ライフサイエンスコーパス: epileptic

1 or face (6) and seizure (5, including 3 non-epileptic).

2 However, sleep also activates epileptic activities in medial temporal regions.

3 nnel function, which may lie at the basis of epileptic activity and neurodevelopmental symptoms in th

4 The increase in interictal epileptic activity before arousals suggests its particip

5 etworks of patients with focal epilepsy, and epileptic activity can exert widespread effects within t

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

7 properties identify areas that are shaped by epileptic activity independent of IED or seizure detecti

8 We investigated whether sleep-related epileptic activity is associated with sleep disruption.

9 Epileptic activity is frequently associated with Alzheim

10 The direct influence of nocturnal epileptic activity on sleep fragmentation remains poorly

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

12 local circuitry gives rise to stereotypical epileptic activity patterns, but these are also influenc

13 ear, which is called ictal fear (IF), due to epileptic activity within the brain defensive survival c

14 Epileptic activity, frequently occurring in glioma patie

15 ntal monomorphic delta waves with absence of epileptic activity.

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

17 nisms that could both amplify and counteract epileptic activity.

18 ngly recognized as potential contributors to epileptic activity.

19 tribution to the emergence or maintenance of epileptic activity.

20 be required for astrocytes to contribute to epileptic activity.

21 y become capable of intrinsically generating epileptic activity.

22 epsy is associated with ictal and interictal epileptic activity.

23 tform The Virtual Brain, we reconstructed 14 epileptic and 5 healthy human (of either sex) brain netw

24 g the granule cells overly quiescent in both epileptic and control mice again disrupted behavioural p

25 a reliable technique to stain microglia from epileptic and glioma patients to examine responses to pu

26 the aim of improving differentiation between epileptic and non-epileptic hippocampi in humans.

27 arity of HFOs properties recorded at rest in epileptic and non-epileptic hippocampi suggests that the

28 ena, it is possible to differentiate between epileptic and non-epileptic hippocampi using a simple od

29 tive amplitude and duration were compared in epileptic and non-epileptic hippocampi.

30 ecycling is of essential importance in human epileptic and psychiatric disorders and our findings may

31 ha-OH steroids that act as anesthetics, anti-epileptics, and anti-depressants.

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

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

34 Principal hippocampal neurons from such epileptic animals display enhanced spike output in respo

35 mplete feedback circuit motifs of normal and epileptic animals revealed that, as a consequence of alt

36 lation can paradoxically trigger seizures in epileptic animals, supporting the notion that gamma-amin

37 In epileptic animals, this system produced a progressive an

38 In epileptic animals, we observed two types of co-occurring

39 oriens-lacunosum moleculare interneurons in epileptic animals.

40 l activation in both control and chronically epileptic animals.

41 udies using chronic EEG (cEEG) revealed that epileptic brain activity shows robust cycles, operating

42 is selectively upregulated within neurons in epileptic brain and report that targeting miR-135a in vi

43 HFOs are a proposed biomarker of epileptic brain tissue and may also be useful for seizur

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

45 ctural features of this projection system in epileptic brain.

46 g to neuroimaging data, we demonstrated that epileptic brains during interictal RS are associated wit

47 working point of the model, indicating that epileptic brains operate closer to a stable equilibrium

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

49 The epileptic burst index increased significantly before aro

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

51 marked sleep stages, arousals, seizures, and epileptic bursts in 36 patients with focal drug-resistan

52 significantly differentially edited between epileptic cases and controls.

53 after status epilepticus (SE) and in chronic epileptic (CE) rats.

54 ion of slow-wave sleep MI of neighboring non-epileptic channels of 47 patients, whose ECoG sampling i

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

56 t rest as well as during a cognitive task in epileptic compared with non-epileptic hippocampi.

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

58 pilocarpine, initiates the development of an epileptic condition resembling human temporal lobe epile

59 Neuronal activity including epileptic conditions generates synchronised calcium tran

60 hose levels are potentially diminished under epileptic conditions.

