ライフサイエンスコーパス: epileptic seizure

1 with impaired consciousness with or without epileptic seizure.

2 ity, neurodegeneration and susceptibility to epileptic seizure.

3 into rapidly evolving brain networks in the epileptic seizure.

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

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

6 logical disorders characterised by recurrent epileptic seizures.

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

8 Traumatic brain injury often leads to epileptic seizures.

9 to sensory stimuli, and a high incidence of epileptic seizures.

10 the effect of the ketogenic diet in reducing epileptic seizures.

11 dence implicates glutamatergic mechanisms in epileptic seizures.

12 attention for their potential involvement in epileptic seizures.

13 temporally correlates with the emergence of epileptic seizures.

14 s such as ischemic stroke, brain trauma, and epileptic seizures.

15 ted in ERK activation and caused spontaneous epileptic seizures.

16 he feedback control of neuronal circuits and epileptic seizures.

17 KO) mice exhibit brain enlargement and fatal epileptic seizures.

18 n parameters, and long-term effect of DBS on epileptic seizures.

19 ion and to the development and expression of epileptic seizures.

20 both control conditions and during prolonged epileptic seizures.

21 le after 30 min of experimental induction of epileptic seizures.

22 e imbalance as a molecular rationale for the epileptic seizures.

23 EEG abnormalities and dose-dependent risk of epileptic seizures.

24 ppocampal excitability and predisposition to epileptic seizures.

25 nt neural activity typically associated with epileptic seizures.

26 ous insults, including cerebral ischemia and epileptic seizures.

27 onized rhythmic oscillations of sleep and of epileptic seizures.

28 psy but there was no other family history of epileptic seizures.

29 and type 1 InsP3R mutants display ataxia and epileptic seizures.

30 erative conditions such as stroke and severe epileptic seizures.

31 nks persistently by approximately 35% during epileptic seizures.

32 control of pharmacologically-resistant focal epileptic seizures.

33 ein, compatible with a lowered threshold for epileptic seizures.

34 to the eyes and present risks of triggering epileptic seizures.

35 s such as impaired movement, memory loss, or epileptic seizures.

36 so play fundamental roles in many aspects of epileptic seizures.

37 nal activity and modulates the occurrence of epileptic seizures.

38 receptor blocker (ARB) therapy could inhibit epileptic seizures.

39 mouse hemicortex, were sufficient to trigger epileptic seizures.

40 of EEG signals can be used as indicators of epileptic seizures.

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

42 ing between different percolation regimes in epileptic seizures.

43 es of emotional expression during prefrontal epileptic seizures.

44 t is often associated with disorders such as epileptic seizures.

45 ve of a lower threshold for the induction of epileptic seizures.

46 observational studies on pregnant women with epileptic seizures.

47 in mice lowers the threshold for triggering epileptic seizures.

48 hippocampal neuronal injury during prolonged epileptic seizures.

49 ippocampus in the occurrence and severity of epileptic seizures.

50 ng the evaluation of gustatory and olfactory epileptic seizures.

51 cation, and thereby reduce susceptibility to epileptic seizures.

52 uronal death induced by proneurotrophins and epileptic seizures.

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

54 central to the initiation and progression of epileptic seizures.

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

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

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

58 enetic activation has been reported to block epileptic seizures.

59 is that astrogliosis is sufficient to induce epileptic seizures.

60 convulsant drug is used for the treatment of epileptic seizures.

61 is can cause hippocampal neuronal loss after epileptic seizures.

62 iched in the hippocampus, often the focus of epileptic seizures.

63 nsidered during the evaluation of vestibular epileptic seizures.

64 hat appears to be related to the presence of epileptic seizures.

65 re classified at 6 months as having definite epileptic seizures, 228 as having possible epileptic sei

66 particular, in an important animal model of epileptic seizures, 4-aminopyridine (4-AP) administratio

67 es for management of neuropathic pain(4) and epileptic seizures(5).

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

69 and the lack of nElavl leads to spontaneous epileptic seizure activity.

70 neocortex on the development of neocortical epileptic seizures after head injury in the rat.

