ライフサイエンスコーパス: hippocampal sclerosis

1 ed in lesional acquired epilepsies (gliomas, hippocampal sclerosis).

2 farcts, arteriolosclerosis, Lewy bodies, and hippocampal sclerosis).

3 tion profile of Watson Grade 1 samples (mild hippocampal sclerosis).

4 but less marked than those in patients with hippocampal sclerosis.

5 of diffusion abnormalities in patients with hippocampal sclerosis.

6 ic spatial task, in patients with unilateral hippocampal sclerosis.

7 d amygdalohippocampal T2-signal increase and hippocampal sclerosis.

8 Ammon horn atrophy in patients with TLE and hippocampal sclerosis.

9 3 and alpha-synuclein pathologies as well as hippocampal sclerosis.

10 o seizures, who had pathologically confirmed hippocampal sclerosis.

11 t common operation performed for adults with hippocampal sclerosis.

12 l model of temporal lobe epilepsy that lacks hippocampal sclerosis.

13 of human mesial temporal lobe epilepsy with hippocampal sclerosis.

14 sease scores and Braak and Braak stage), and hippocampal sclerosis.

15 eterotopia is not invariably associated with hippocampal sclerosis.

16 ith mesial temporal lobe epilepsy (MTLE) and hippocampal sclerosis.

17 zures may all contribute to the evolution of hippocampal sclerosis.

18 ergoing surgery for refractory seizures with hippocampal sclerosis.

19 s observed in two cases with combined AD and hippocampal sclerosis.

20 ay contribute to the epileptogenic nature of hippocampal sclerosis.

21 ial temporal lobe epilepsy due to unilateral hippocampal sclerosis.

22 g 80% (203 of 254 individuals) in those with hippocampal sclerosis.

23 ents with mesial temporal lobe epilepsy with hippocampal sclerosis.

24 3.1%), followed by TDP-43 pathology, AD, and hippocampal sclerosis.

25 nsactive response DNA-binding protein 43, or hippocampal sclerosis.

26 ient with focal cortical dysplasia IIIa with hippocampal sclerosis.

27 en the case in human patients, presents with hippocampal sclerosis.

28 ents display a pattern of neuron loss called hippocampal sclerosis.

29 A-binding protein 43 (TDP-43) pathology, and hippocampal sclerosis.

30 r malformation, and 71.5% (2108 of 2948) for hippocampal sclerosis.

31 es of temporal lobe epilepsy with or without hippocampal sclerosis.

32 tion was evident for all lesions, except for hippocampal sclerosis.

33 sease, including cerebrovascular disease and hippocampal sclerosis.

34 lepsy in adults and is often associated with hippocampal sclerosis.

35 mon being mesial temporal lobe epilepsy with hippocampal sclerosis.

36 ease in all the groups except for those with hippocampal sclerosis.

37 opic infarcts, 10.8% to Lewy bodies, 5.2% to hippocampal sclerosis, 11.7% to transactive response DNA

38 n contrast, LATE (35% versus 8%, P < 0.001), hippocampal sclerosis (15% versus 3%, P = 0.02), argyrop

39 al medial temporal lobe epilepsy (25/26 left hippocampal sclerosis, 16/20 right hippocampal sclerosis

40 s with unilateral temporal lobe epilepsy and hippocampal sclerosis (24 left) and 26 healthy control s

41 ormations of cortical development (5.4%) and hippocampal sclerosis (4.1%).

42 t (6.11 +/- 4 single-nucleotide variants) or hippocampal sclerosis (5.1 +/- 3.04 single-nucleotide va

43 % CI 1.6 to 3.8 for normal MRI compared with hippocampal sclerosis), a history of secondarily general

44 a mouse model of temporal lobe epilepsy with hippocampal sclerosis, a closed-loop system and selectiv

45 laterally in humans after TBI and resembling hippocampal sclerosis, a hallmark of temporal-lobe epile

46 nd fusiform gyrus whereas patients with left hippocampal sclerosis activated only right posterior hip

47 Automated and Interpretable Detection of Hippocampal Sclerosis (AID-HS) is an open-source pipelin

48 c resonance imaging (MRI) or MRI evidence of hippocampal sclerosis and >=2-year postsurgical follow-u

49 ople with mesial temporal lobe epilepsy with hippocampal sclerosis and 3591 control subjects.

50 esial temporal lobe epilepsy associated with hippocampal sclerosis and 44 healthy controls.

