ライフサイエンスコーパス: epilepticus

1 ngle febrile, unprovoked seizures, or status epilepticus).

2 ally in patients with complex partial status epilepticus.

3 red in the evaluation of the child in status epilepticus.

4 sions to be weaned with resolution of status epilepticus.

5 ered first-line therapy for pediatric status epilepticus.

6 ered in young children with recurrent status epilepticus.

7 iatric patients with super-refractory status epilepticus.

8 pocampus of humans who died following status epilepticus.

9 raphic seizures, or 3) electrographic status epilepticus.

10 ll on our cohort of ICU patients with status epilepticus.

11 nd albumin with course and outcome of status epilepticus.

12 transportability to ICU patients with status epilepticus.

13 om coma, and for guiding treatment of status epilepticus.

14 dentify patients with poor outcome of status epilepticus.

15 ns for outcome in adult patients with status epilepticus.

16 ion after traumatic injury and during status epilepticus.

17 s assessed during the first 3 days of status epilepticus.

18 kB promotes epileptogenesis caused by status epilepticus.

19 s predicted poor outcome and death in status epilepticus.

20 for the treatment of super-refractory status epilepticus.

21 es in refractory and super-refractory status epilepticus.

22 a non-harmful seizure episode before status epilepticus.

23 but not in intact brain or following status epilepticus.

24 5 weeks following pilocarpine-induced status epilepticus.

25 ented with genes hypomethylated after status epilepticus.

26 er termination of pilocarpine-induced status epilepticus.

27 had their acute episode of convulsive status epilepticus.

28 s in recent years in the treatment of status epilepticus.

29 convulsions and idiopathic convulsive status epilepticus.

30 ncreased in the hippocampus following status epilepticus.

31 populations of cortical neurons after status epilepticus.

32 ignaling in the hippocampus following status epilepticus.

33 times given in cryptogenic refractory status epilepticus.

34 er intra-amygdala kainic acid-induced status epilepticus.

35 outcomes in patients with convulsive status epilepticus.

36 auditory discrimination had incident status epilepticus.

37 are alone in patients with convulsive status epilepticus.

38 e context of a stroke-like episode or status epilepticus.

39 ts admitted to the ICU for convulsive status epilepticus.

40 juries, including pilocarpine-induced status epilepticus.

41 tients with nonprincipal diagnoses of status epilepticus.

42 ts admitted to the ICU for convulsive status epilepticus.

43 Of 467 patients with incident status epilepticus, 238 returned to baseline (51.1%), 162 had n

44 the third stage (stage of refractory status epilepticus), a variety of anaesthetics and nonpharmacol

45 Our analysis demonstrates that status epilepticus after admission for sepsis in the United Sta

46 B mice (n = 127) that had experienced status epilepticus after systemic treatment with pilocarpine 31

47 showed altered DNA methylation after status epilepticus alone or status epilepticus that followed se

48 rizing agent mimicking the episode of status epilepticus, also results in an increase in miR21 and a

49 0 days of their episode of convulsive status epilepticus and 16 during follow-up.

50 limbic encephalitis, the pathology of status epilepticus and Ammon's horn sclerosis, and the systemat

51 t inhibition of TrkB commencing after status epilepticus and continued for 2 weeks prevents recurrent

52 induced status epilepticus, and after status epilepticus and daily treatment beginning 24 hours later

53 dds for the development of refractory status epilepticus and death (with every 1g/L: odds ratio 0.91,

54 iated with higher rates of refractory status epilepticus and death (with every 1mg/L: odds ratio 1.01

55 Outcomes were defined as refractory status epilepticus and death.

56 ogression between 2 and 5 months post-status epilepticus and drastically reduced the frequency of spo

57 rch to enable early identification of status epilepticus and efficacy of anti-epileptic drugs will be

58 tion changes in the hippocampus after status epilepticus and epileptic tolerance in adult mice.

59 rm decision making on drug therapy in status epilepticus and help develop safer and more effective tr

60 me-wide DNA methylation changes after status epilepticus and in epileptic tolerance, which may contri

61 f pharmacologic therapy in refractory status epilepticus and intracranial hypertension.

