ライフサイエンスコーパス: encephalopathy

1 s an overlap with 'early infantile epileptic encephalopathy'.

2 e model of cerebral palsy (Hypoxic-Ischaemic Encephalopathy).

3 nvasive GBS disease presenting with neonatal encephalopathy.

4 ated stillbirth, preterm birth, and neonatal encephalopathy.

5 e 18 months in infants with hypoxic-ischemic encephalopathy.

6 nths of age adjusted for center and level of encephalopathy.

7 y potential in patients with anoxic-ischemic encephalopathy.

8 ypathology, which includes chronic traumatic encephalopathy.

9 neurodegenerative disease chronic traumatic encephalopathy.

10 urological deterioration attributed to JCPyV encephalopathy.

11 get for therapeutic intervention in diabetic encephalopathy.

12 's disease and patterns of chronic traumatic encephalopathy.

13 e condition referred to as chronic traumatic encephalopathy.

14 as a cause of autosomal recessive epileptic encephalopathy.

15 of Alzheimer's disease and chronic traumatic encephalopathy.

16 ng Alzheimer's disease and chronic traumatic encephalopathy.

17 ), even after adjustment for MELD or hepatic encephalopathy.

18 atient with a severe form of infantile onset encephalopathy.

19 s to assess cerebral edema in severe hepatic encephalopathy.

20 nt of rapidly progressive motor weakness and encephalopathy.

21 risk for human exposure to bovine spongiform encephalopathy.

22 e diseases known as transmissible spongiform encephalopathy.

23 ssociated with higher rates of early hepatic encephalopathy.

24 ally, HT may not benefit infants with severe encephalopathy.

25 are at risk of developing chronic traumatic encephalopathy.

26 e in UBA5 underlies a severe infantile-onset encephalopathy.

27 a cause of death other than hypoxic-ischemic encephalopathy.

28 neonatal multisystemic disease to late-onset encephalopathy.

29 trophil exhaustion, and exacerbating hepatic encephalopathy.

30 s well as presence or absence of ascites and encephalopathy.

31 ing in two unrelated children with epileptic encephalopathy.

32 eding, death, treatment failure, and hepatic encephalopathy.

33 ansplantation in an infant with ethylmalonic encephalopathy.

34 ols in the diagnostics of neonatal bilirubin encephalopathy.

35 in the evaluation of neonates with bilirubin encephalopathy.

36 leading to the genetic disease ethylmalonic encephalopathy.

37 o reduce excitability in patients with KCNQ2 encephalopathy.

38 f 7000 (UR, 0-19000) presented with neonatal encephalopathy.

39 d ratio at waitlisting, and less ascites and encephalopathy.

40 without increasing the incidence of hepatic encephalopathy.

41 n, as KCNQ2 variants could lead to epileptic encephalopathy.

42 8 months among infants with hypoxic-ischemic encephalopathy.

43 in TRAPPC12 result in progressive childhood encephalopathy.

44 in the first week of life with seizures and encephalopathy.

45 history of chronic headaches and progressive encephalopathy.

46 viduals who presented early with severe AIDS encephalopathy.

47 ation, may develop in CMS patients and cause encephalopathy.

48 neurodegenerative disease chronic traumatic encephalopathy.

49 irus (CHAV), which is responsible for deadly encephalopathies.

50 is of genetic epilepsies including epileptic encephalopathies.

51 genes associated with early-onset epileptic encephalopathies.

52 e diseases known as transmissible spongiform encephalopathies.

53 a new molecular entity within the epileptic encephalopathies.

54 to be the most helpful in the evaluation of encephalopathies.

55 high resistance to transmissible spongiform encephalopathies.

56 n (33% vs 13%; P = .02), less frequently had encephalopathy (10% vs 29%; P = .01), and had better out

57 encephalopathy, or early infantile epileptic encephalopathy 13 (EIEE13), is caused predominantly by d

58 lowed by dysautonomia (16 patients [8%]) and encephalopathy (15 patients [8%]); 164 patients (85%) ha

59 R] 1.59 [95% CI 1.13-2.20]; p=0.01), hepatic encephalopathy (2.81 [1.72-4.42]; p=0.0004), diameter of

60 r ataxia, dysmetria, or dysarthria, 38%; and encephalopathy, 27%.

