ライフサイエンスコーパス: encephalopathy

1 mpensation (ascites, variceal hemorrhage, or encephalopathy).

2 nary, cardiac and renal failure, ascites and encephalopathy.

3 associated with developmental and epileptic encephalopathy.

4 for term infants with hypoxic-ischaemic (HI) encephalopathy.

5 -term rifaximin treatment to prevent hepatic encephalopathy.

6 ated with GRIN2A developmental and epileptic encephalopathy.

7 o be a frequent cause of recessive epileptic encephalopathy.

8 inical efficacy in the management of hepatic encephalopathy.

9 wo patients with developmental and epileptic encephalopathy.

10 ients with intractable early onset epileptic encephalopathy.

11 es (>=45), age, sex, race, life support, and encephalopathy.

12 ding hypertension and KCNQ5 loss-of-function encephalopathy.

13 eurovascular coupling (NVC) in newborns with encephalopathy.

14 severe hypo or hypernatremia, and grade 3-4 encephalopathy.

15 el causal gene for early infantile epileptic encephalopathy.

16 eceived therapeutic hypothermia for neonatal encephalopathy.

17 pontaneous bacterial peritonitis and hepatic encephalopathy.

18 ascites without increasing rates of hepatic encephalopathy.

19 lay, autism spectrum disorder, and epileptic encephalopathy.

20 -term rifaximin treatment to prevent hepatic encephalopathy.

21 e SCN8A gene cause early infantile epileptic encephalopathy.

22 rate encephalopathy, and 13 (25%) had severe encephalopathy.

23 abnormalities observed years after neonatal encephalopathy.

24 s to prevent refeeding syndrome and Wernicke encephalopathy.

25 l syndrome associated with chronic traumatic encephalopathy.

26 ed glutamate homeostasis and severe neonatal encephalopathy.

27 known disease-associated genes for epileptic encephalopathy.

28 man nucleoporin NUP214 causing acute febrile encephalopathy.

29 loma, following treatment for severe CRS and encephalopathy.

30 g as treatment-resistant infantile epileptic encephalopathy.

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

32 8 months among infants with hypoxic-ischemic encephalopathy.

33 eceived >=5 days of ceftaroline, 3 developed encephalopathy.

34 nvasive GBS disease presenting with neonatal encephalopathy.

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

36 -Goutieres syndrome, a hereditary autoimmune encephalopathy.

37 t not limited to developmental and epileptic encephalopathy.

38 Forty-five patients (83%) had high grade encephalopathy.

39 as Alzheimer's disease and chronic traumatic encephalopathy.

40 emorrhage, and acute hemorrhagic necrotizing encephalopathy.

41 athic ventricular arrhythmias, and epileptic encephalopathy.

42 ized epilepsy to developmental and epileptic encephalopathy.

43 ve supranuclear palsy, and chronic traumatic encephalopathy.

44 ons, may be a cause of antibiotic-associated encephalopathy.

45 ng Alzheimer's disease and chronic traumatic encephalopathy.

46 ental outcome eighteen months after neonatal encephalopathy.

47 ol for rapid risk stratification in neonatal encephalopathy.

48 eath and moderate-to-severe hypoxic-ischemic encephalopathy.

49 ts from donors with AD and chronic traumatic encephalopathy.

50 d prolong survival in a mouse model of SCN8A encephalopathy.

51 studies have reported ceftaroline-associated encephalopathy.

52 lay, autism spectrum disorder, and epileptic encephalopathy.

53 evelopmental delay and early-onset epileptic encephalopathy.

54 ized epilepsy to developmental and epileptic encephalopathies.

55 lly associated with transmissible spongiform encephalopathies.

56 d potassium channel produce severe epileptic encephalopathies.

57 rontotemporal dementia and chronic traumatic encephalopathy(1).