51 ents with mesial temporal lobe epilepsy with hippocampal sclerosis and 75 neurologically healthy cont

52 ople with mesial temporal lobe epilepsy with hippocampal sclerosis and 7552 control subjects, with va

53 All three patients with asymmetrical hippocampal sclerosis and all nine patients with unilate

54 Hippocampal sclerosis and benign tumors were associated

55 sely delineate structural abnormalities like hippocampal sclerosis and focal cortical dysplasia in ep

56 al lobe epilepsy (TLE) is commonly caused by hippocampal sclerosis and is frequently resistant to dru

57 phase, Braak stage, cerebrovascular disease, hippocampal sclerosis and Pathological 43-kDa transactiv

58 oreactive deposits, alpha-synucleinopathies, hippocampal sclerosis and prion disease) based on a neur

59 e dentate gyrus translate to the severity of hippocampal sclerosis and seizure burden in chronic epil

60 disease pathology, cerebrovascular disease, hippocampal sclerosis and the altered expression of thre

61 one of the three patients with asymmetrical hippocampal sclerosis and three of the nine patients wit

62 y in limbic areas with or without coexisting hippocampal sclerosis and/or AD neuropathological change

63 lobar degeneration, cerebrovascular disease, hippocampal sclerosis, and no known pathology were exami

64 white matter, as was cortical astrogliosis, hippocampal sclerosis, and status marmoratus of the basa

65 logy, vascular brain pathologies, Lewy body, hippocampal sclerosis, and TAR DNA-binding protein 43.

66 ampal volume was related to AD pathology and hippocampal sclerosis, and the effects of hippocampal sc

67 age-related TDP-43 encephalopathy (LATE) and hippocampal sclerosis; and five vascular measures: chron

68 ecially disturbances in episodic memory, and hippocampal sclerosis are common in temporal lobe epilep

69 izures in mesial temporal lobe epilepsy with hippocampal sclerosis are typically drug-resistant, and

70 temporal lobe seizure onset, had ipsilateral hippocampal sclerosis as the only brain lesion, and unde

71 Age of death and clinical features of hippocampal sclerosis associated with ageing (with or wi

72 There was no association between cases with hippocampal sclerosis associated with ageing and apolipo

73 en our ability to discriminate patients with hippocampal sclerosis associated with ageing clinically,

74 y but low word list recall distinguished the hippocampal sclerosis associated with ageing group at in

75 a first step in clinical differentiation of hippocampal sclerosis associated with ageing versus pure

76 udinal cognitive profile of 43 patients with hippocampal sclerosis associated with ageing was compare

77 o hippocampal sclerosis in the aged brain as hippocampal sclerosis associated with ageing.

78 al and pathological features associated with hippocampal sclerosis associated with ageing.

79 Much remains unknown about hippocampal sclerosis associated with ageing.

80 h Braak stage and the presence of TDP-43 and hippocampal sclerosis associated with global cognitive f

81 Furthermore, in patients with confirmed hippocampal sclerosis at post-mortem examination, stereo

82 e response DNA-binding protein 43 pathology, hippocampal sclerosis, atherosclerosis, gross infarcts)

83 5/26 left hippocampal sclerosis, 16/20 right hippocampal sclerosis) before and after anterior tempora

84 ssociated with amyloid plaques, tangles, and hippocampal sclerosis but not neocortical Lewy bodies or

85 sonance images in about 15% of patients with hippocampal sclerosis, but most such patients are exclud

86 Four infants had bilateral hippocampal sclerosis by magnetic resonance scans, inclu

87 Compared with the autopsies, hippocampal sclerosis cases with decreased neuron densit

88 alopathy (LATE), argyrophilic grain disease, hippocampal sclerosis, cerebral amyloid angiopathy, and

89 butors to dementia were AD, neocortical LBD, hippocampal sclerosis, cerebral amyloid angiopathy, and

90 tau tangle density, neocortical Lewy bodies, hippocampal sclerosis, chronic gross and microscopic cer

91 from 27 patients subsequently proved to have hippocampal sclerosis demonstrated extrahippocampal stru

92 Hippocampal sclerosis describes a pattern of neuronal lo

93 pocampus, whereas patients with preoperative hippocampal sclerosis did not exhibit significant declin

94 mporal reorganization in patients with right hippocampal sclerosis during face encoding were not asso

95 eorganization observed in patients with left hippocampal sclerosis during word encoding and bilateral

96 ents with refractory partial epilepsy due to hippocampal sclerosis fail to become seizure free after

97 12 patients with unilateral MTLE and hippocampal sclerosis (five left and seven right MTLE) a

98 c across meta-analyses: febrile convulsions, hippocampal sclerosis, focal abnormal MRI, Single-Photon

99 The most common categories were hippocampal sclerosis, found in 36.4% of the patients (8

100 ere reduced, whereas Braak stage, TDP-43 and hippocampal sclerosis frequency increased.