61 as well as pharmacological interventions and epileptic conditions.

62 -specific synaptic reorganization underlying epileptic cortical circuits and provide new insights int

63 Human epileptic cortices presenting type II focal cortical dys

64 e mouse model of temporal lobe epilepsy, the epileptic dentate gyrus excessively recruits granule cel

65 to explain these observations, and find that epileptic DG networks organize into disjoint, cell-type

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

67 changes in action potential waveform during epileptic discharges, but acquiring similar evidence in

68 Dravet Syndrome is a severe childhood epileptic disorder caused by haploinsufficiency of the S

69 2 channel and hnRNP U are strongly linked to epileptic disorders and intellectual disability.

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

71 erstanding of epileptic propagation and anti-epileptic drug action.

72 Standard anti-epileptic drug monotherapy was ineffective in the patien

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

74 e extracting the features of two common anti-epileptic drugs (levetiracetam and lamotrigine) in an in

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

76 cing poor seizure control with existing anti-epileptic drugs.

77 ly reproduces EEG data from both healthy and epileptic EEG signals, but it also predicts EEG features

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

79 Developmental and epileptic encephalopathies (DEE) are a heterogeneous gro

80 The developmental and epileptic encephalopathies (DEEs) are heterogeneous diso

81 es have been identified in developmental and epileptic encephalopathies (DEEs), but correlating genet

82 ort additional risk genes for schizophrenia, epileptic encephalopathies and CHD.

83 2 channels are also strongly associated with epileptic encephalopathies and intellectual disability i

84 Epileptic encephalopathies are a devastating group of se

85 Developmental and epileptic encephalopathies are a heterogeneous group of

86 Developmental epileptic encephalopathies are devastating disorders cha

87 on, and with the neonatal or infantile onset epileptic encephalopathies due to KCNQ2 GoF.

88 NCE STATEMENT KCNT1 mutations lead to severe epileptic encephalopathies for which there are no effect

89 Many epileptic encephalopathies have a genetic aetiology and

90 ic movements in the context of developmental epileptic encephalopathies is an increasingly recognized

91 as a causative factor for developmental and epileptic encephalopathies of infancy and childhood with

92 family Q (KCNQ) dysfunction can cause severe epileptic encephalopathies that are resistant to modern

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

94 the unique association of developmental and epileptic encephalopathies, cleft palate, joint contract

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

96 m-activated potassium channel produce severe epileptic encephalopathies.

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

98 ic generalized epilepsy to developmental and epileptic encephalopathies.

99 SCN8A encephalopathy is a developmental and epileptic encephalopathy (DEE) caused by de novo gain-of

100 like features, and seizures or developmental epileptic encephalopathy (DEE).

101 ) 2.1, are associated with developmental and epileptic encephalopathy (DEE).

102 ations in K(v)7.2 and K(v)7.3 subunits cause epileptic encephalopathy (EE), yet the underlying pathog

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

104 n of TBC1D24 associated with early infantile epileptic encephalopathy (EIEE).

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

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

107 s with high risk for sudden death, including epileptic encephalopathy and cardiac arrhythmia.

108 gical disorders, from drug-refractory lethal epileptic encephalopathy and DOORS syndrome (deafness, o

109 d GABRA5 as a causative gene for early onset epileptic encephalopathy and expands the mutant GABRA1 p

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

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

112 ave been increasingly identified in neonatal epileptic encephalopathy and more recently also in early

113 with a range of global developmental delay, epileptic encephalopathy and primary or progressive micr

114 a cause of infantile-onset developmental and epileptic encephalopathy and underline the critical role

115 Two unrelated individuals with epileptic encephalopathy carry a de novo variant in the

116 3 patients (eight previously described) with epileptic encephalopathy carrying either novel or known

117 e describe a new syndromic developmental and epileptic encephalopathy caused by bi-allelic loss-of-fu

118 is a rare, treatment-resistant developmental epileptic encephalopathy characterised by multiple types

119 ome (DS) is a catastrophic developmental and epileptic encephalopathy characterized by severe, pharma

120 16L) linked to severe infancy or early-onset epileptic encephalopathy exhibited markedly defective co

121 or genetic generalized and developmental and epileptic encephalopathy patients but also for lesional

122 gories tested, followed by developmental and epileptic encephalopathy patients.