61 irus listing diagnoses (69% vs 56%), hepatic encephalopathy (36% vs 31%), height (161.9 vs 177.0 cm),

62 For spongiform encephalopathies, a real prion can be transmitted among

63 m the development of experimental autoimmune encephalopathy, a model of the autoimmune disease multip

64 to Alzheimer's disease and chronic traumatic encephalopathy, a successful tau therapeutic for PSP mig

65 tween three subgroups of patients with KCNA2 encephalopathy according to the electrophysiological fea

66 , 46.4; 95% CI, 42.2-51.0), hypoxic ischemic encephalopathy (adjusted HR, 23.6; 95% CI, 20.6-27.1), a

67 a universally fatal transmissible spongiform encephalopathy affecting cervids, and natural infection

68 Dravet syndrome, an epileptic encephalopathy affecting children, largely results from

69 Cerebral malaria, a reversible encephalopathy affecting young children, is a medical em

70 neurologic impairment and chronic traumatic encephalopathy after traumatic brain injury (TBI).

71 may play a pathological role during hepatic encephalopathy, although precisely how they dysregulate

72 are also strongly associated with epileptic encephalopathies and intellectual disability in humans,

73 re) at 18 to 22 months adjusted for level of encephalopathy and age at randomization.

74 e diseases, such as transmissible spongiform encephalopathy and Alzheimer disease.

75 nerative diseases, such as chronic traumatic encephalopathy and Alzheimer disease; however, neither t

76 neurologic events with stepwise dosing were encephalopathy and aphasia (each 9%) and tremor, speech

77 treated early and thoroughly, it results in encephalopathy and death.

78 ctive TBCD function underlies a recognizable encephalopathy and drives accelerated microtubule polyme

79 Prompt recognition of hyponatremic encephalopathy and early treatment with hypertonic salin

80 de novo mutations in patients with epileptic encephalopathy and for common susceptibility variants as

81 causative for a developmental and epileptic encephalopathy and have elucidated the role of atypical

82 ised by early, rapidly progressive postnatal encephalopathy and intractable seizures, leading to seve

83 lirubinemia (SNH) and the onset of bilirubin encephalopathy and kernicterus result in part from delay

84 by a remarkably similar phenotype (infantile encephalopathy and largely normal brain MRI) to that of

85 Cerebral edema is common in severe hepatic encephalopathy and may be life threatening.

86 , acute kidney injury, septic shock, hepatic encephalopathy and model for end stage liver disease wer

87 ational age, had signs of moderate to severe encephalopathy and moderately or severely abnormal backg

88 ified two additional patients with infantile encephalopathy and partially overlapping clinical featur

89 ion period, which was defined as symptoms of encephalopathy and plasma ammonia level exceeding 200 mu

90 e-mediated encephalopathy; lymphoma, hepatic encephalopathy and progressive multifocal leukoencephalo

91 e (PRES), also called the acute hypertensive encephalopathy and reversible posterior leukoencephalopa

92 Pertussis is associated with encephalopathy and seizures in infants.

93 GluN2B(p.P553T) can contribute to Rett-like encephalopathy and that their potentiation by D-serine t

94 cles involving risk factors for hyponatremic encephalopathy and treatment of hyponatremic encephalopa

95 Insufficiency with Hyperbilirubinemia and/or Encephalopathy and/or Renal Failure dataset with adoptio

96 Insufficiency with Hyperbilirubinemia and/or Encephalopathy and/or Renal Failure trial by applying th

97 Insufficiency with Hyperbilirubinemia and/or Encephalopathy and/or Renal Failure trial.

98 ssion (Ohtahara syndrome and early myoclonic encephalopathy) and evaluate genotype-phenotype correlat

99 oped progressive neurological deterioration (encephalopathy) and we wished to investigate this.

100 ovenous thrombosis, 11 with hypoxic ischemic encephalopathy, and 5 with neonatal arterial ischemic st

101 ere diagnosed as having posterior reversible encephalopathy, and 7 patients (1.6%) died.

102 s 3.0 g/dL, 28% had ascites, 18% had hepatic encephalopathy, and 83% were Child class B or C.

103 including hyperbilirubinemia, coagulopathy, encephalopathy, and ascites formation.

104 in liver function, coagulation, incidence of encephalopathy, and creatinine.

105 s, including stroke, traumatic brain injury, encephalopathy, and dementia.

106 Hemodynamic changes, incidence of hepatic encephalopathy, and long-term (>3 months) need for parac

107 essive supranuclear palsy, chronic traumatic encephalopathy, and other tauopathies.