58 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

59 Thirteen patients (25%) had mild encephalopathy, 27 (50%) had moderate encephalopathy, an

60 P = 0.001), with higher incidence of hepatic encephalopathy (50% versus 27.5%; P = 0.04), hyponatremi

61 P = 0.001), with higher incidence of hepatic encephalopathy (50% vs. 27.5%; P = 0.04), hyponatremia (

62 ommonly occurring neurological symptoms were encephalopathy (57%), headache (42%), tremor (38%), apha

63 ntion following reports of chronic traumatic encephalopathy, a progressive tauopathy.

64 Acute bilirubin encephalopathy (ABE) and kernicterus spectrum disorder (

65 Secondary outcomes included encephalopathy, acute renal failure, mechanical ventilat

66 Presented is the first case of fatal JCV encephalopathy after immunosuppressive therapy that incl

67 onal risk genes for schizophrenia, epileptic encephalopathies and CHD.

68 Emerging reports of encephalopathies and similar ailments with the detection

69 h risk for sudden death, including epileptic encephalopathy and cardiac arrhythmia.

70 T cells concomitantly act to mitigate MuPyV-encephalopathy and control viral infection.

71 complications of severe disease (eg, hypoxic encephalopathy and critical care neuropathy) from those

72 One patient presented with encephalopathy and developed prolonged myoclonus in the

73 rders, from drug-refractory lethal epileptic encephalopathy and DOORS syndrome (deafness, onychodystr

74 onset and lethality in mouse models of SCN8A encephalopathy and Dravet syndrome.

75 s a causative gene for early onset epileptic encephalopathy and expands the mutant GABRA1 phenotypic

76 ice recapitulate cardinal features of STXBP1 encephalopathy and indicate that GABAergic synaptic dysf

77 ith some complications, particularly hepatic encephalopathy and infections.

78 It is the manifestation of acute encephalopathy and is variably called acute brain failur

79 y, and was associated with increased risk of encephalopathy and mechanical ventilation.

80 Improvements in encephalopathy and medical stabilization did not rapidly

81 ncreasingly identified in neonatal epileptic encephalopathy and more recently also in early-onset epi

82 diabetes, cognitive deficits associated with encephalopathy and myelopathy also occur.

83 nge of global developmental delay, epileptic encephalopathy and primary or progressive microcephaly.

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

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

86 infantile-onset developmental and epileptic encephalopathy and underline the critical role of the FH

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

88 rifaximin after hospitalization for hepatic encephalopathy) and outcomes (30-day readmissions and su

89 d mild encephalopathy, 27 (50%) had moderate encephalopathy, and 13 (25%) had severe encephalopathy.

90 , frontotemporal dementia, chronic traumatic encephalopathy, and Alzheimer's disease.

91 tonia, global developmental delay, epileptic encephalopathy, and dysmorphic features.

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

93 gan Failure Assessment score, renal failure, encephalopathy, and mechanical ventilation (adjusted odd

94 infection include granule cell neuronopathy, encephalopathy, and meningitis.

95 congenital microcephaly, infantile epileptic encephalopathy, and profound developmental delay were fo

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

97 d with global developmental delay, epileptic encephalopathy, and spasticity, and ten individuals with

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

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

100 on disease; sheep scrapie; bovine spongiform encephalopathy; and chronic wasting disease.

101 Developmental and epileptic encephalopathies are a heterogeneous group of early-onse

102 Developmental epileptic encephalopathies are devastating disorders characterized

103 GRIN2D-mediated developmental and epileptic encephalopathy, as well as the potential benefit of prec

104 s; >=3 Elixhauser score; presence of hepatic encephalopathy, ascites, variceal bleeding, hepatocellul

105 class >=3, and 72% had a history of hepatic encephalopathy, ascites, varices, hepatorenal syndrome,

106 Human cerebral malaria (HCM), a severe encephalopathy associated with Plasmodium falciparum inf

107 /=36 weeks' gestation) with hypoxic-ischemic encephalopathy at 18 US centers in the Eunice Kennedy Sh

108 ICU with moderate-to-severe hypoxic-ischemic encephalopathy at day 1 to 5 during hospitalization occu

109 CU) with moderate-to-severe hypoxic-ischemic encephalopathy at day 1 to 5 during hospitalization.

110 2005, two cases of natural bovine spongiform encephalopathies (BSE) have been reported in goats.