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

124 neurotransmission contribute to early onset epileptic encephalopathy phenotypes.

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

126 novo genetic variant found in patients with epileptic encephalopathy that changes a residue located

127 on reported in 14 unrelated individuals with epileptic encephalopathy that included seizure onset in

128 esent with developmental and early infantile epileptic encephalopathy that is far more severe than ty

129 Dravet syndrome (DS) is an epileptic encephalopathy that still lacks biomarkers for

130 m channel gene are linked to early-infantile epileptic encephalopathy type 13, also known as SCN8A-re

131 ause a severe, early onset developmental and epileptic encephalopathy via an unclear mechanism.

132 quired focal epilepsy, and developmental and epileptic encephalopathy were included.

133 in 36 cases from 25 families presenting with epileptic encephalopathy with developmental delay and hy

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

135 f the sodium channel gene SCN8A result in an epileptic encephalopathy with refractory seizures, devel

136 with hypotonia, global developmental delay, epileptic encephalopathy, and dysmorphic features.

137 uals with congenital microcephaly, infantile epileptic encephalopathy, and profound developmental del

138 d presented with global developmental delay, epileptic encephalopathy, and spasticity, and ten indivi

139 hanisms of GRIN2D-mediated developmental and epileptic encephalopathy, as well as the potential benef

140 variants, presenting with developmental and epileptic encephalopathy, characterized by early-infanti

141 ales who typically present with severe early epileptic encephalopathy, global developmental delay, mo

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

143 ch delay/apraxia to severe developmental and epileptic encephalopathy, often within the epilepsy-apha

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

145 All affected individuals presented with epileptic encephalopathy, severe neurodevelopmental dela

146 riant in two patients with developmental and epileptic encephalopathy.

147 in six patients with intractable early onset epileptic encephalopathy.

148 A is a novel causal gene for early infantile epileptic encephalopathy.

149 pmental delay, autism spectrum disorder, and epileptic encephalopathy.

150 ions in the SCN8A gene cause early infantile epileptic encephalopathy.

151 study of known disease-associated genes for epileptic encephalopathy.

152 manifesting as treatment-resistant infantile epileptic encephalopathy.

153 cluding but not limited to developmental and epileptic encephalopathy.

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

155 ome, idiopathic ventricular arrhythmias, and epileptic encephalopathy.

156 ic generalized epilepsy to developmental and epileptic encephalopathy.

157 ies associated with GRIN2A developmental and epileptic encephalopathy.

158 pmental delay, autism spectrum disorder, and epileptic encephalopathy.

159 hibiting developmental delay and early-onset epileptic encephalopathy.

160 a new gene associated with developmental and epileptic encephalopathy.

161 e likely to be a frequent cause of recessive epileptic encephalopathy.

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

163 for synaptic plasticity in the emergence of epileptic foci.

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

165 us, initiate in regions uniquely outside the epileptic focus, elicit marked increases of multiunit ac

166 with contralateral side of the brain in each epileptic group: left mesial temporal sclerosis (LMTS) a

167 ng differentiation between epileptic and non-epileptic hippocampi in humans.

168 erties recorded at rest in epileptic and non-epileptic hippocampi suggests that they cannot be used a

169 e to differentiate between epileptic and non-epileptic hippocampi using a simple odd-ball task.

170 These reductions were not observed in non-epileptic hippocampi.

171 duration were compared in epileptic and non-epileptic hippocampi.

172 deviations in brain metabolites characterize epileptic hippocampi.

173 ognitive task in epileptic compared with non-epileptic hippocampi.

174 icant reductions of HFOs rates were found in epileptic hippocampi.

