ライフサイエンスコーパス: status epilepticus

1 fter single febrile, unprovoked seizures, or status epilepticus).

2 especially in patients with complex partial status epilepticus.

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

4 ic infusions to be weaned with resolution of status epilepticus.

5 considered first-line therapy for pediatric status epilepticus.

6 considered in young children with recurrent status epilepticus.

7 n 2 pediatric patients with super-refractory status epilepticus.

8 the hippocampus of humans who died following status epilepticus.

9 lectrographic seizures, or 3) electrographic status epilepticus.

10 ably well on our cohort of ICU patients with status epilepticus.

11 otein and albumin with course and outcome of status epilepticus.

12 nd its transportability to ICU patients with status epilepticus.

13 very from coma, and for guiding treatment of status epilepticus.

14 ng to identify patients with poor outcome of status epilepticus.

15 functions for outcome in adult patients with status epilepticus.

16 protection after traumatic injury and during status epilepticus.

17 tein was assessed during the first 3 days of status epilepticus.

18 ptor TrkB promotes epileptogenesis caused by status epilepticus.

19 effects predicted poor outcome and death in status epilepticus.

20 ilable for the treatment of super-refractory status epilepticus.

21 therapies in refractory and super-refractory status epilepticus.

22 sure to a non-harmful seizure episode before status epilepticus.

23 stroke, but not in intact brain or following status epilepticus.

24 izures 5 weeks following pilocarpine-induced status epilepticus.

25 rrepresented with genes hypomethylated after status epilepticus.

26 1 h after termination of pilocarpine-induced status epilepticus.

27 n they had their acute episode of convulsive status epilepticus.

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

29 ebrile convulsions and idiopathic convulsive status epilepticus.

30 , are increased in the hippocampus following status epilepticus.

31 select populations of cortical neurons after status epilepticus.

32 hin-3 signaling in the hippocampus following status epilepticus.

33 is sometimes given in cryptogenic refractory status epilepticus.

34 psy after intra-amygdala kainic acid-induced status epilepticus.

35 rologic outcomes in patients with convulsive status epilepticus.

36 ment in auditory discrimination had incident status epilepticus.

37 ndard care alone in patients with convulsive status epilepticus.

38 s in the context of a stroke-like episode or status epilepticus.

39 patients admitted to the ICU for convulsive status epilepticus.

40 enic injuries, including pilocarpine-induced status epilepticus.

41 ated patients with nonprincipal diagnoses of status epilepticus.

42 patients admitted to the ICU for convulsive status epilepticus.

43 Of 467 patients with incident status epilepticus, 238 returned to baseline (51.1%), 16

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

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

46 FVB mice (n = 127) that had experienced status epilepticus after systemic treatment with pilocar

47 1 genes showed altered DNA methylation after status epilepticus alone or status epilepticus that foll

48 depolarizing agent mimicking the episode of status epilepticus, also results in an increase in miR21

49 ithin 30 days of their episode of convulsive status epilepticus and 16 during follow-up.

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

51 ate that inhibition of TrkB commencing after status epilepticus and continued for 2 weeks prevents re

52 arpine-induced status epilepticus, and after status epilepticus and daily treatment beginning 24 hour

53 lower odds for the development of refractory status epilepticus and death (with every 1g/L: odds rati

54 e associated with higher rates of refractory status epilepticus and death (with every 1mg/L: odds rat

55 Outcomes were defined as refractory status epilepticus and death.

56 ease progression between 2 and 5 months post-status epilepticus and drastically reduced the frequency

57 r research to enable early identification of status epilepticus and efficacy of anti-epileptic drugs

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

59 ay inform decision making on drug therapy in status epilepticus and help develop safer and more effec

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

61 ation of pharmacologic therapy in refractory status epilepticus and intracranial hypertension.