71 nd persistent prevention and modification of epileptic seizures after head injury with a cooling prot

72 nd persistent prevention and modification of epileptic seizures after head injury with a cooling prot

73 Rate of epileptic seizures after initiation of amantadine treatm

74 Epileptic seizures also repress Cbln1 and are found to e

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

76 fast hemodynamic changes during inter-ictal epileptic seizures and 2) temperature variations during

77 e epileptic seizures, 228 as having possible epileptic seizures and 220 as having febrile seizures.

78 y 5 and GCS at day 10, rate of ICU delirium, epileptic seizures and all-cause mortality at 90 days.

79 whether these pathogenic mechanisms underlie epileptic seizures and behavioral comorbidities remains

80 Loss of consciousness is a hallmark of many epileptic seizures and carries risks of serious injury a

81 AC in cortical gray matter may contribute to epileptic seizures and cell death in diverse diseases of

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

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

84 ribe in detail the dosage effect of CNVs for epileptic seizures and further elucidates its role in th

85 e treatment of patients with psychogenic non-epileptic seizures and generates ideas for future resear

86 s, which possibly leads to the initiation of epileptic seizures and ictal events.

87 ypes including resistance to kainite-induced epileptic seizures and neuronal toxicity.

88 w-carbohydrate (ketogenic) diet might reduce epileptic seizures and offer neuroprotection in part bec

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

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

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

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

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

94 tributes to the variability in occurrence of epileptic seizures, and (4) the window for antiepileptog

95 severe intellectual disability, early-onset epileptic seizures, and amelogenesis imperfecta.

96 ary studies of patients with focal dystonia, epileptic seizures, and auditory hallucinations indicate

97 pilocarpine-treated animals began to display epileptic seizures, and CB(1) receptor expression was ch

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

99 ng slow wave sleep, anaesthesia, generalized epileptic seizures, and disorders of consciousness, such

100 FGF22-deficient mice are resistant to epileptic seizures, and FGF7-deficient mice are prone to

101 d following acute insults such as stroke and epileptic seizures, and following electroconvulsive ther

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

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

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

105 system are involved in learning and memory, epileptic seizures, and processing the amyloid precursor

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

107 Epileptic seizures are a common and poorly understood co

108 esized that the pathologic brain dynamics of epileptic seizures are an emergent property of microscal

109 Epileptic seizures are associated with increased risks o

110 Epileptic seizures are associated with increases in hipp

111 Epileptic seizures are characterized by periods of hyper

112 Epileptic seizures are characterized by periods of recur

113 e relationships between brain metabolism and epileptic seizures are complex and bidirectional, produc

114 ction during seizures.SIGNIFICANCE STATEMENT Epileptic seizures are debilitating and impair normal br

115 Epileptic seizures are debilitating because of the clini

116 Epileptic seizures are generally unpredictable and arise

117 While epileptic seizures are known to often manifest also with

118 r ex vivo and in vivo data, we conclude that epileptic seizures are manifested as the first symptom w

119 Epileptic seizures are traditionally characterized as th

120 vioral domains, as well as hyperactivity and epileptic seizures, as have been reported in humans with

121 s (RE), a childhood disease characterized by epileptic seizures associated with progressive destructi

122 isoaspartate and typically succumb to fatal epileptic seizures at 4-10 weeks of age.

123 a 91% accuracy in classifying seven types of epileptic seizure attacks, which outperformed the 65%, 7

124 e potential to monitor and forecast risk for epileptic seizures based on changes in 24-h patterns in

125 tion, are used in the literature to identify epileptic seizures based on EEG signals.

126 ms for the recognition and categorization of epileptic seizures based on EEG signals.

127 1970s engineers designed systems to predict epileptic seizures based upon quantitative changes in th

128 lmost 40 years, neuroscientists thought that epileptic seizures began abruptly, just a few seconds be

129 tion actually reduces sleep disturbances and epileptic seizures; both are seen in AD patients.

130 re of these syndromes is a predisposition to epileptic seizures but each is associated with different

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

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

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

134 ing a clinically proven dataset of over 3047 epileptic seizure cases.