62 trographic seizures or electrographic status epilepticus and mortality or short-term neurologic outco

63 n the contralateral hippocampus after status epilepticus and resulted in more frequent spontaneous se

64 nd sedation and times to cessation of status epilepticus and return to baseline mental status.

65 nd demographic factors at the time of status epilepticus and subsequent risk of death.

66 to 5 weeks before pilocarpine-induced status epilepticus and these cells were then eliminated beginni

67 Mice that had experienced status epilepticus and were treated for 2 months with rapamycin

68 ents, including inhospital mortality, status epilepticus, and acute kidney injury, was similar in bot

69 mice 5 days after pilocarpine-induced status epilepticus, and after status epilepticus and daily trea

70 tients with encephalitis, seizures or status epilepticus, and antibodies to unknown neuropil antigens

71 izure onset after pilocarpine-induced status epilepticus, and attenuated subsequent progressive incre

72 ed as a strategy for super-refractory status epilepticus, and better evidence for their use may becom

73 suggests a dynamical understanding of status epilepticus, and demonstrates an accessible system for s

74 ould also be focused on the causes of status epilepticus, and immunological therapy is sometimes give

75 years after an episode of convulsive status epilepticus, and investigate its predictors from a paedi

76 ain lesions, seizures that evolved to status epilepticus, and neurologic sequelae.

77 suppression, generalized suppression, status epilepticus, and nonreactivity.

78 eatments directed at the cause of the status epilepticus, and of supportive ITU care is also emphasiz

79 with intractable seizures/convulsive status epilepticus, and the rest died as a complication of thei

80 rographic seizures and electrographic status epilepticus are associated with higher mortality or wors

81 rographic seizures and electrographic status epilepticus are common in critically ill children.

82 Albumin levels measured early in status epilepticus are independently associated with refractory

83 truly refractory and super-refractory status epilepticus are seen infrequently at any given instituti

84 The definition of status epilepticus as a prolonged seizure or a series of seizur

85 ardized and age-standardized rates of status epilepticus as the underlying cause of death in the Unit

86 HHV-7 primary infection with febrile status epilepticus as well as the role of reactivation of laten

87 be related with course and outcome in status epilepticus, as changes of cytokine levels and blood-bra

88 vs. computed tomography in new-onset status epilepticus, as well as high rates of identification of

89 and midazolam significantly increased status epilepticus-associated neuronal injury in various brain

90 In the first stage (stage of early status epilepticus), buccal midazolam has become an important o

91 years following childhood convulsive status epilepticus but most deaths are not seizure related.

92 Electrographic status epilepticus, but not electrographic seizures, is associa

93 n vehicle-treated mice 2 months after status epilepticus, but remained at only 63% of controls in rap

94 ary efficacy outcome was cessation of status epilepticus by 10 minutes without recurrence within 30 m

95 Finally, induction of status epilepticus by intrahippocampal injection of pilocarpine

96 to accurately predict the outcome of status epilepticus by measures of discrimination and calibratio

97 g evidence suggests that seizures and status epilepticus can be immune-mediated.

98 transient inhibition commencing after status epilepticus can prevent these long-lasting devastating c

99 mortality after admission for sepsis, status epilepticus carried a higher risk of death.

100 Lastly, kainate-induced status epilepticus causes GIRK1 and GIRK2 cleavage in the hippo

101 If status epilepticus continued at 12 minutes, fosphenytoin was ad

102 The prognosis of convulsive status epilepticus (CSE), a common childhood medical neurologic

103 dition characterized by recurrence of status epilepticus despite use of deep general anesthesia, and

104 ons, likely reflecting an increase in status epilepticus diagnoses through improved diagnostic sensit

105 The history of status epilepticus, diagnosis of psychosis and positron emissio

106 es at ICU admission and occurrence of status epilepticus during ICU stay were not associated with neu

107 Mortality in status epilepticus during sepsis decreased from 43% in 1988 to

108 d focal epilepsies with an electrical status epilepticus during slow sleep-like EEG pattern (six pati

109 ng experimental prolonged FS (febrile status epilepticus; eFSE).