111 e similarly exposed to the bovine spongiform encephalopathy (BSE) agent.

112 rongly regulated since the bovine spongiform encephalopathy (BSE) crisis.

113 Bovine spongiform encephalopathy (BSE) is a TSE that occurs in cattle and

114 Bovine Spongiform Encephalopathy (BSE) is the only animal prion which has

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

116 Two unrelated individuals with epileptic encephalopathy carry a de novo variant in the gene encod

117 a new syndromic developmental and epileptic encephalopathy caused by bi-allelic loss-of-function var

118 treatment-resistant developmental epileptic encephalopathy characterised by multiple types of freque

119 s a catastrophic developmental and epileptic encephalopathy characterized by severe, pharmacoresistan

120 presenting with developmental and epileptic encephalopathy, characterized by early-infantile onset e

121 e association of developmental and epileptic encephalopathies, cleft palate, joint contractures and/o

122 Encephalopathy complicates beta-lactam therapy, particul

123 om Alzheimer's disease and chronic traumatic encephalopathy (CTE) (in which both 3R and 4R isoforms a

124 The term chronic traumatic encephalopathy (CTE) has recently entered public conscio

125 ic changes consistent with chronic traumatic encephalopathy (CTE) have been reported in ASF players,

126 Chronic traumatic encephalopathy (CTE) in particular is associated with re

127 Chronic traumatic encephalopathy (CTE) is a neurodegenerative disease asso

128 Chronic traumatic encephalopathy (CTE) is a neurodegenerative disease that

129 Chronic traumatic encephalopathy (CTE) is a neurodegenerative disease that

130 Chronic traumatic encephalopathy (CTE) is a neurodegenerative disorder tha

131 Chronic traumatic encephalopathy (CTE) is a neurodegenerative tauopathy th

132 Chronic traumatic encephalopathy (CTE) is associated with repeated traumat

133 In the 20th century, chronic traumatic encephalopathy (CTE) was conceptualized as a neurologica

134 o late life development of chronic traumatic encephalopathy (CTE), a neurodegenerative disorder histo

135 th recent work focusing on chronic traumatic encephalopathy (CTE).

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

137 erative disease, including chronic traumatic encephalopathy (CTE).

138 Developmental and epileptic encephalopathies (DEE) are a heterogeneous group of diso

139 ephalopathy is a developmental and epileptic encephalopathy (DEE) caused by de novo gain-of-function

140 res, and seizures or developmental epileptic encephalopathy (DEE).

141 associated with developmental and epileptic encephalopathy (DEE).

142 The developmental and epileptic encephalopathies (DEEs) are heterogeneous disorders with

143 en identified in developmental and epileptic encephalopathies (DEEs), but correlating genetic finding

144 Hospital admission with encephalopathy, defined as a main diagnosis of delirium,

145 /deterioration were poor performance status, encephalopathy, diabetes, high Model for End-stage Liver

146 tice of therapeutic hypothermia for neonatal encephalopathy, disability rates and the severity spectr

147 th the neonatal or infantile onset epileptic encephalopathies due to KCNQ2 GoF.

148 e model of MS is the experimental autoimmune encephalopathy (EAE) induced by immunization of mice wit

149 K(v)7.2 and K(v)7.3 subunits cause epileptic encephalopathy (EE), yet the underlying pathogenetic mec

150 24 associated with early infantile epileptic encephalopathy (EIEE).

151 ere complications with neonatal epilepsy and encephalopathy (EIEE25).

152 Example of COVID-19 CNS disease include encephalopathy, encephalitis, acute disseminated encepha

153 isorders, collectively referred to as STXBP1 encephalopathy, encompass a broad spectrum of neurologic

154 d to severe infancy or early-onset epileptic encephalopathy exhibited markedly defective conduction.