135 Recurrent high-frequency epileptic seizures cause progressive hippocampal scleros

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

137 ression of K(v)7 channels is associated with epileptic seizures, cognitive and behavioral deficits, a

138 In epileptic seizures consciousness is often transiently lo

139 patterns and an increased susceptibility to epileptic seizures consistent with an impairment of cort

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

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

142 ural circuitry that address the question "Do epileptic seizures damage the brain?"

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

144 he proposed methodology, the overall average epileptic seizure detection performance is increased to

145 roposed work intends to develop an automated epileptic seizure detection system with an improved perf

146 omated mechanisms for designing an EEG-based epileptic seizure detection system.

147 Understanding how epileptic seizures develop or identifying diagnostic ind

148 trophies), strokes and stroke-like episodes, epileptic seizures, developmental delay, and demyelinati

149 e behavioural testing have shed light on how epileptic seizures disrupt the consciousness system.

150 ce display frequent myoclonus and occasional epileptic seizures, documented by electroencephalographi

151 a-analysis to assess the association between epileptic seizures during pregnancy and adverse pregnanc

152 Epileptic seizures during pregnancy may increase the ris

153 deo-telemetry database who had 30 documented epileptic seizures during video-EEG recording and who la

154 Sporadic epileptic seizure emergencies (SEs) require rapid treatm

155 Epileptic seizure emergencies are life-threatening condi

156 HEP occur prior to FS and compare this with epileptic seizures (ES).

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

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

159 ewly diagnosed, previously untreated partial epileptic seizures from 44 European centres and randomly

160 Detection and classification of epileptic seizures from the EEG signals have gained sign

161 that under unperturbed conditions and during epileptic seizures, galanin exerts a sedative influence

162 e regions and networks involved during focal epileptic seizure generation in humans.

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

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

165 In clinical neuroscience, epileptic seizures have been associated with the sudden

166 e the diagnostic features of psychogenic non-epileptic seizures have been better characterized in rec

167 Patients with partial epileptic seizures have focal regions that periodically

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

169 By observing the march of epileptic seizures he developed the idea of somatotopic

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

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

172 y lead to neuropsychiatric disorders such as epileptic seizures if carried so far as to engross part

173 by 0.5 to 2 degrees C inhibited the onset of epileptic seizures in a dose-dependent fashion.

174 molecular model explaining the occurrence of epileptic seizures in association with malignant gliomas

175 providing a noninvasive tool for localizing epileptic seizures in humans because of its high spatial

176 have been identified as a likely trigger of epileptic seizures in mesial temporal lobe epilepsy (MTL

177 ed convulsive and non-convulsive spontaneous epileptic seizures in mice and rats.

178 ave been identified in which mutations cause epileptic seizures in mice.

179 integrins, and have been thought to underlie epileptic seizures in patients with cortical malformatio

180 Pilocarpine injection induces epileptic seizures in rodents, an experimental paradigm

181 oscopic lights or repeated sounds can induce epileptic seizures in susceptible individuals.

182 tant in the development and/or generation of epileptic seizures in this mouse strain and may be a sig

183 ults of radiofrequency surgery indicate that epileptic seizures in this syndrome originate and propag

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

185 ncy treatment of acute febrile and afebrile (epileptic) seizures in children.

186 Epileptic seizures induce aberrant neurogenesis from res

187 The identification of epileptic seizure-induced alterations on the brain relat

188 nd collaborators show the key role of Bim in epileptic seizure-induced neuronal injury and identify t

189 ed form of cellular events that occur during epileptic seizure initiation.

190 Epileptic seizures involve a cortical excitation-inhibit

191 An epileptic seizure is defined as a sudden occurrence of t

192 An epileptic seizure is frequently the presenting sign of i

193 vulsive therapy (ECT), wherein a generalized epileptic seizure is induced, is a treatment for major d

194 The current gold standard for detecting epileptic seizures is in-hospital video-Electroencephalo

195 onal processes implicated in the etiology of epileptic seizures, learning, and memory (see the relate

196 ibe a novel method of adaptively controlling epileptic seizure-like events in hippocampal brain slice

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

198 rom a small number of patients, suggest that epileptic seizures may begin as a cascade of electrophys

199 Tissue acidosis following ischaemia and epileptic seizures may contribute to neuronal damage, wh

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

201 Finally, we find that a mechanically-induced epileptic seizure model (easily shocked "bang-sensitive"

202 Hyperexcitable, learning-enhanced, and epileptic seizure models have comparably elevated intera

203 The first step is recognition of epileptic seizures; next is classification of epilepsy t

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

205 logical syndrome of infancy characterized by epileptic seizures of cerebellar origin.