62 en electrographic seizures or electrographic status epilepticus and mortality or short-term neurologi

63 ccurred after 1 month of pilocarpine-induced status epilepticus and persisted during the chronic phas

64 evels in the contralateral hippocampus after status epilepticus and resulted in more frequent spontan

65 rence and sedation and times to cessation of status epilepticus and return to baseline mental status.

66 nical and demographic factors at the time of status epilepticus and subsequent risk of death.

67 orn up to 5 weeks before pilocarpine-induced status epilepticus and these cells were then eliminated

68 Mice that had experienced status epilepticus and were treated for 2 months with ra

69 erse events, including inhospital mortality, status epilepticus, and acute kidney injury, was similar

70 ce, in mice 5 days after pilocarpine-induced status epilepticus, and after status epilepticus and dai

71 140 patients with encephalitis, seizures or status epilepticus, and antibodies to unknown neuropil a

72 ayed seizure onset after pilocarpine-induced status epilepticus, and attenuated subsequent progressiv

73 described as a strategy for super-refractory status epilepticus, and better evidence for their use ma

74 ation, suggests a dynamical understanding of status epilepticus, and demonstrates an accessible syste

75 ment should also be focused on the causes of status epilepticus, and immunological therapy is sometim

76 ithin 8 years after an episode of convulsive status epilepticus, and investigate its predictors from

77 uded brain lesions, seizures that evolved to status epilepticus, and neurologic sequelae.

78 burst-suppression, generalized suppression, status epilepticus, and nonreactivity.

79 e of treatments directed at the cause of the status epilepticus, and of supportive ITU care is also e

80 ociated with intractable seizures/convulsive status epilepticus, and the rest died as a complication

81 r electrographic seizures and electrographic status epilepticus are associated with higher mortality

82 Electrographic seizures and electrographic status epilepticus are common in critically ill children

83 Albumin levels measured early in status epilepticus are independently associated with ref

84 ses of truly refractory and super-refractory status epilepticus are seen infrequently at any given in

85 The definition of status epilepticus as a prolonged seizure or a series of

86 onstandardized and age-standardized rates of status epilepticus as the underlying cause of death in t

87 -6B and HHV-7 primary infection with febrile status epilepticus as well as the role of reactivation o

88 n, may be related with course and outcome in status epilepticus, as changes of cytokine levels and bl

89 of MRI vs. computed tomography in new-onset status epilepticus, as well as high rates of identificat

90 rbital and midazolam significantly increased status epilepticus-associated neuronal injury in various

91 In the first stage (stage of early status epilepticus), buccal midazolam has become an impo

92 ithin 8 years following childhood convulsive status epilepticus but most deaths are not seizure relat

93 Electrographic status epilepticus, but not electrographic seizures, is

94 trols in vehicle-treated mice 2 months after status epilepticus, but remained at only 63% of controls

95 he primary efficacy outcome was cessation of status epilepticus by 10 minutes without recurrence with

96 Finally, induction of status epilepticus by intrahippocampal injection of pilo

97 ability to accurately predict the outcome of status epilepticus by measures of discrimination and cal

98 creasing evidence suggests that seizures and status epilepticus can be immune-mediated.

99 That transient inhibition commencing after status epilepticus can prevent these long-lasting devast

100 ion in mortality after admission for sepsis, status epilepticus carried a higher risk of death.

101 Lastly, kainate-induced status epilepticus causes GIRK1 and GIRK2 cleavage in th

102 If status epilepticus continued at 12 minutes, fosphenytoin

103 The prognosis of convulsive status epilepticus (CSE), a common childhood medical neu

104 s a condition characterized by recurrence of status epilepticus despite use of deep general anesthesi

105 alizations, likely reflecting an increase in status epilepticus diagnoses through improved diagnostic

106 The history of status epilepticus, diagnosis of psychosis and positron

107 failures at ICU admission and occurrence of status epilepticus during ICU stay were not associated w

108 Mortality in status epilepticus during sepsis decreased from 43% in 1

109 ts), and focal epilepsies with an electrical status epilepticus during slow sleep-like EEG pattern (s

110 following experimental prolonged FS (febrile status epilepticus; eFSE).