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

156 ENT KCNT1 mutations lead to severe epileptic encephalopathies for which there are no effective treatm

157 e evaluated along with validated measures of encephalopathy (Glasgow Coma Scale), multiple organ syst

158 ypically present with severe early epileptic encephalopathy, global developmental delay, motor dysfun

159 nd haematoma infection, grade 4 hypertensive encephalopathy, grade 3 acute cardiac failure, and grade

160 asures acquired soon after birth in neonatal encephalopathy had the highest accuracy to predict neurd

161 Encephalopathy has been reported for 93 patients in tota

162 ons between LFI scores, ascites, and hepatic encephalopathy (HE) and mortality.

163 al hypertension without a history of hepatic encephalopathy (HE) and reviewed medical and pharmacy re

164 Hepatic encephalopathy (HE) can cause major morbidity despite st

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

166 Hepatic encephalopathy (HE) is a serious neurologic complication

167 Cirrhosis and hepatic encephalopathy (HE) is associated with an altered gut-li

168 Hepatic encephalopathy (HE) is associated with poor quality of l

169 to be central to the pathogenesis of hepatic encephalopathy (HE), but its prognostic role in patients

170 Patients may develop hepatic encephalopathy (HE), pulmonary hypertension (PaHT), or l

171 can lead to acute liver failure and hepatic encephalopathy (HE).

172 o some complications including overt hepatic encephalopathy (HE).

173 h cirrhosis (62% with ascites and/or hepatic encephalopathy [HE]) who were within 7 days of bleeding

174 Encephalopathy, hepatic, and renal dysfunction manifeste

175 gender, black race, the presence of ascites, encephalopathy, hepatocellular carcinoma, and higher Cha

176 ase (ESLD) events including ascites, hepatic encephalopathy, hepatocellular carcinoma, esophageal var

177 Hypoxic-ischaemic encephalopathy (HIE) affects 2-4/1000 live term births.

178 : Asphyxiated neonates with hypoxic ischemic encephalopathy (HIE) are at risk of myocardial dysfuncti

179 Neonatal hypoxic-ischaemic encephalopathy (HIE) is a leading cause of death and dis

180 Hypoxic ischemic encephalopathy (HIE) is a major cause of neonatal mortal

181 erized by cardiomyopathy, corneal opacities, encephalopathy, hypotonia, and seizures in whom a monoal

182 condary objective was to compare the risk of encephalopathy in baclofen users vs nonusers.

183 thic babies recruited to the Hypothermia for Encephalopathy in Low and middle-income countries (HELIX

184 Here we modeled STXBP1 encephalopathy in mice and found that Stxbp1 haploinsuff

185 have linked the muscle relaxant baclofen to encephalopathy in patients with chronic kidney disease (

186 ts in the context of developmental epileptic encephalopathies is an increasingly recognized phenomeno

187 SCN8A encephalopathy is a developmental and epileptic encephal

188 Hepatic encephalopathy is a frequent and debilitating complicati

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

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

191 due to limbic-predominant age-related TDP-43 encephalopathy (LATE) and Alzheimer's disease.

192 athy: limbic-predominant, age-related TDP-43 encephalopathy (LATE) and the underlying neuropathologic

193 ntity, limbic-predominant age-related TDP-43 encephalopathy (LATE).

194 Severe hepatic encephalopathy, low body mass index (<18.5) and diabetes

195 roups of baclofen users had a higher risk of encephalopathy (<20 mg/d weighted RR, 5.90 [95% CI, 3.59

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

197 This opportunistic encephalopathy mainly affects immunodepressed patients w

198 rnational normalized ratio [INR] >= 1.5) and encephalopathy, may occur during pregnancy either as a p

199 severity of hyponatremia was associated with encephalopathy, mechanical ventilation, and decreased pr

200 Minimal hepatic encephalopathy (MHE) is a subclinical cognitive impairme

201 Mitochondrial neurogastrointestinal encephalopathy (MNGIE), due to mutations in TYMP, often

202 eral hyperexcitabability including seizures, encephalopathy, myoclonus, tremor and spasticity, with i

203 Five major categories emerged: (i) encephalopathies (n = 10) with delirium/psychosis and no

204 s (n = 5), varices/bleeding (n = 7), hepatic encephalopathy (n = 4), hepatocellular cancer (HCC) scre

205 and dexamethasone (pneumonia [n=1], hepatic encephalopathy [n=1]).