101 Mice stimulated for 24 hours developed hippocampal sclerosis, granule cell mossy fiber sproutin

102 transactive response DNA-binding protein 43, hippocampal sclerosis, gross infarcts, and microinfarcts

103 tmortem findings on 1 patient suggested that hippocampal sclerosis had developed following the clinic

104 actory temporal lobe epilepsy and unilateral hippocampal sclerosis had repeat volumetric magnetic res

105 al tumour (LEAT), vascular malformation, and hippocampal sclerosis had the best seizure outcome at 2

106 re laterality, and rostro-caudal location of hippocampal sclerosis has not been examined in the conte

107 actory temporal lobe epilepsy and unilateral hippocampal sclerosis have progressive hippocampal atrop

108 inated inclusions (FTLD-U) in the setting of hippocampal sclerosis (HpScl) and Alzheimer's disease (A

109 change (ADNC), Lewy-related pathology (LRP), hippocampal sclerosis (HS) and cerebral amyloid angiopat

110 n a better clinicopathological definition of hippocampal sclerosis (HS) and end folium sclerosis (EFS

111 er febrile status epilepticus (FSE) produces hippocampal sclerosis (HS) and temporal lobe epilepsy (T

112 One patient with pre-existing hippocampal sclerosis (HS) did not develop progressive h

113 Hippocampal sclerosis (HS) is a common histopathological

114 stingly, this risk is lower in patients with hippocampal sclerosis (HS) relative to those without HS

115 ral lobe epilepsy (TLE) patients show marked hippocampal sclerosis (HS) upon pathological examination

116 (AD) and mesial temporal lobe epilepsy with hippocampal sclerosis (HS)) and their matched healthy co

117 asia (IIa and b), hippocampi with or without hippocampal sclerosis (HS), and available controls were

118 Hippocampal sclerosis (HS), defined as severe neuronal l

119 ed to determine, in patients with or without hippocampal sclerosis (HS), if there was a correlation b

120 Hippocampal sclerosis (HS), the most common pathology as

121 different subtypes of FTLD-TDP as well as in hippocampal sclerosis (HS), which represents a non-FTLD

122 tients with temporal lobe epilepsy (TLE) and hippocampal sclerosis (HS).

123 al lobe epilepsy (mTLE) caused by unilateral hippocampal sclerosis (HS).

124 unilateral temporal lobe epilepsy (TLE) with hippocampal sclerosis (HS-TLE, n = 26) was studied as an

125 focal cortical dysplasia (FCD; 14 cases) and hippocampal sclerosis (HS; eight cases).

126 Hippocampal sclerosis (HS; n = 16), non-HS (n = 10), and

127 ry in hippocampi from three groups: TLE with hippocampal sclerosis (HS; n = 17), epileptic hippocampi

128 Hippocampal sclerosis, identified in 40% (bilateral in 4

129 oinfarcts, cystic infarcts, Lewy bodies, and hippocampal sclerosis in all studies.

130 l attempts to replicate the human pattern of hippocampal sclerosis in animals indicate that prolonged

131 Similar to human patients, hippocampal sclerosis in sea lions was unilateral in 79%

132 different underlying causes, and we refer to hippocampal sclerosis in the aged brain as hippocampal s

133 rences were most pronounced in patients with hippocampal sclerosis in the ipsilateral parahippocampal

134 lected expression patterns of risk genes for hippocampal sclerosis in TLE and for generalized epileps

135 nt in temporal lobe epilepsy with or without hippocampal sclerosis, in addition to a common methylati

136 he three patients with bilateral symmetrical hippocampal sclerosis, in one of the three asymmetrical

137 Hippocampal sclerosis is a relatively common neuropathol

138 tant, and mesial temporal lobe epilepsy with hippocampal sclerosis is frequently associated with impo

139 These results indicate that classic hippocampal sclerosis is uniquely produced by a single e

140 cause of mesial temporal lobe epilepsy with hippocampal sclerosis is unknown, but there is an associ