108 ular mechanisms underlying bilirubin-induced encephalopathy, and searching for potential therapies fo

109 e marrow transplant as a result of undefined encephalopathy, and the other remained in remission 10 m

110 Heliox improves respiratory acidosis, encephalopathy, and the respiratory rate more quickly th

111 and compared them to 21 CMS patients without encephalopathy, and to 15 healthy control subjects witho

112 defined as hepatic decompensation (ascites, encephalopathy, and variceal bleeding), hepatocellular c

113 sferred to the treating center with moderate encephalopathy, and were randomized at a mean (SD) of 16

114 ogy is prominently seen in chronic traumatic encephalopathy, and whether human neuroimaging observati

115 Epileptic encephalopathies are a devastating group of severe child

116 Infantile encephalopathies are a group of clinically and biologica

117 new molecular target for patients with KCNQ2 encephalopathy, as partial inhibition of these channels

118 We report a case of atypical JCPyV encephalopathy associated with cerebral venous sinus thr

119 /=36 weeks' gestation) with hypoxic-ischemic encephalopathy at 18 US centers in the Eunice Kennedy Sh

120 disability for infants with hypoxic-ischemic encephalopathy at 36 weeks' or later gestation.

121 children, presenting with acute episodes of encephalopathy, bilateral symmetric brain lesions, and h

122 pathological properties of bovine spongiform encephalopathy (BSE) and variant Creutzfeldt-Jakob disea

123 However, since the bovine spongiform encephalopathy (BSE) crisis, their use has been strictly

124 sease (CWD) in cervids and bovine spongiform encephalopathy (BSE) in cattle are prion diseases that a

125 t-Jakob disease (vCJD) and bovine spongiform encephalopathy (BSE) prions are two of the prion strains

126 icobasal degeneration, and chronic traumatic encephalopathy, but did not label nonpathological, paren

127 ttle include the classical bovine spongiform encephalopathy (C-BSE) and the atypical H-type BSE (H-BS

128 The causes of encephalopathy can be either non-genetic or genetic.

129 Chronic traumatic encephalopathy can occur after sporting injuries, so we

130 f a 4-year-old Rett-like patient with severe encephalopathy carrying a missense de novo mutation in G

131 (eight previously described) with epileptic encephalopathy carrying either novel or known KCNA2 muta

132 childhood onset, severe autosomal recessive encephalopathy characterized by extreme cerebellar atrop

133 Here, we report a syndromic neonatal encephalopathy characterized by profound developmental d

134 cle and triggers hypermethioninemia, hepatic encephalopathy, cognitive impairment, and seizures.

135 tes with moderate or severe hypoxic-ischemic encephalopathy, cooling for longer than 72 hours, coolin

136 ed with the development of chronic traumatic encephalopathy (CTE) and Alzheimer's disease.

137 Chronic traumatic encephalopathy (CTE) refers to pathologic changes that h

138 he more recently described chronic traumatic encephalopathy (CTE).

139 l conditions, particularly chronic traumatic encephalopathy (CTE).

140 Developmental and epileptic encephalopathy (DEE) is a group of conditions characteri

141 Transient encephalopathy developed in approximately one in three p

142 ized tonic clonic seizures and the epileptic encephalopathy, Dravet syndrome.

143 s a pathophysiological cause for early-onset encephalopathies due to abnormal protein ufmylation.

144 mice are associated with a severe epileptic encephalopathy due to a dominant negative effect of the

145 bunit gene GABRB1 in children with epileptic encephalopathies (EEs) Lennox-Gastaut syndrome (LGS) or

146 the etiology of developmental and epileptic encephalopathies (EEs), highlighting their genetic heter

147 Patients with early infantile epileptic encephalopathy (EIEE) are at increased risk for sudden u

148 Patients with early infantile epileptic encephalopathy (EIEE) experience severe seizures and cog

149 ic phenotypes, including infantile epileptic encephalopathy (EIEE), suggestive of a gain of pathologi

150 Early infantile epileptic encephalopathy (EIEE)-associated mutations in MUNC18-1 c

151 se in the adults appears broader as cases of encephalopathy, encephalitis, meningitis, myelitis, and

152 ion with moderate or severe hypoxic-ischemic encephalopathy enrolled at 6 to 24 hours after birth.

153 ified in patients with early-onset epileptic encephalopathy (EOEE) and profound developmental delay.