110 on, seizures including non-convulsive status epilepticus, endocrinopathy, or thiamine deficiency.

111 Seventy-eight status epilepticus episodes (54%) had good outcomes (Glasgow Ou

112 Among status epilepticus episodes treated by third-line antiepileptic

113 Predictors of poor outcome among all status epilepticus episodes were older age (odds ratio 1.06; 95

114 Predictors of mortality among all status epilepticus episodes were treatment with third-line anti

115 de updates on identifying children in status epilepticus, etiologic considerations, and the rationale

116 Status epilepticus etiologies included subtherapeutic antiepile

117 8.85; 95% CI, 4.87-16.08), myoclonic status epilepticus (false-positive rate, 0.05; 95% CI, 0.02-0.1

118 prospectively demographics, clinical status epilepticus features, treatment, and outcome at discharg

119 Cessation of status epilepticus for 10 minutes without recurrence within 30

120 All consecutive patients with status epilepticus from 2005 to 2009 were selected from a prosp

121 long-standing hypothesis that febrile status epilepticus (FSE) can cause brain injury, particularly t

122 Whether febrile status epilepticus (FSE) produces hippocampal sclerosis (HS) an

123 rder, arises in children with febrile status epilepticus (FSE).

124 associated with poorer outcome after status epilepticus; furthermore, it portends higher infection r

125 g-resistant epilepsies and refractory status epilepticus has been further defined and is expected to

126 blood-brain barrier breakdown during status epilepticus have been demonstrated.

127 ons, which in their most severe form, status epilepticus, have a high mortality rate if not quickly t

128 first London-Innsbruck Colloquium on Status Epilepticus, held in London in April 2007.

129 mortality and the marked increase in status epilepticus hospitalizations, likely reflecting an incre

130 tivity in 209 of 374 (55%), including status epilepticus in 102 of 374 (27%).

131 ures in 41 (20.5%) and electrographic status epilepticus in 43 (21.5%).

132 d its predictors following convulsive status epilepticus in childhood are uncertain.

133 ng a surveillance study of convulsive status epilepticus in childhood.

134 is review discusses the management of status epilepticus in children, including both anticonvulsant m

135 pilepticus (RSE) and super-refractory status epilepticus in children.

136 port of allopregnanolone use to treat status epilepticus in children.

137 neralized convulsive or nonconvulsive status epilepticus in coma.

138 omise for prevention of TLE caused by status epilepticus in humans.

139 ted P2X7R responses after focal-onset status epilepticus in mice, comparing changes in the damaged, i

140 ginning 1 d after pilocarpine-induced status epilepticus in mice, would suppress mossy fiber sproutin

141 ic diet as treatment for uncontrolled status epilepticus in pediatric patients.

142 Using a recently developed model of status epilepticus in postnatal day 7 rat pups that results in

143 -year study period, the prevalence of status epilepticus in primary admissions of septic patients inc

144 cipant who had surgery and 3 cases of status epilepticus in the medical group.

145 Doose syndrome), Dravet syndrome, and status epilepticus (including FIRES syndrome).

146 ill present the current definition of status epilepticus, including a recently modified operational d

147 he definition and general approach to status epilepticus, including resource use, should evolve with

148 Seizure activity, in particular status epilepticus, increases cerebral amino acid transport wit

149 Results following pilocarpine-induced status epilepticus indicate that neuronal COX-2 promotes early

150 n a well-characterized mouse model of status epilepticus-induced epilepsy (systemic pilocarpine).