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

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

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

178 The occurrence of non-epileptic hyperkinetic movements in the context of devel

179 ule cells (DGCs) generated in response to an epileptic insult develop features that promote increased

180 y which SE transforms a brain from normal to epileptic may reveal novel targets for preventive and di

181 iation of modulation index (MI) from the non-epileptic mean (rated by z-score) improved the performan

182 of statistical deviation of MI from the non-epileptic mean on invasive recording is technically feas

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

184 ts and was responsive to treatment with anti-epileptic medications in almost all.

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

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

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

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

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

190 al granule cell hyperactivity in chronically epileptic mice via either of two distinct inhibitory che

191 We found that CA1 place cells in epileptic mice were unstable and completely remapped acr

192 CA1 and dentate gyrus in pilocarpine-treated epileptic mice with silicon probes during head-fixed vir

193 itulated spatial memory deficits observed in epileptic mice.

194 firing between the CA1 and dentate gyrus in epileptic mice.

195 stereological analyses in several models of epileptic mice.

196 ee microRNAs reduced spontaneous seizures in epileptic mice.

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

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

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

200 In the cross-frequency epileptic network, secondary generalization was associat

201 In the within-frequency epileptic network, we found that the seizure onset zone

202 individualized brain regions outside of the epileptic network.

203 ed excitation-inhibition interactions of the epileptic network.

204 dom, but represent an electrically connected epileptic network.

205 ls are required to generate both features of epileptic networks (i.e., spontaneous interictal populat

206 rtant new hypotheses regarding the nature of epileptic networks and mechanisms of seizure onset.

207 Epileptic networks are characterized by two outputs: bri

208 esearch groups have published methods to map epileptic networks but applying them to improve patient

209 ateralization of MTLE may represent distinct epileptic networks in patients with right versus left MT

210 HP component is markedly reduced in male rat epileptic neurons, whereas the NKA-sAHP component is not

211 polarization (sAHP), which is reduced in the epileptic neurons.

212 also to normalization of the spike output of epileptic neurons.

213 The outcome was epileptic (non-eclamptic) seizure captured using diary r

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

215 agents included eight antibiotics, two anti-epileptics, one anti-psychotic, and one anti-inflammator

216 kes were expertly identified, and interictal epileptic oscillations across the neural activity freque

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

218 ics and in defining clinical localization of epileptic pathology.

219 and the global coupling in the virtual human epileptic patient brain network models (BNMs), complemen

220 n the initiation of pathological activity in epileptic patients and experimental animal models of tem

221 lectin in tissue slices from female and male epileptic patients diagnosed with mesial temporal lobe e

222 Many epileptic patients do not achieve adequate seizure contr

223 he human hippocampal formation, performed in epileptic patients for clinical reasons, and highlight t

224 's findings based on electric stimulation of epileptic patients led them to hypothesize that a sensor

225 This article focuses on adult epileptic patients, reviewing the updated clinical crite

226 provide a method of suppressing seizures in epileptic patients.

227 ify the source of seizures in drug-resistant epileptic patients.

228 posterior superior temporal gyrus (pSTG) of epileptic patients.

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

230 outing and recurrent seizures in the chronic epileptic phase.

231 t with pyridoxine significantly improved the epileptic phenotype and extended lifespan in plpbp-/- an

232 sed in inhibitory interneurons, explains the epileptic phenotype.

233 an intermediate phenotype that contribute to epileptic phenotypes and that are potential drug targets

234 lts in the exacerbation of hyperactivity and epileptic phenotypes.

235 cerebellum, making it capable of generating epileptic population activity.

236 se neuronal excitability consistent with the epileptic potential of FHF2 variants.

237 s, provides a mechanistic explanation of the epileptic processes during the interictal RS period.

238 ortant implications for our understanding of epileptic propagation and anti-epileptic drug action.

239 AB and EB populations of DGCs recorded from epileptic rats received increased excitatory input compa

240 factor (GDNF) directly to the hippocampus of epileptic rats.

