ライフサイエンスコーパス: epileptogenic

1 nodes with a short transition time as highly epileptogenic.

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

3 prise brain regions that are not necessarily 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 Comparing to a well-known epileptogenic agent kainic acid (KA), CTZ affects neuron

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

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

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

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

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

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

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

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

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

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

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

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

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

23 ccurrence were significantly associated with epileptogenic areas.

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

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

26 00 Hz) frequency range, may be signatures of epileptogenic brain and involved in the generation of se

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

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

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

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

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

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

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

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

35 eizure activity analogous to recordings from epileptogenic brain tissue.

36 t neurophysiological processes in normal and epileptogenic brain.

37 ental oscillations that are signatures of an epileptogenic brain.

38 ly recognized as potential biomarkers of the epileptogenic brain.

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

40 structural disorganization exists in occult epileptogenic cerebral lesions.

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

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

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

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

45 The epileptogenic cortex had only marginally increased gluta

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

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

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

49 ts with intracranial recordings can identify epileptogenic cortex.

50 at of structural brain lesions surrounded by epileptogenic cortex.

51 patient-specific dynamical network models of epileptogenic cortex.

52 lation between glucose PET abnormalities and epileptogenic cortical regions.

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

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

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

56 us sclerosis (TSC) is the presence of highly epileptogenic dysplastic cerebral cortex (tubers) compos

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

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

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

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

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

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

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

64 t in synaptic transmission as well as in the epileptogenic effects of kainate.

65 mpus, an action that could contribute to the epileptogenic effects of kainate.

66 We studied the short- and long-term epileptogenic effects of massed stimulation (MS) of the

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

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

69 equence of temporal lobe seizures and not an epileptogenic entity.

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 Identification of epileptogenic foci in patients with refractory epilepsy

74 ore promising tool for the identification of epileptogenic foci than interictal SPECT or scalp EEG in

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

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

77 ide an additional method for localization of epileptogenic foci.

78 r postictal SPECT (n=23) for localization of epileptogenic foci.

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

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

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

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

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

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

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

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

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

88 as and eventually contribute to the cortical epileptogenic focus.

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

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

91 The epileptogenic hippocampus had surprisingly high basal gl

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

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

94 lite deviations consistently lateralized the epileptogenic hippocampus.

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

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

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

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

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

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

101 After epileptogenic injuries, dentate granule cell axons (moss

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

103 susceptibility of the human dentate gyrus to epileptogenic injuries.

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

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

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

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

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

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

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

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

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

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

114 neuronal integration can be disrupted by an epileptogenic insult.

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

116 Epileptogenic insults may often involve prolonged excita

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

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

119 al stimulation is used to produce controlled epileptogenic insults.

120 ippocampal dentate gyrus and increases after epileptogenic insults.

121 considered for patients exposed to potential epileptogenic insults.

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

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

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

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

126 When an epileptogenic lesion is present, antiepileptic drugs alo

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

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

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

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

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

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

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

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

135 One potential epileptogenic mechanism is loss of GABAergic interneuron

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

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

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

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

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

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

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

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

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

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

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

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

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

149 icient disconnection of an anterior temporal epileptogenic network.

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

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

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

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

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

155 ically relevant biomarkers characteristic of epileptogenic networks.

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

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

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

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

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

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

162 ) if MEG spike sources colocalize with focal epileptogenic pathology, and (3) if MEG can identify the

163 In 5 of 6 patients with focal epileptogenic pathology, MEG spike sources were colocali

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

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

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

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

168 optogenetic strategy can reverse an in vitro epileptogenic phenotype.

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

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

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

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

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

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

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

176 ysregulation of HCNs might contribute to the epileptogenic process.

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

178 lutamatergic network that contributes to the epileptogenic process.

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

180 has been hypothesized to participate in the epileptogenic processes.

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

182 sphere in 2), and overlapped or bordered the epileptogenic region in 12.

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

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

185 l damage, and reduced inhibition in a highly epileptogenic region of the dentate gyrus.

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

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

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

189 epileptogenicity, and the delineation of the epileptogenic region.

190 formation that helps to identify the primary epileptogenic region.

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

192 orrelated highly with phosphorylation in the epileptogenic region.

193 for any rate constants measured outside the epileptogenic region.

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

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

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

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

198 Identifying epileptogenic regions in the temporal lobe using magneti

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

200 nces in cortical organization render neurons epileptogenic remains controversial.

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

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

203 ith TLE had hippocampal abnormalities on the epileptogenic side.

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

205 zures evoked focally from area tempestas, an epileptogenic site in the deep rostral piriform cortex.

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

207 ptide thyrotropin-releasing hormone (TRH) in epileptogenic sites, we examined soman-induced convulsio

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

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

210 t THIP, were significantly reduced following epileptogenic stimulation.

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

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

213 nterictal single neuronal burst discharge in epileptogenic structures stresses the difference between

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

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

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

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

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

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

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

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

222 t account for all failures; extrahippocampal epileptogenic tissue must persist in some patients.

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

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

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

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

227 g the years after neurosurgical resection of epileptogenic tissue.

228 we performed transcriptome analysis on human epileptogenic tissue.

229 quence to high gamma oscillations present in epileptogenic tissue.

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

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

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

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

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

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

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

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

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

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

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

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

242 sources were localized in the region of the epileptogenic zone as ultimately defined by all clinical

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

259 c pathology, and (3) if MEG can identify the epileptogenic zone when scalp ictal electroencephalogram

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

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

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

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

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

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

266 HFOs appear excellent markers for the epileptogenic zone.

267 It can potentially identify the epileptogenic zone.

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

269 ients with TLE retrospectively confirmed the epileptogenic zone.

270 al epilepsy and regional connectivity at the epileptogenic zone.

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

272 with no biomarker precisely delineating the epileptogenic zone.

273 elines for presurgical identification of the epileptogenic zone.

274 izing information on the ictal processes and epileptogenic zone.

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

276 ltimate goal being the clinical treatment of epileptogenic zones.

277 aluable data for presurgical localization of epileptogenic zones.