151 Status epilepticus induces a cascade of protein expression chan

152 Treatment with pY816 following status epilepticus inhibited TLE and prevented anxiety-like dis

153 For subjects in status epilepticus, intramuscular midazolam is at least as safe

154 Status epilepticus is a common neurologic emergency in children

155 Status epilepticus is a common neurologic emergency with signif

156 Status epilepticus is a common neurological emergency with cons

157 Super-refractory status epilepticus is a condition characterized by recurrence o

158 Super-refractory status epilepticus is a life-threatening condition.

159 Status epilepticus is also increasingly identified in the inpat

160 Status epilepticus is an acute neurologic emergency, the incide

161 Status epilepticus is an emergency; however, prompt treatment o

162 Rapid management of status epilepticus is associated with a greater likelihood of s

163 er, prompt treatment of patients with status epilepticus is challenging.

164 Status epilepticus is common in neonates and infants, and is as

165 Super-refractory status epilepticus is defined as status epilepticus that contin

166 Status epilepticus is reported with continuous electroencephalo

167 owchart for managing super-refractory status epilepticus is suggested.

168 impairments at the time of convulsive status epilepticus is the main risk factor for mortality within

169 The treatment of tonic-clonic status epilepticus is usually divided into three stages.

170 We found that febrile status epilepticus, lasting an average of 64 min, increased the

171 n barrier pathology in rats following status epilepticus, late electrocorticography to identify epile

172 Pilocarpine-induced status epilepticus led to a significant increase in the number

173 not transplanted- pulmonary congestion with epilepticus (likely not related) versus transplanted inf

174 Having a predetermined status epilepticus management pathway can expedite management.

175 After pilocarpine-induced status epilepticus, many granule cells born into the postseizur

176 vel of suspicion for the diagnosis of status epilepticus may be indicated in those patients with cent

177 s was initiated using the pilocarpine status epilepticus model in male and female mice.

178 dered epileptic using the pilocarpine-status epilepticus model of epilepsy were monitored continuousl

179 rning and accelerated forgetting in a status epilepticus model of mesial temporal lobe epilepsy in ra

180 he second stage (stage of established status epilepticus) modern treatment choices include valproate,

181 iol use, the most common of which was status epilepticus (n=9 [6%]).

182 that progressed to hydrocephalus and status epilepticus necessitating a medically induced coma.

183 encephalitis with seizures (one with status epilepticus needing pharmacologically induced coma; one

184 3.75; p < .001), and first episode of status epilepticus (odds ratio 3.73; 95% confidence interval 1.

185 worse developmental outcome included status epilepticus (odds ratio = 3.1; confidence interval = 1.5

186 Convulsive status epilepticus often results in permanent neurologic impair

187 ssions for sepsis was associated with status epilepticus, older age, and Black and Native American/Es

188 firmed status epilepticus, refractory status epilepticus on day 1, "super-refractory" status epilepti

189 The attributable role of convulsive status epilepticus on mortality remains uncertain, but appears

190 rate of progression to EEG-confirmed status epilepticus on the first day was lower in the hypothermi

191 g-term effects of pilocarpine-induced status epilepticus on vesicular release and recycling in hippoc

192 ents with higher levels of albumin at status epilepticus onset had significant lower odds for the dev

193 ncreased C-reactive protein levels at status epilepticus onset were associated with higher rates of r

194 Albumin was assessed at admission and status epilepticus onset, and C-reactive protein was assessed d

195 l of consciousness were determined at status epilepticus onset, in order to calculate the Status Epil

196 e male patients) developed refractory status epilepticus or epilepsia partialis continua along with e

197 s of kainic acid (20 mg/kg) to induce status epilepticus or the vehicle (saline).

198 ncephalitis with seizures, refractory status epilepticus, or both.

199 pecific impact of therapeutic coma on status epilepticus outcome.