206 a potentiate the risk of developing neonatal encephalopathy (NE) and adverse outcome.

207 es optimal therapy for infants with neonatal encephalopathy (NE) in high-resource settings.

208 Neonatal encephalopathy (NE) is a significant worldwide problem w

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

210 lling of brain sections of chronic traumatic encephalopathy obtained from the Brain Bank.

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

212 The primary outcome, hospitalization with encephalopathy, occurred in 108/9707 (1.11%) patients wh

213 In multivariate analysis, hepatic encephalopathy (odds ratio [OR], 2.728; 95% confidence i

214 ative factor for developmental and epileptic encephalopathies of infancy and childhood with diverse c

215 s (adult cardiac arrest and hypoxic-ischemic encephalopathy of newborns) or intraoperative hypothermi

216 s (adult cardiac arrest and hypoxic-ischemic encephalopathy of newborns).

217 exploring the underlying pathophysiology of encephalopathy of prematurity employ significant insults

218 Encephalopathy of prematurity encompasses the multifacet

219 refore, we aimed to develop a representative encephalopathy of prematurity small animal model only de

220 n, and can develop a severe condition called encephalopathy of prematurity(3).

221 praxia to severe developmental and epileptic encephalopathy, often within the epilepsy-aphasia spectr

222 n contraindicated by the presence of hepatic encephalopathy or hepatorenal syndrome.

223 ilation and risk of death, hypoxic ischaemic encephalopathy or respiratory arrest did not vary with e

224 ilation, and risk of death, hypoxic ischemic encephalopathy or respiratory arrest.

225 e of rifaximin after a discharge for hepatic encephalopathy (OR 2.09 [1.80, 2.43]), and reduced risk

226 osis (no ascites, gastrointestinal bleeding, encephalopathy, or jaundice) without esophageal varices

227 h CC (no ascites, gastrointestinal bleeding, encephalopathy, or jaundice) without esophageal varices

228 acute liver injury (ALI; INR >= 2.0 with no encephalopathy), over two decades.

229 In univariate analysis, history of hepatic encephalopathy (P = 0.033), immunosuppressant treatment

230 isease, vascular dementia, chronic traumatic encephalopathy), P7C3-A20 may have widespread clinical u

231 generalized and developmental and epileptic encephalopathy patients but also for lesional focal epil

232 Compared to other encephalopathy patients with KCNA2 mutations, the proban

233 ted, followed by developmental and epileptic encephalopathy patients.

234 ed clinical events (39% ascites, 24% hepatic encephalopathy); patients who progressed had higher base

235 smission contribute to early onset epileptic encephalopathy phenotypes.

236 Antecedents of hepatic encephalopathy, pre-LT sodium serum levels, and donor ag

237 Ethylmalonic encephalopathy protein 1 (ETHE1) and molybdenum cofactor

238 Symptoms of encephalopathy range from mild confusion and aphasia to

239 bustness of NVC wavelet analysis in Neonatal Encephalopathy related to HIE.

240 s, AD, Pick's disease, and chronic traumatic encephalopathy, represent the end points of Tau's molecu

241 Sepsis-associated encephalopathy (SAE) is an acutely progressing brain dys

242 s were administered the Psychometric Hepatic Encephalopathy Score and animal naming test to detect MH

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

244 was diagnosed when the Psychometric Hepatic Encephalopathy Score was <=-4.

245 ctious or autoimmune causes, and can lead to encephalopathy, seizures, focal neurological deficits, n

246 ffected individuals presented with epileptic encephalopathy, severe neurodevelopmental delay (often w

247 Encephalopathy severity and adrenergic agonist medicatio

248 ts (4.90 vs 1.48 hr) and was correlated with encephalopathy severity by Glasgow Coma Scale in critica

249 nts but dampened and delayed with increasing encephalopathy severity.