141 ly common, and not typically associated with hippocampal sclerosis, is an appropriate target for cont

142 Neurofibrillary tangles (NFTs), hippocampal sclerosis, lacunar infarcts, hyaline atheros

143 se neurodegenerative diseases (i.e. LATE-NC, hippocampal sclerosis, Lewy bodies), and cerebrovascular

144 thologic traits, mtDNAcn was associated with hippocampal sclerosis, macroscopic infarctions and CAA a

145 or more diagnoses, including dual pathology, hippocampal sclerosis, malformation of cortical dysplasi

146 Hippocampal sclerosis may be reliably identified, quanti

147 sial temporal lobe epilepsy with and without hippocampal sclerosis (mTLE + HS and mTLE -HS) to invest

148 ries with mesial temporal lobe epilepsy with hippocampal sclerosis (MTLE-HS) and to elucidate the cli

149 d 1249 patients: temporal lobe epilepsy with hippocampal sclerosis (n = 599), temporal lobe epilepsy

150 ubset of cases with neuropathology-confirmed hippocampal sclerosis (n=106).

151 osis positive patients compared with 9.7% of hippocampal sclerosis negative patients.

152 ern of selective neuron loss called "classic hippocampal sclerosis." No single experimental injury ha

153 Hippocampal sclerosis of ageing (HS-A)-severe cell loss

154 a subsample of frontal cortex sections from hippocampal sclerosis of ageing (n = 15) and control (n

155 yses incorporate 226 cases of autopsy-proven hippocampal sclerosis of ageing and 1792 controls.

156 Arteriolosclerosis appears specific to hippocampal sclerosis of ageing brains, because brains w

157 Hippocampal sclerosis of ageing is a prevalent brain dis

158 rodmann area 9) was strongly associated with hippocampal sclerosis of ageing pathology (P < 0.001).

159 ntre) showing a specific association between hippocampal sclerosis of ageing pathology and arteriolos

160 We found no evidence of associations between hippocampal sclerosis of ageing pathology and lacunar in

161 Individuals with hippocampal sclerosis of ageing pathology did not show i

162 e correlation between arteriolosclerosis and hippocampal sclerosis of ageing pathology was strong in

163 dimensions that were unchanged in cases with hippocampal sclerosis of ageing versus controls.

164 In frontal cortex of cases with hippocampal sclerosis of ageing, smooth muscle actin-imm

165 acts multiple brain areas and contributes to hippocampal sclerosis of ageing.

166 ltifocal epileptiform discharges (n = 4) and hippocampal sclerosis on magnetic resonance imaging (n =

167 erosis and all nine patients with unilateral hippocampal sclerosis on MRI showed unilateral reduction

168 mesial temporal lobe epilepsy and unilateral hippocampal sclerosis on MRI than was subsequently histo

169 to have unilateral or bilateral asymmetrical hippocampal sclerosis on MRI.

170 No evidence of hippocampal sclerosis or dysplasia was present on brain

171 Eighty-two patients with hippocampal sclerosis or normal magnetic resonance imagi

172 a-amyloid levels (beta = - 0.15, p = 0.023), hippocampal sclerosis (OR = 0.56, p = 0.0015) and cerebr

173 age-related TDP-43 encephalopathy (LATE-NC), hippocampal sclerosis, other cerebrovascular conditions]

174 c resonance imaging (MRI) or MRI evidence of hippocampal sclerosis over a 10-year period.

175 out "high"-level ADNC, Lewy body disease, or hippocampal sclerosis pathologies; this group was enrich

176 ears correlated with increased prevalence of hippocampal sclerosis pathology and decreased prevalence

177 Hippocampal sclerosis pathology can be associated with d

178 t the disease is usually bilateral even when hippocampal sclerosis pathology is not obvious by haemat

179 in older adults, with or without coexisting hippocampal sclerosis pathology.

180 Hippocampi from hippocampal sclerosis patients (n = 28) and temporal mas

181 sclerosis, in one of the three asymmetrical hippocampal sclerosis patients and in six of the nine un

182 for changes in neuron densities showed that hippocampal sclerosis patients had increased AMPA and NM

183 s patients and in six of the nine unilateral hippocampal sclerosis patients.

184 43 immunohistochemistry was seen in 89.9% of hippocampal sclerosis positive patients compared with 9.