111 infection, seizures including non-convulsive status epilepticus, endocrinopathy, or thiamine deficien

112 Seventy-eight status epilepticus episodes (54%) had good outcomes (Gla

113 Among status epilepticus episodes treated by third-line antiep

114 Predictors of poor outcome among all status epilepticus episodes were older age (odds ratio 1

115 Predictors of mortality among all status epilepticus episodes were treatment with third-li

116 o provide updates on identifying children in status epilepticus, etiologic considerations, and the ra

117 Status epilepticus etiologies included subtherapeutic an

118 ratio, 8.85; 95% CI, 4.87-16.08), myoclonic status epilepticus (false-positive rate, 0.05; 95% CI, 0

119 ecorded prospectively demographics, clinical status epilepticus features, treatment, and outcome at d

120 Cessation of status epilepticus for 10 minutes without recurrence wit

121 All consecutive patients with status epilepticus from 2005 to 2009 were selected from

122 e is a long-standing hypothesis that febrile status epilepticus (FSE) can cause brain injury, particu

123 Whether febrile status epilepticus (FSE) produces hippocampal sclerosis

124 in disorder, arises in children with febrile status epilepticus (FSE).

125 coma is associated with poorer outcome after status epilepticus; furthermore, it portends higher infe

126 of drug-resistant epilepsies and refractory status epilepticus has been further defined and is expec

127 els and blood-brain barrier breakdown during status epilepticus have been demonstrated.

128 conditions, which in their most severe form, status epilepticus, have a high mortality rate if not qu

129 nce the first London-Innsbruck Colloquium on Status Epilepticus, held in London in April 2007.

130 related mortality and the marked increase in status epilepticus hospitalizations, likely reflecting a

131 form activity in 209 of 374 (55%), including status epilepticus in 102 of 374 (27%).

132 ic seizures in 41 (20.5%) and electrographic status epilepticus in 43 (21.5%).

133 lity and its predictors following convulsive status epilepticus in childhood are uncertain.

134 ed during a surveillance study of convulsive status epilepticus in childhood.

135 This review discusses the management of status epilepticus in children, including both anticonvu

136 tatus epilepticus (RSE) and super-refractory status epilepticus in children.

137 irst report of allopregnanolone use to treat status epilepticus in children.

138 with generalized convulsive or nonconvulsive status epilepticus in coma.

139 with promise for prevention of TLE caused by status epilepticus in humans.

140 vestigated P2X7R responses after focal-onset status epilepticus in mice, comparing changes in the dam

141 cin, beginning 1 d after pilocarpine-induced status epilepticus in mice, would suppress mossy fiber s

142 ketogenic diet as treatment for uncontrolled status epilepticus in pediatric patients.

143 Using a recently developed model of status epilepticus in postnatal day 7 rat pups that resu

144 the 21-year study period, the prevalence of status epilepticus in primary admissions of septic patie

145 a participant who had surgery and 3 cases of status epilepticus in the medical group.

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

147 We will present the current definition of status epilepticus, including a recently modified operat

148 The definition and general approach to status epilepticus, including resource use, should evolv

149 Seizure activity, in particular status epilepticus, increases cerebral amino acid transp

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

151 made in a well-characterized mouse model of status epilepticus-induced epilepsy (systemic pilocarpin

152 Status epilepticus induces a cascade of protein expressi

153 Treatment with pY816 following status epilepticus inhibited TLE and prevented anxiety-l

154 For subjects in status epilepticus, intramuscular midazolam is at least

155 Status epilepticus is a common neurologic emergency in c

156 Status epilepticus is a common neurologic emergency with

157 Status epilepticus is a common neurological emergency wi

158 Super-refractory status epilepticus is a condition characterized by recur

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

160 Status epilepticus is also increasingly identified in th

161 Status epilepticus is an acute neurologic emergency, the

162 Status epilepticus is an emergency; however, prompt trea

163 Rapid management of status epilepticus is associated with a greater likeliho

164 ; however, prompt treatment of patients with status epilepticus is challenging.