250 Although these developmental encephalopathies share many clinical features, clear dif

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

252 between disrupted transcriptome rhythms and encephalopathy suggests a path for future work to elucid

253 high MELD score, low serum albumin, ascites, encephalopathy), surgery-related characteristics (emerge

254 Patients with encephalopathy suspected of having nonconvulsive seizure

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

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

257 Furthermore, TBI patients with traumatic encephalopathy syndrome showed higher 11C-PBB3 binding c

258 d multiorgan dysfunction, CAR-T-cell-related encephalopathy syndrome with altered mental status and n

259 of cytokine release syndrome and CAR-related encephalopathy syndrome, and IL-6 blockade and steroids

260 matter segment than those without traumatic encephalopathy syndrome, and regional assessments reveal

261 d diagnostic clinical criteria for traumatic encephalopathy syndrome, in particular the inclusion of

262 dial infarction, n = 1; posterior reversible encephalopathy syndrome, n = 1; and intracranial hemorrh

263 proposed as diagnostic features of traumatic encephalopathy syndrome, the putative clinical syndrome

264 re cytokine release syndrome and CAR-related encephalopathy syndrome, which can occur within hours or

265 symptoms based on the criteria of traumatic encephalopathy syndrome.

266 KCNQ) dysfunction can cause severe epileptic encephalopathies that are resistant to modern anticonvul

267 tic variant found in patients with epileptic encephalopathy that changes a residue located in the ion

268 d in 14 unrelated individuals with epileptic encephalopathy that included seizure onset in the prenat

269 sine degradation characterized by a specific encephalopathy that is caused by toxic accumulation of l

270 developmental and early infantile epileptic encephalopathy that is far more severe than typical SCN1

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

272 c diseases, or any alternative diagnoses for encephalopathy that were apparent within 6 h of birth.

273 In neonatal encephalopathy, the clinical manifestations of injury ca

274 uroimaging findings resembling mitochondrial encephalopathy to milder manifestation of adolescent-ons

275 is responsible for transmissible spongiform encephalopathies (TSE).

276 imilarities between transmissible spongiform encephalopathies (TSEs) and other protein misfolding dis

277 d with the onset of transmissible spongiform encephalopathies (TSEs).

278 ion of PLPBP variants included mitochondrial encephalopathy (two patients), folinic acid-responsive e

279 gene are linked to early-infantile epileptic encephalopathy type 13, also known as SCN8A-related epil

280 ronic wasting disease and transmissible mink encephalopathy uncovered that incomplete PrP(Sc) glycosy

281 ns, neuropathology (transmissible spongiform encephalopathy vacuolation and prion protein deposition)

282 uroprognostic approaches to hypoxic-ischemic encephalopathy vary among physicians and are often not c

283 ere, early onset developmental and epileptic encephalopathy via an unclear mechanism.

284 nt resource use, and the presence of hepatic encephalopathy was an additional predictor of higher inp

285 prescribed baclofen, the 30-day incidence of encephalopathy was increased among those prescribed high

286 Anoxic encephalopathy was most frequent and P-PASS higher (16.9

287 renal replacement therapy, grade 3/4 hepatic encephalopathy, WBC count, and albumin.

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

289 al epilepsy, and developmental and epileptic encephalopathy were included.

290 id hemorrhage, and postcardiac arrest anoxic encephalopathy were selected.

291 fied by AD, patients with ascites or hepatic encephalopathy were significantly more likely to develop

292 c drugs can favor the development of hepatic encephalopathy, whereas drugs undergoing extensive liver

293 on (ascites, variceal hemorrhage and hepatic encephalopathy), which defines the transition from compe

294 PyV encephalitis in wild-type mice causes an encephalopathy, which is markedly exacerbated in mice de

295 Early-infantile encephalopathies with epilepsy are devastating condition

296 MECP2 duplication disorder are developmental encephalopathies with shared and distinct features.

297 s from 25 families presenting with epileptic encephalopathy with developmental delay and hypotonia.

298 (VARS) in ten patients with a developmental encephalopathy with microcephaly, often associated with

299 utosomal dominant form of dementia, familial encephalopathy with neuroserpin inclusion bodies (FENIB)

300 um channel gene SCN8A result in an epileptic encephalopathy with refractory seizures, developmental d