200 ctivity after ischemia, less frequent status epilepticus (p < 0.05), and earlier return of sleep stat

201 One hundred thirty-five consecutive status epilepticus patients were analyzed.

202 Among 171 status epilepticus patients with a mean age of 64.1 years (+/-

203 ion-standardized hospitalizations for status epilepticus per 100 000 persons increased by 56.4% (inci

204 younger than 18 years with convulsive status epilepticus presenting to 1 of 11 US academic pediatric

205 Prolonged seizures (status epilepticus) produce pathophysiological changes in the h

206 xcessive activation of TrkB caused by status epilepticus promotes development of temporal lobe epilep

207 ic regression analysis disclosed that status epilepticus, psychosis and cognitive dysfunction were st

208 is purpose, we used two distinct post-status epilepticus rat models, in which epilepsy was induced wi

209 for refractory generalised convulsive status epilepticus, rather than additional trials of second-lin

210 duced to 63% of controls 5 days after status epilepticus, recovered to 93% of controls in vehicle-tre

211 therapy, including those cases where status epilepticus recurs on the reduction or withdrawal of ana

212 oencephalographically (EEG) confirmed status epilepticus, refractory status epilepticus on day 1, "su

213 arameters reported include control of status epilepticus, relapse on withdrawal, breakthrough seizure

214 s-sectional studies including 408 304 status epilepticus-related hospital visits using generalizable

215 d to estimate population-standardized status epilepticus-related hospitalization rates using Internat

216 imited data exist detailing trends in status epilepticus-related hospitalizations and mortality.

217 Status epilepticus-related hospitalizations were categorized by

218 exists between the relatively stable status epilepticus-related mortality and the marked increase in

219 Age-standardized status epilepticus-related mortality per 1 000 000 persons incr

220 frequency in patients with convulsive status epilepticus remains unknown.

221 In contrast, prolonged seizures (status epilepticus) repeatedly approach, but do not cross, the

222 Uncontrolled episodes of status epilepticus require intensive care treatment and the lit

223 lepticus on day 1, "super-refractory" status epilepticus (resistant to general anesthesia), and funct

224 use model in which a brief episode of status epilepticus results in chronic recurrent seizures, anxie

225 in approach in controlling refractory status epilepticus (RSE) and super-refractory status epilepticu

226 Status epilepticus (SE) can cause brain damage and lead to neur

227 r locale of enhanced pTrkB induced by status epilepticus (SE) evoked by infusion of kainic acid into

228 levant question is whether early post-status epilepticus (SE) evoked chloride dysregulation is import

229 r restraining seizures, cannot thwart status epilepticus (SE) induced neurodegeneration or down-strea

230 Status epilepticus (SE) is a common neurological emergency for

231 Status epilepticus (SE) is a common neurological emergency, whi

232 Status epilepticus (SE) is a life-threatening condition that ca

233 Status epilepticus (SE) is a life-threatening disease that has

234 seizure tests and pilocarpine-induced status epilepticus (SE) model.

235 neralized convulsive or nonconvulsive status epilepticus (SE) that continued despite initial first- a

236 ed a rat model of pilocarpine-induced status epilepticus (SE) to investigate HIF-1alpha expression an

237 The generalized seizures of status epilepticus (SE) trigger a series of molecular and cellu

238 Status epilepticus (SE) triggers pathological changes to hippoc

239 s in determining KCC2 activity during status epilepticus (SE) using knockin mice in which S940 is mut

240 As epileptogenic insult, a status epilepticus (SE) was induced in rats by lithium pilocarp

241 ain several months after induction of status epilepticus (SE) when compared to control rats.

242 Status epilepticus (SE), a medical emergency that is typically

243 in 50% of rats reduced threshold for status epilepticus (SE), accelerated epileptogenesis, and once

244 dal neurons after pilocarpine-induced status epilepticus (SE), accompanied by loss of HCN1 channel pr

245 With as little as a 5 min duration of status epilepticus (SE), gamma-H2AX increased in CA1, CA3, and

246 hat in the mouse pilocarpine model of status epilepticus (SE), systemic administration of TG6-10-1 co

247 t-born DGCs after pilocarpine-induced status epilepticus (SE), whereas normotopic DGCs synapse onto b

248 in mice following pilocarpine-induced status epilepticus (SE).

249 r before or after pilocarpine-induced status epilepticus (SE).

250 ncluding the benzodiazepine-resistant status epilepticus (SE).

251 ransmission in the hippocampus during status epilepticus (SE).

252 y pilocarpine- or kainic acid-induced status epilepticus (SE).