165 Status epilepticus is common in neonates and infants, an

166 Super-refractory status epilepticus is defined as status epilepticus that

167 Status epilepticus is reported with continuous electroen

168 and flowchart for managing super-refractory status epilepticus is suggested.

169 ogical impairments at the time of convulsive status epilepticus is the main risk factor for mortality

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

171 We found that febrile status epilepticus, lasting an average of 64 min, increa

172 od-brain barrier pathology in rats following status epilepticus, late electrocorticography to identif

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

174 Having a predetermined status epilepticus management pathway can expedite manag

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

176 high level of suspicion for the diagnosis of status epilepticus may be indicated in those patients wi

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

178 ice rendered epileptic using the pilocarpine-status epilepticus model of epilepsy were monitored cont

179 ric learning and accelerated forgetting in a status epilepticus model of mesial temporal lobe epileps

180 In the second stage (stage of established status epilepticus) modern treatment choices include val

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

182 eadache that progressed to hydrocephalus and status epilepticus necessitating a medically induced com

183 six had encephalitis with seizures (one with status epilepticus needing pharmacologically induced com

184 2.31-13.75; p < .001), and first episode of status epilepticus (odds ratio 3.73; 95% confidence inte

185 cting a worse developmental outcome included status epilepticus (odds ratio = 3.1; confidence interva

186 Convulsive status epilepticus often results in permanent neurologic

187 er admissions for sepsis was associated with status epilepticus, older age, and Black and Native Amer

188 EG) confirmed status epilepticus, refractory status epilepticus on day 1, "super-refractory" status e

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

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

191 the long-term effects of pilocarpine-induced status epilepticus on vesicular release and recycling in

192 Patients with higher levels of albumin at status epilepticus onset had significant lower odds for

193 Increased C-reactive protein levels at status epilepticus onset were associated with higher rat

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

195 nd level of consciousness were determined at status epilepticus onset, in order to calculate the Stat

196 rs; five male patients) developed refractory status epilepticus or epilepsia partialis continua along

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

198 rm of encephalitis with seizures, refractory status epilepticus, or both.

199 s the specific impact of therapeutic coma on status epilepticus outcome.

200 izure activity after ischemia, less frequent status epilepticus (p < 0.05), and earlier return of sle

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

202 Among 171 status epilepticus patients with a mean age of 64.1 year

203 population-standardized hospitalizations for status epilepticus per 100 000 persons increased by 56.4

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

205 Prolonged seizures (status epilepticus) produce pathophysiological changes i

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

207 logistic regression analysis disclosed that status epilepticus, psychosis and cognitive dysfunction

208 For this purpose, we used two distinct post-status epilepticus rat models, in which epilepsy was ind

209 agents for refractory generalised convulsive status epilepticus, rather than additional trials of sec

210 was reduced to 63% of controls 5 days after status epilepticus, recovered to 93% of controls in vehi

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

212 electroencephalographically (EEG) confirmed status epilepticus, refractory status epilepticus on day

213 tcome parameters reported include control of status epilepticus, relapse on withdrawal, breakthrough

214 al cross-sectional studies including 408 304 status epilepticus-related hospital visits using general

215 ere used to estimate population-standardized status epilepticus-related hospitalization rates using I

216 , yet limited data exist detailing trends in status epilepticus-related hospitalizations and mortalit

217 Status epilepticus-related hospitalizations were categor

218 connect exists between the relatively stable status epilepticus-related mortality and the marked incr

219 Age-standardized status epilepticus-related mortality per 1 000 000 perso

220 y, its frequency in patients with convulsive status epilepticus remains unknown.

