic regions, in agreement with the data.

212 nces in cortical organization render neurons epileptogenic remains controversial.

213 NA causes phenotypic abnormalities including epileptogenic responses and cognitive dysfunction.

214 s rather than reduces seizure, indicating an epileptogenic role for loss-of-function Cacna1h gene var

215 red to MRI) procedure was used to locate the epileptogenic seizure focus with SPECT.

216 y of hippocampal digitations occurred on the epileptogenic side in all patients with TLE and also on

217 ith TLE had hippocampal abnormalities on the epileptogenic side.

218 ies the TGF-beta pathway as a novel putative epileptogenic signaling cascade and therapeutic target f

219 evoked from area tempestas (AT), a discrete epileptogenic site in the rostral piriform cortex.

220 veal a novel form of neural plasticity, that epileptogenic stimulation can selectively downregulate e

221 ation of tonic GABA inhibition after chronic epileptogenic stimulation of rat hippocampal cultures.

222 t THIP, were significantly reduced following epileptogenic stimulation.

223 hippocampus (VHC) is also more sensitive to epileptogenic stimuli than the dorsal hippocampus (DHC),

224 responses to SPES are functional markers of epileptogenic structural abnormalities, and can identify

225 es of higher magnitude and discriminated the epileptogenic structures more accurately when compared t

226 Our results suggest that epileptogenic susceptibility in AS patients is a consequ

227 eizure, with a relative disconnection of the epileptogenic temporal lobe in the interictal period.

228 to secondary seizure generalization from the epileptogenic temporal lobe to broader brain networks in

229 a relative decreased correlation between the epileptogenic temporal region and remaining cortex durin

230 by a surge of cross-correlated perfusion in epileptogenic temporal-limbic structures during a seizur

231 clerosis and identify novel targets for anti-epileptogenic therapeutic intervention.

232 cepts and targets for anticonvulsant or anti-epileptogenic therapy.

233 Some varieties are intrinsically epileptogenic; these include FCD and heterotopia.

234 ntered on: (1) improving the localization of epileptogenic tissue beyond that of state-of-the-art str

235 om Emx-Cre; Clock(flox/flox) mouse and human epileptogenic tissue exhibit decreased spontaneous inhib

236 (HFOs; 80-500 Hz) seem better biomarkers for epileptogenic tissue than spikes.

237 HFES effects on epileptogenic tissue were immediate and also outlasted t

238 obe epilepsy surgery is to remove sufficient epileptogenic tissue without compromising post-operative

239 g the years after neurosurgical resection of epileptogenic tissue.

240 illations (HFOs) are important biomarkers of epileptogenic tissue.

241 Output Cycles Kaput (CLOCK) is decreased in epileptogenic tissue.

242 we performed transcriptome analysis on human epileptogenic tissue.

243 quence to high gamma oscillations present in epileptogenic tissue.

244 erved depending on the lateralization of the epileptogenic TL.

245 Therefore, after epileptogenic treatments that kill hilar mossy cells, mo

246 mossy fiber sprouting from developing after epileptogenic treatments, its potential role in the path

247 f cortical lesions, however, identifying the epileptogenic tuber(s) is difficult and often requires i

248 to be a useful tool in the identification of epileptogenic tubers and has improved the outcome of sur

249 tonin synthesis is increased interictally in epileptogenic tubers in patients with TSC.

250 date, the underlying mechanism is unique for epileptogenic variants and involves differential beta su

251 al treatment in epilepsy is effective if the epileptogenic zone (EZ) can be correctly localized and c

252 nd postures (HPs) as localizing signs of the epileptogenic zone (EZ) in patients with frontal or temp

253 olymicrogyria (PMG) types and the associated epileptogenic zone (EZ), as defined by stereoelectroence

254 ther these abnormalities are specific to the epileptogenic zone (EZ), we characterized in vivo whole-

255 tory partial epilepsy are referred to as the epileptogenic zone (EZ).

256 HFES was delivered directly to the epileptogenic zone (local closed-loop) in four patients

257 e compared with the presumed location of the epileptogenic zone (PEZ) as determined by video-EEG and

258 Localization results were compared with epileptogenic zone and resected cortex for congruence as

259 ations sources (80-200 Hz) with the presumed epileptogenic zone and the resected cortex were 75.0% an

260 is a promising technique for localizing the epileptogenic zone and would be enhanced by the ability

261 Their link to the epileptogenic zone argues that their study will teach us

262 ictal VHFOs are more specific biomarkers for epileptogenic zone compared to traditional HFOs.

263 l data that guide surgical resections of the epileptogenic zone for medically refractory epilepsy.

264 equires thorough investigation to define the epileptogenic zone for surgical treatment.

265 resection for a 35-year-old patient with an epileptogenic zone identified in the anterior temporal l

266 enic zone), it may not constitute the entire epileptogenic zone in all cases.

267 of (18)F-FMZ PET for the localization of the epileptogenic zone in patients with drug-resistant tempo

268 il (FMZ) PET more specifically localizes the epileptogenic zone in patients with medically refractory

269 omatogenic zone appears to correspond to the epileptogenic zone in rolandic epilepsy (sensory-motor s

270 For patients with the epileptogenic zone in the noneloquent cortex, seizure fo

271 a clinical tool for the localization of the epileptogenic zone in the presurgical evaluation of drug

272 A complete resection of the epileptogenic zone is required for seizure-free life.

273 There is evidence that the epileptogenic zone is spatially distributed and also, in

274 ug-resistant focal epilepsy, excision of the epileptogenic zone is the most effective treatment appro

275 The predominance of FRs within the epileptogenic zone not only during NREM sleep, but also

276 scillations sources were discordant with the epileptogenic zone or resection area, patient has an odd

277 rovided a surgical option for patients whose epileptogenic zone resides in the eloquent cortex.

278 ficantly more reliable marker of the primary epileptogenic zone than the presence of either intericta

279 nd appear to be more specific biomarkers for epileptogenic zone when compared to traditional HFOs.

280 ain responsible for generating seizures (the epileptogenic zone), it may not constitute the entire ep

281 iding in the noninvasive localization of the epileptogenic zone).

282 s-fMRI SOZ can be used as a biomarker of the epileptogenic zone, and postoperative rs-fMRI normalizat

283 Anterior HPC specimens from the patients' epileptogenic zone, defined by electrocorticography, wer

284 an now provide an accurate assessment of the epileptogenic zone, thereby permitting improved identifi

285 peaks ('leading regions') are located in the epileptogenic zone, whereas sites in which late, seconda

286 ty (21/31 [68%]) for the localization of the epileptogenic zone, with a more restricted abnormality t

287 ails due to an incomplete delineation of the epileptogenic zone.

288 with no biomarker precisely delineating the epileptogenic zone.

289 elines for presurgical identification of the epileptogenic zone.

290 izing information on the ictal processes and epileptogenic zone.

291 HFOs appear excellent markers for the epileptogenic zone.

292 urgery due to the imprecise determination of epileptogenic zone.

293 It can potentially identify the epileptogenic zone.

294 resective surgery after determination of the epileptogenic zone.

295 ably not the most important component of the epileptogenic zone.

296 ogenicity biomarkers for localization of the epileptogenic zone.

297 ients with TLE retrospectively confirmed the epileptogenic zone.

298 al epilepsy and regional connectivity at the epileptogenic zone.

299 izure-free interictal EEG data are higher in epileptogenic zones as compared with nearby normal areas

300 ltimate goal being the clinical treatment of epileptogenic zones.