253 E was provoked by kainic acid-induced status epilepticus (SE).

254 uding trauma, stroke, infections, and status epilepticus (SE).

255 t brain insults, such as ischemia and status epilepticus (SE).

256 ty pharmacologically induced in vivo [status epilepticus (SE)].

257 After severe seizures (e.g., status epilepticus [SE]) and some other conditions, newborn GCs

258 ment of a child with super-refractory status epilepticus secondary to FIRES.

259 tics revealed good calibration of the Status Epilepticus Severity Score (chi-square goodness-of-fit t

260 ion of the predictive accuracy of the Status Epilepticus Severity Score and its transportability to I

261 curve for prediction of death by the Status Epilepticus Severity Score had an area under the curve o

262 nation and calibration indicated that Status Epilepticus Severity Score performed reasonably well on

263 validity and transportability of the Status Epilepticus Severity Score prediction functions for outc

264 icus onset, in order to calculate the Status Epilepticus Severity Score.

265 sses the advances in the treatment of status epilepticus since the first London-Innsbruck Colloquium

266 rolonged seizures in super-refractory status epilepticus (SRSE) have been shown to cause neuronal dea

267 Super-refractory status epilepticus (SRSE) is a life-threatening form of status

268 sures of occurrence of first seizure, status epilepticus, stroke-like episode, and death.

269 ters resulted in immediate relapse of status epilepticus, suggesting a pivotal role of deep brain sti

270 ndon, UK (the north London convulsive status epilepticus surveillance study cohort; NLSTEPSS).

271 tory status epilepticus is defined as status epilepticus that continues or recurs 24 h or more after

272 (SRSE) is a life-threatening form of status epilepticus that continues or recurs despite 24 hours or

273 boy with a prolonged super-refractory status epilepticus that eventually resolved after commencing de

274 ion after status epilepticus alone or status epilepticus that followed seizure preconditioning, with

275 In stage 2 and stage 3 of status epilepticus, the therapies have almost invariably been a

276 d that, following pilocarpine-induced status epilepticus, there are two independent changes in HCN fu

277 1-2 months after pilocarpine-induced status epilepticus, there were significant increases in mossy f

278 idelines for management of refractory status epilepticus; this is, however, based on weak evidence.

279 lorazepam for children and adults in status epilepticus treated by paramedics.

280 rials, such as the ESETT (Established Status Epilepticus Treatment Trial), compare effectiveness of a

281 espiratory effects of these agents in status epilepticus treatment.

282 ng pediatric patients with convulsive status epilepticus, treatment with lorazepam did not result in

283 Status epilepticus was also more common among later years, youn

284 ultivariable analysis, electrographic status epilepticus was associated with an increased risk of mor

285 Status epilepticus was convulsive in 132 cases (92%).

286 Refractory status epilepticus was defined as generalized convulsive or non

287 ical scoring system for patients with status epilepticus was developed for predicting outcome, planni

288 gical impairments prior to convulsive status epilepticus was the only independent risk factor for mor

289 lizations were categorized by whether status epilepticus was the principal diagnosis, whether the pat

290 In 2010, status epilepticus was the reported underlying cause of death i

291 quired epilepsy induced by electrical status epilepticus, we show that oxidative stress occurs in bot

292 ved their acute episode of convulsive status epilepticus were not at a significantly increased risk o

293 y develop epilepsy after experiencing status epilepticus when naturally exposed to domoic acid.

294 treatment option in super-refractory status epilepticus when other treatment options have failed.

295 altered in structure and function by status epilepticus, which could contribute to the development o

296 itically ill patients with convulsive status epilepticus who were receiving mechanical ventilation to

297 ith 11 episodes of serial seizures or status epilepticus, who underwent MRI and (18)F-FET PET, were s

298 diagnostic evaluation of the child in status epilepticus will help identify causes, which may require

299 Prevention of status epilepticus with regular medication and emergency protoc

300 and subsequently developed refractory status epilepticus, with dramatic electroclinical improvement u