241 The propagation of epileptic seizure activity in the brain is a widespread

242 An epileptic seizure can trigger a headache during (ictal)

243 proic acid (VPA) is a drug commonly used for epileptic seizure control.

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

245 ncer or diabetes, may discriminate a general epileptic seizure odor (different from body odours of th

246 ure (picrotoxin) to determine the effects of epileptic seizure on the activity of trigeminovascular A

247 ely recognized as a network disease in which epileptic seizure propagation is likely coordinated by d

248 e to provide clinical guidance in support of epileptic seizure treatments in practice.

249 which are known to be overproduced during an epileptic seizure, may contribute to postictal sleep and

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

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

252 ating disorders characterized by intractable epileptic seizures and developmental delay.

253 s have resulted in the new classification of epileptic seizures and epilepsies.

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

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

256 oceuticals to enable accurate forecasting of epileptic seizures and therapy.

257 While epileptic seizures are known to often manifest also with

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

259 Recurrent high-frequency epileptic seizures cause progressive hippocampal scleros

260 ene associated with autism-like symptoms and epileptic seizures for further proof of pathogenicity.

261 Investigations of the mechanisms generating epileptic seizures have primarily focused on neurons.

262 RKi) have recently been applied to alleviate epileptic seizures in tuberous sclerosis complex (TSC).

263 no study has yet tested the possibility that epileptic seizures may be reflected in an olfactory prof

264 Epileptic seizures potently modulate hippocampal adult n

265 t, but accompanied by hypothermia and severe epileptic seizures preceding death.

266 Epileptic seizures represent altered neuronal network dy

267 Then, we formulate the abatement of epileptic seizures to a closed-loop tracking control pro

268 We proposed an automatic method to detect epileptic seizures using an imaged-EEG representation of

269 KO mice lacked epileptic seizures when fed a low lysine/high PN diet.

270 chniques for the detection and prediction of epileptic seizures with electroencephalogram (EEG).

271 e novel insights into the pathophysiology of epileptic seizures with respect to ANS function, and, wh

272 ot detected in patients with psychogenic non-epileptic seizures, and did not result from medication t

273 n the treatment of sleep disorders, anxiety, epileptic seizures, and many others.

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

275 risks to users, including psychosis, stroke, epileptic seizures, and they can kill.

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

277 We show, for neural systems prone to epileptic seizures, that such a reduction in diffusivity

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

279 logical disorders characterised by recurrent epileptic seizures.

280 works occurs resulting in the onset of focal epileptic seizures.

281 in mice lowers the threshold for triggering epileptic seizures.

282 hippocampal neuronal injury during prolonged epileptic seizures.

283 ippocampus in the occurrence and severity of epileptic seizures.

284 ng the evaluation of gustatory and olfactory epileptic seizures.

285 cation, and thereby reduce susceptibility to epileptic seizures.

286 n the brain of freely moving mice undergoing epileptic seizures.

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

288 Epileptic spasms are a hallmark of severe seizure disord

289 Our findings provide evidence that epileptic spasms can arise from the neocortex and reveal

290 he first month of life, mainly consisting of epileptic spasms or myoclonic seizures.

291 states as a mechanism capable of initiating epileptic spasms will likely provide new targets for int

292 vidence has been growing that in addition to epileptic spikes high frequency oscillations (HFOs) are

293 Epileptic spikes were detected automatically.

294 Interictal epileptic spikes were expertly identified, and intericta

295 es, presented by the propagating patterns of epileptic spikes, as well as temporal correlations decli

296 Understanding the nature of epileptic state transitions remains a major goal for epi

297 s of multiple temporal lobe epilepsy and non-epileptic subjects.

298 tes of slow wave rhythms are more intense in epileptic than control animals and occasionally appear s

299 urine-induced motility of human microglia in epileptic tissue is similar to that of rodent microglia

300 As a result, the epileptic zone in the BECTS patients appears to exhibit