154 Early-onset epileptic encephalopathy (EOEE) represents a heterogeneous group o

155 r carcinoma, hepatic decompensation (hepatic encephalopathy, esophageal varices, ascites, or portal h

156 iological agents in transmissible spongiform encephalopathies, exhibit remarkable resistance to most

157 In patients with hyponatremic encephalopathy exhibiting neurologic manifestations, a b

158 f acute myocardial infarction, septic shock, encephalopathy, general deterioration in physical health

159 0.05) and increased with severity of hepatic encephalopathy (grade 0-2 vs 3/4) and systemic inflammat

160 Those patients with advanced hepatic encephalopathy (grade 3/4) or high systemic inflammatory

161 mutations in UNC80 and persistent hypotonia, encephalopathy, growth failure, and severe intellectual

162 ogenic determinants underlying the epileptic encephalopathies has grown rapidly.

163 Many epileptic encephalopathies have a genetic aetiology and are often

164 a prion disease of cattle, bovine spongiform encephalopathy-have been reported from 12 countries.

165 useful to objectively diagnose/grade hepatic encephalopathy (HE) across its spectrum of severity.

166 died the association of ammonia with hepatic encephalopathy (HE) and 21-day transplant-free survival

167 mechanisms behind the development of hepatic encephalopathy (HE) are unclear, although hyperammonemia

168 The pathogenesis of hepatic encephalopathy (HE) in cirrhosis is multifactorial and a

169 tors (PPIs) may be a risk factor for hepatic encephalopathy (HE) in patients with cirrhosis, possibly

170 Recurrent hepatic encephalopathy (HE) is a leading cause of readmission de

171 BACKGROUND & AIMS: Hepatic encephalopathy (HE) is a serious complication of cirrhos

172 Hepatic encephalopathy (HE) is a serious complication of cirrhos

173 rides (NADs) have been used to treat hepatic encephalopathy (HE) since 1966.

174 Screening for hepatic encephalopathy (HE) that does not cause obvious disorien

175 ression for all readmissions and for hepatic encephalopathy (HE), renal/metabolic, and infection-rela

176 epsy is a risk factor for developing hepatic encephalopathy (HE), which is a strong predictor of mort

177 ated with brain dysfunction known as hepatic encephalopathy (HE).

178 Encephalopathy, hepatic, and renal dysfunction manifeste

179 tropic substances, mental confusion, hepatic encephalopathy, hepatocellular carcinoma, severe anemia,

180 derate and severe neonatal hypoxic-ischaemic encephalopathy (HIE), the leading cause of permanent bra

181 ortem samples from neonates that suffered HI encephalopathy (HIE).

182 le T2h and complex T2h with hypoxic-ischemic encephalopathy (HIE).

183 t episodic metabolic crises characterized by encephalopathy, hypoglycemia, rhabdomyolysis, arrhythmia

184 Among term infants with hypoxic-ischemic encephalopathy, hypothermia initiated at 6 to 24 hours a

185 including influenza-associated encephalitis/encephalopathy (IAE).

186 including influenza associated encephalitis/encephalopathy (IAE).

187 ents with inherited thiamine defects causing encephalopathy in childhood, identifying outcome predict

188 encephalopathy and treatment of hyponatremic encephalopathy in critical illness.

189 in the development of progressive multifocal encephalopathy in immunocompromised individuals.

190 investigation suggests an outbreak of acute encephalopathy in Muzaffarpur associated with both hypog

191 Suspected cases of Wernicke's encephalopathy in other fedratinib trials led to study t

192 y, and intellectual disability and epileptic encephalopathy in particular.

193 The difficulty of diagnosing Wernicke's encephalopathy in the critical care setting is reviewed.

194 The encephalopathies include many age-related electroclinica

195 l to 17 mug/L argue against hypoxic-ischemic encephalopathy incompatible with reawakening.

196 stuffs in order to prevent Bovine Spongiform Encephalopathy infection and diffusion, however the legi

197 ids, ribavirin use, the presence of ascites, encephalopathy, insomnia, and depression.

198 sorders: autism spectrum disorder, epileptic encephalopathy, intellectual disability and schizophreni

199 eurotoxicity during transmissible spongiform encephalopathies is undisputed, the physiological role o

200 A encephalopathy.SIGNIFICANCE STATEMENTSCN8A encephalopathy is a devastating neurological disorder th

201 Ethylmalonic encephalopathy is a fatal, rapidly progressive mitochond

202 Hyponatremic encephalopathy is a frequently encountered problem in th

203 Hepatic encephalopathy is a serious neurological complication of

204 Chronic traumatic encephalopathy is a tauopathy associated with RBT that h

205 Progressive childhood encephalopathy is an etiologically heterogeneous conditi

206 This encephalopathy is characterized by coma and is thought t

207 here pathology in cases of chronic traumatic encephalopathy is observed.