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

222 Uncontrolled episodes of status epilepticus require intensive care treatment and

223 tus epilepticus on day 1, "super-refractory" status epilepticus (resistant to general anesthesia), an

224 ed a mouse model in which a brief episode of status epilepticus results in chronic recurrent seizures

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

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

227 cellular locale of enhanced pTrkB induced by status epilepticus (SE) evoked by infusion of kainic aci

228 ally relevant question is whether early post-status epilepticus (SE) evoked chloride dysregulation is

229 cial for restraining seizures, cannot thwart status epilepticus (SE) induced neurodegeneration or dow

230 Status epilepticus (SE) is a common neurological emergen

231 Status epilepticus (SE) is a common neurological emergen

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

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

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

235 d as generalized convulsive or nonconvulsive status epilepticus (SE) that continued despite initial f

236 , we used a rat model of pilocarpine-induced status epilepticus (SE) to investigate HIF-1alpha expres

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

238 Status epilepticus (SE) triggers pathological changes to

239 ss plays in determining KCC2 activity during status epilepticus (SE) using knockin mice in which S940

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

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

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

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

244 pyramidal neurons after pilocarpine-induced status epilepticus (SE), accompanied by loss of HCN1 cha

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

246 found that in the mouse pilocarpine model of status epilepticus (SE), systemic administration of TG6-

247 to adult-born DGCs after pilocarpine-induced status epilepticus (SE), whereas normotopic DGCs synapse

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

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

250 odels including the benzodiazepine-resistant status epilepticus (SE).

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

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

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

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

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

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

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

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

259 statistics revealed good calibration of the Status Epilepticus Severity Score (chi-square goodness-o

260 validation of the predictive accuracy of the Status Epilepticus Severity Score and its transportabili

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

262 iscrimination and calibration indicated that Status Epilepticus Severity Score performed reasonably w

263 xternal validity and transportability of the Status Epilepticus Severity Score prediction functions f

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

265 w discusses the advances in the treatment of status epilepticus since the first London-Innsbruck Coll

266 ance: Prolonged seizures in super-refractory status epilepticus (SRSE) have been shown to cause neuro

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

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

269 parameters resulted in immediate relapse of status epilepticus, suggesting a pivotal role of deep br

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

271 -refractory status epilepticus is defined as status epilepticus that continues or recurs 24 h or more

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

273 ar-old boy with a prolonged super-refractory status epilepticus that eventually resolved after commen

274 ethylation after status epilepticus alone or status epilepticus that followed seizure preconditioning

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

276 e showed that, following pilocarpine-induced status epilepticus, there are two independent changes in

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

278 d in guidelines for management of refractory status epilepticus; this is, however, based on weak evid

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

280 nical trials, such as the ESETT (Established Status Epilepticus Treatment Trial), compare effectivene

281 c and respiratory effects of these agents in status epilepticus treatment.

282 Among pediatric patients with convulsive status epilepticus, treatment with lorazepam did not res

283 Status epilepticus was also more common among later year

284 In multivariable analysis, electrographic status epilepticus was associated with an increased risk

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

286 Refractory status epilepticus was defined as generalized convulsive

287 A clinical scoring system for patients with status epilepticus was developed for predicting outcome,

288 neurological impairments prior to convulsive status epilepticus was the only independent risk factor

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

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

291 l of acquired epilepsy induced by electrical status epilepticus, we show that oxidative stress occurs

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

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

294 ay be a treatment option in super-refractory status epilepticus when other treatment options have fai

295 stently altered in structure and function by status epilepticus, which could contribute to the develo

296 270 critically ill patients with convulsive status epilepticus who were receiving mechanical ventila

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

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

299 Prevention of status epilepticus with regular medication and emergency

300 er proband subsequently developed refractory status epilepticus, with dramatic electroclinical improv