185 TLE with hippocampal sclerosis presented a significantly higher b

186 w international consensus classification for hippocampal sclerosis proposed by the International Leag

187 Mesial temporal lobe epilepsy with hippocampal sclerosis represents the most common epileps

188 quent memory in patients with left and right hippocampal sclerosis, respectively, representing effect

189 osed the alternative hypothesis that classic hippocampal sclerosis results from a single excitatory e

190 Patients with right hippocampal sclerosis showed increased temporal activati

191 left hippocampus whereas patients with left hippocampal sclerosis showed significant additional righ

192 ll three patients with bilateral symmetrical hippocampal sclerosis showed significant bilateral reduc

193 d three of the nine patients with unilateral hippocampal sclerosis showed significant reductions of F

194 Patients with right hippocampal sclerosis showed subsequent visual memory ef

195 hese findings suggest that tangle pathology, hippocampal sclerosis, TDP-43 and perforant pathway syna

196 myloid angiopathy, cerebral atherosclerosis, hippocampal sclerosis, TDP-43 cytoplasmic inclusions and

197 ontrolling for amyloid plaques, tangles, and hippocampal sclerosis, TDP-43 pathology was associated w

198 ymmetry was more pronounced in patients with hippocampal sclerosis than in those without.

199 In hippocampal sclerosis, the findings of increased apathy

200 mmonic and perforant pathways that accompany hippocampal sclerosis, the pathological hallmark of this

201 on with outcome for epilepsy associated with hippocampal sclerosis, this figure is low.

202 er symmetrical on MRI (bilateral symmetrical hippocampal sclerosis; three patients) or bilateral but

203 or bilateral but asymmetrical (asymmetrical hippocampal sclerosis; three patients), and in nine pati

204 lation in mesial temporal lobe epilepsy with hippocampal sclerosis tissue as well as gene networks in

205 ging research in temporal lobe epilepsy with hippocampal sclerosis (TLE-HS) has identified brain atro

206 (DREs), such as temporal lobe epilepsy with hippocampal sclerosis (TLE-HS), and mTOR pathway-related

207 est series of autopsy-verified patients with hippocampal sclerosis to date, we characterized the clin

208 with associated another principal lesion as hippocampal sclerosis, tumor, vascular malformation or a

209 atients with intractable mTLE and unilateral hippocampal sclerosis underwent comprehensive presurgica

210 Hippocampal sclerosis was associated with increased apat

211 re freedom and histopathological evidence of hippocampal sclerosis was not found.

212 -grade tumor were the most common causes and hippocampal sclerosis was rare.

213 In addition, hippocampal sclerosis was specific to participants with

214 -resistant focal epilepsy requiring surgery, hippocampal sclerosis was the most common histopathologi

215 Gross and microscopic cerebral infarcts and hippocampal sclerosis were also identified.

216 infarcts, Lewy bodies, TDP-43 pathology, and hippocampal sclerosis were associated with progressive c

217 nd hippocampal sclerosis, and the effects of hippocampal sclerosis were greater for subjects with low

218 ed Wada result or the presence of unilateral hippocampal sclerosis, whereas none of the patients with

219 on of inflammatory processes associated with hippocampal sclerosis which warrants further studies elu

220 nd a quantitative MRI diagnosis of bilateral hippocampal sclerosis, which appeared either symmetrical

221 equency epileptic seizures cause progressive hippocampal sclerosis, which is associated with caspase-

222 ases with substantial lesions in the form of hippocampal sclerosis, which suggests that neuronal loss

223 eport 10 right-handed TLE patients with left hippocampal sclerosis who underwent left hippocampal res

224 pileptic patients (11 women) with unilateral hippocampal sclerosis, who served as a hippocampal lesio

225 ases with mesial temporal lobe epilepsy with hippocampal sclerosis with (overall n = 757) and without

226 onal analysis showed that patients with left hippocampal sclerosis with better verbal memory addition

227 nal analysis showed that patients with right hippocampal sclerosis with better visual memory activate

228 ation for mesial temporal lobe epilepsy with hippocampal sclerosis with febrile seizures at the sodiu

229 anding of mesial temporal lobe epilepsy with hippocampal sclerosis with febrile seizures, and open av

230 dant neocortical amyloid-beta deposition and hippocampal sclerosis with its attendant TDP-43 patholog

231 cBZR in mesial temporal lobe epilepsy due to hippocampal sclerosis with optimal sensitivity.

232 tensive neuronal injury that defines classic hippocampal sclerosis, without giving any clinical indic