208 c brain injury, now termed chronic traumatic encephalopathy, is acknowledged as being a complex, mixe

209 e recently described NALCN-related infantile encephalopathy, is increasingly recognized.

210 loss of gene function of which causes severe encephalopathy, is required for inhibitory synaptic func

211 line were highly suggestive of mitochondrial encephalopathy, lactic acidosis and stroke-like episodes

212 ic aciduria, dystonia-deafness, hepatopathy, encephalopathy, Leigh-like syndrome (MEGDHEL) syndrome i

213 bust Alzheimer disease and chronic traumatic encephalopathy-like conditions that manifest in a singul

214 In mice with ethylmalonic encephalopathy, liver-targeted adeno-associated virus-me

215 associated with older age, dialysis, hepatic encephalopathy, longer length of stay, and higher white

216 mimic cases, and 10% had an immune-mediated encephalopathy; lymphoma, hepatic encephalopathy and pro

217 ests that the effect of lactulose on hepatic encephalopathy may not be related to alteration in gut m

218 At admission, 3 patients had hepatic encephalopathy; median levels of prothrombin time, INR,

219 osis of liver cirrhosis with minimal hepatic encephalopathy (MHE) disease was developed.

220 ve connectivity patterns for minimal hepatic encephalopathy (MHE) using large-scale intrinsic connect

221 Neonatal encephalopathy (NE) is a leading cause of child mortalit

222 or modification of interventions in neonatal encephalopathy (NE).

223 n the trastuzumab emtansine group [metabolic encephalopathy, neutropenic sepsis, and acute myeloid le

224 Serious encephalopathy occurred in 3 patients (11%); 2 cases wer

225 that human infection with bovine spongiform encephalopathy occurred in Saudi Arabia.

226 Epileptic encephalopathies of infancy and childhood comprise a lar

227 ng disease (CWD), a transmissible spongiform encephalopathy of cervids, was first documented nearly 5

228 ng disease (CWD), a transmissible spongiform encephalopathy of cervids, was first documented nearly 5

229 ry preterm infants are at risk of developing encephalopathy of prematurity and long-term neurodevelop

230 Using a mouse model where encephalopathy of prematurity is induced by systemic int

231 rs, and 14 patients with infantile epileptic encephalopathy, of which 13 had severe neurodevelopmenta

232 ts with cirrhosis and bouts of overt hepatic encephalopathy (OHE) are missing.

233 a series of 101 persons with early myoclonic encephalopathy, Ohtahara syndrome, and infantile spasms.

234 inical manifestations are headache, subacute encephalopathy, optic papillitis, inflammatory myelitis,

235 of chronic liver disease, and no ascites or encephalopathy or other associated clinical symptoms.

236 SCN8A encephalopathy, or early infantile epileptic encephalopa

237 combined phenotype with hypomyelination and encephalopathy (p.Asn414Lys), as well as milder phenotyp

238 ing on patients with a spectrum of epileptic encephalopathy phenotypes, and we identified five novel

239 s may be major contributors to the epileptic encephalopathy phenotypes.

240 nt illness, or of severe pertussis (seizure, encephalopathy, pneumonia, and/or hospitalization).

241 seizures associated with a severe epileptic encephalopathy presenting in the first 2 years of life,

242 33.5 degrees C for neonatal hypoxic-ischemic encephalopathy reduces death or disability, but rates co

243 subunit, Ndufs4, develop a fatal progressive encephalopathy resembling Leigh syndrome and die at appr

244 oxidase to sulfide poisoning in ethylmalonic encephalopathy, resulting from the deficiency in a mitoc

245 ng normobaric 11% O2 in mice with late-stage encephalopathy reverses their established neurological d

246 Weighing progressive multifocal encephalopathy risk associated with >/=24 months of nata

247 sorders: autism spectrum disorder, epileptic encephalopathy, schizophrenia, and severe intellectual d

248 linical evaluation, the Psychometric Hepatic Encephalopathy Score (PHES), and EEG recording with both

249 Respiratory rate, pH, PaCO2, and encephalopathy score improved significantly faster with

250 Affected patients develop hepatic encephalopathy, seizures, and severe cognitive impairmen

251 potentially fatal early infantile epileptic encephalopathy, severe developmental delay, and other fe

252 f hippocampal neurons in this model of SCN8A encephalopathy.SIGNIFICANCE STATEMENTSCN8A encephalopath