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

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

208 seizures (FS) known also as psychogenic non-epileptic seizures or dissociative seizures, present wit

209 whose absence or modification either causes epileptic seizures or, conversely, limits epileptogenesi

210 In patients with impaired consciousness, epileptic seizure, or temporal lobe symptoms of new onse

211 Brain injuries by physical trauma, epileptic seizures, or microbial infection upset the osm

212 Epileptic seizures, particularly infantile spasms, are o

213 behavioral abnormalities, cognitive decline, epileptic seizures, peripheral nerve hyperexcitability a

214 Some evidence suggests that psychogenic non-epileptic seizures (PNES) are associated with increased

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

216 60 consecutive patients with psychogenic non-epileptic seizures (PNES), 5-10 years after diagnosis.

217 dies of long-term outcome in psychogenic non-epileptic seizures (PNES), and none of long-term healthc

218 Epileptic seizures potently modulate hippocampal adult n

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

220 nstrate the utility of the method by mapping epileptic seizures progression through cortical circuits

221 ntral nervous system characterized by severe epileptic seizures, progressive degeneration of a single

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

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

224 Epileptic seizures recorded with stereo-EEG can take a f

225 Epileptic seizures reflect a pathological brain state ch

226 Epileptic seizures represent altered neuronal network dy

227 Epileptic seizures represent dysfunctional neural networ

228 on Depdc5(c/-) mice showed that spontaneous epileptic seizures resulting in a SUDEP-like event are n

229 orm discharges on EEG may indicate increased epileptic seizure risk.

230 ue plasminogen activator, and so explain the epileptic seizures seen in individuals with more severe

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

232 Epileptic seizures should be considered as potential sid

233 ies of epilepsy action mechanisms underlying epileptic seizures should be lightened.

234 to subsequent pathologic challenges such as epileptic seizures.SIGNIFICANCE STATEMENT Adult physiolo

235 In contrast, regions associated with epileptic seizures, such as the hippocampus, did not exh

236 among the females, were prone to spontaneous epileptic seizures, suggesting that USF is important in

237 ociated with a substitution of V404 increase epileptic seizure susceptibility.

238 pared with 30 matching live controls with 92 epileptic seizures taken from the same database.

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

240 sm are considered downstream consequences of epileptic seizures that begin at the synaptic level.

241 vances in the understanding and treatment of epileptic seizures that derive from a non-neurocentric v

242 inactivated 1 (LGI1) protein induces severe epileptic seizures that leads to death.

243 r focal neurological deficits (not including epileptic seizure) that were definitely or possibly rela

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

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

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

247 citation may constitute a mechanism by which epileptic seizures trigger compensatory interictal netwo

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

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

250 The research aims to identify epileptic seizures using EEG records automatically.

251 e closed-loop pharmacological suppression of epileptic seizures via feedback from electroencephalogra

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

253 eurons caused by focal cerebral ischemia and epileptic seizures was exacerbated in TNFR-KO mice, indi

254 ited at the time of their first diagnosis of epileptic seizures was undertaken; in those classified 6

255 data to diagnose epilepsy following a single epileptic seizure; we find that a prediction model expla

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

257 Epileptic seizures were assessed by 5-electrode video-el

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

259 sive electrical activity in the brain causes epileptic seizures which can be detected through Electro

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

261 hality by 8 months of age due to spontaneous epileptic seizures, which is preceded by persistent brai

262 nized activities, including those underlying epileptic seizures, which often appear as a transformati

263 evelopment of epilepsy and the generation of epileptic seizures will require delineation of the aberr

264 evelopment of epilepsy and the generation of epileptic seizures will undoubtedly benefit from researc

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

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

267 e frequently implicated in the generation of epileptic seizures, with temporal lobe epilepsy constitu

268 eased GABAergic inhibition, and can generate epileptic seizures within 1 month of lesioning.