253 Older age and encephalopathy, significantly associated with P-OMS, are

254 spastic quadriplegia, and an infantile onset encephalopathy, suggesting multiple cell types may be in

255 Hyponatremic encephalopathy, symptomatic cerebral edema due to a low

256 cades have passed since posterior reversible encephalopathy syndrome (PRES) was first described in 19

257 Posterior reversible encephalopathy syndrome (PRES), also called the acute hy

258 A 34% incidence of posterior reversible encephalopathy syndrome was noted in the first 6 months.

259 arterial hypertension, posterior reversible encephalopathy syndrome, seizures, depressed level of co

260 f probable, possible, and unlikely traumatic encephalopathy syndrome, with included discussion regard

261 epetitive exposure to head trauma: traumatic encephalopathy syndrome.

262 included: IAE (10) including distinct acute encephalopathy syndromes, simple febrile seizures (14),

263 cluded IAE (n = 10) including distinct acute encephalopathy syndromes, simple febrile seizures (n = 1

264 zheimer's disease (AD) and chronic traumatic encephalopathy, tau pathology is accompanied usually by

265 llenge and the outbreak of bovine spongiform encephalopathy that occurred in the late 1980s and 1990s

266 he G-CSF plus stem-cell infusion group), and encephalopathy (three patients in the G-CSF plus stem-ce

267 which might also reduce the risk of hepatic encephalopathy through an increase in skeletal muscle ma

268 riod hyper (HY) strain of transmissible mink encephalopathy (TME).

269 pic/clinical severity, ranging from neonatal encephalopathy to mild psychiatric abnormalities were ob

270 common, with severity ranging from epileptic encephalopathy to well-controlled seizures.

271 ere, using the same transmissible spongiform encephalopathy (TSE) animal model, our aim was to determ

272 sistant PrP without transmissible spongiform encephalopathy (TSE) clinical signs or notable glial act

273 model for studying transmissible spongiform encephalopathy (TSE) infection.

274 Transmissible spongiform encephalopathies (TSEs) are fatal neurological disorders

275 , pregnancy-related transmissible spongiform encephalopathies (TSEs) have been implicated in several

276 Human transmissible spongiform encephalopathies (TSEs) or prion diseases are a group of

277 Prion diseases, or transmissible spongiform encephalopathies (TSEs), are a group of rare progressive

278 In transmissible spongiform encephalopathies (TSEs), which are lethal neurodegenerat

279 p, one of whom was admitted to hospital with encephalopathy twice).

280 e decreases cerebral edema in severe hepatic encephalopathy utilizing a quantitative technique to mea

281 Articles relevant to Wernicke's encephalopathy, vitamin and electrolyte deficiencies in

282 The 1-year probability of remaining free of encephalopathy was 65% for each group.

283 Post-TIPS overt hepatic encephalopathy was present in 14 patients (34%).

284 Overall, hepatic encephalopathy was similar in both groups (45 of 111 pat

285 how these mutations contribute to epileptic encephalopathies, we compared the effects of the mutatio

286 ng a cohort of 57 individuals with epileptic encephalopathy, we ascertained two unrelated affected in

287 rain MRI) to that of NALCN-related infantile encephalopathy, we identified a locus on 2q34 in which w

288 h symptoms that may mimic or mask Wernicke's encephalopathy, we suggest abandoning the banana bag and

289 tify genetic causes of early onset epileptic encephalopathies with burst suppression (Ohtahara syndro

290 We found that (i) encephalopathies with infantile/childhood onset epilepsi

291 racterize the genetic landscape of epileptic encephalopathy with burst suppression, without brain mal

292 AD3A genes on the other displays later-onset encephalopathy with cerebellar atrophy, ataxia and dysto

293 syndrome (FIRES) is a devastating epileptic encephalopathy with limited treatment options and an unc

294 symptoms of early-onset fatal mitochondrial encephalopathy with liver disease, including defects in

295 t patients had repeated episodes of subacute encephalopathy with motor regression, irritability and s

296 Dravet syndrome is an infant-onset epileptic encephalopathy with multiple seizure types that are ofte

297 Progressive encephalopathy with oedema, hypsarrhythmia and optic atr

298 Progressive encephalopathy with oedema, hypsarrhythmia, and optic at

299 Early hepatic encephalopathy (within 1 year) was significantly more fr

300 osis of Ohtahara syndrome or early myoclonic encephalopathy without malformations of cortical develop