ライフサイエンスコーパス: MTLE

1 MTLE has been well characterised and can usually be iden

2 MTLE was associated with a regional reduction in fibre d

3 cordings, SPECT studies, and MR images of 32 MTLE patients and of a subgroup of 11 patients with path

4 e epilepsy (MTLE) without MRI abnormalities (MTLE-NMRI) represent a challenge for diagnosis of the un

5 etwork excitability dynamics in epilepsy and MTLE.

6 as present in the neocortex of both NTLE and MTLE patients in similar concentrations.

7 dies, we tested the hypothesis that NTLE and MTLE subtypes of human epilepsy might differ in regards

8 nd synaptic reorganization that characterize MTLE are not seen.

9 At the Clinic, MTLE had been recognized to be familial in 2 patients on

10 Historically, we have considered MTLE a single disorder, but it may be time to view it as

11 pocampal neuronal loss and gliosis), defines MTLE.

12 ng patients with newly intractable disabling MTLE, resective surgery plus AED treatment resulted in a

13 12 years) had mesial temporal lobe epilepsy (MTLE) and disabling seizues for no more than 2 consecuti

14 patients with mesial temporal lobe epilepsy (MTLE) and hippocampal sclerosis.

15 ouse model of mesial temporal lobe epilepsy (MTLE) as well as in hippocampal tissue resected from ind

16 Mesial temporal lobe epilepsy (MTLE) is a common medically refractory neurological dise

17 Medial temporal lobe epilepsy (MTLE) is associated with limbic atrophy involving the hi

18 knowledge of mesial-temporal-lobe epilepsy (MTLE) is extensive, yet still insufficient to draw final

19 The cause of mesial temporal lobe epilepsy (MTLE) is often unknown.

20 nal damage in medial temporal lobe epilepsy (MTLE) may lead to the development of aberrant connection

21 s in acquired mesial temporal lobe epilepsy (MTLE) remains unknown.

22 rast to prior mesial temporal lobe epilepsy (MTLE) studies, seizure-free intervals between the initia

23 izures in the mesial temporal lobe epilepsy (MTLE) syndrome.

24 patients with mesial temporal lobe epilepsy (MTLE) using the technique of composite subtraction ictal

25 progresses to mesial-temporal lobe epilepsy (MTLE) with dual pathology.

26 Patients with mesial temporal lobe epilepsy (MTLE) without MRI abnormalities (MTLE-NMRI) represent a

27 imal model of mesial temporal lobe epilepsy (MTLE), a disease accompanied with cognitive impairment.

28 patients with mesial temporal lobe epilepsy (MTLE), but recently pHFOs have also been recorded with c

29 c seizures in mesial temporal lobe epilepsy (MTLE), but the underlying mechanism remains unclear.

30 iagnosed with mesial temporal lobe epilepsy (MTLE), e.g., in hippocampal (HPC) pathology.

31 patients with mesial temporal lobe epilepsy (MTLE).

32 y intractable mesial temporal lobe epilepsy (MTLE).

33 patients with mesial temporal lobe epilepsy (MTLE).

34 patients with mesial temporal lobe epilepsy (MTLE; n = 64), those with extratemporal lobe (XTLE; n =

35 onlesional MTLE actually represents familial MTLE (FMTLE).

36 zures) was 1645 (95% CI = 1448,1830) and for MTLE subjects (774 seizures) was 1500 (95% CI = 1324,163

37 t randomised trial of surgical treatment for MTLE, questions remain about the neurological consequenc

38 ation (DBS) of grey matter has been used for MTLE with limited success.

39 The chronological similarity between human MTLE and PLS rat epilepsy suggests that limbic seizure o

40 subject as follows: epilepsy, specifying if MTLE; manifestations suspicious for epilepsy; or unaffec

41 In MTLE, NE concentrations in the CA1 subfield of the Pyram

42 The enzyme activity was lower by 38% in MTLE vs non-MTLE (mean 0.0060 [SD 0.0031] vs 0.0097 [0.0

43 tulate that the loss of perivascular AQP4 in MTLE is likely to result in a perturbed flux of water th

44 efined pattern of hippocampal deformation in MTLE patients compared with matched controls.

45 chanism which results in glutamate excess in MTLE remains unknown.

46 hanism affecting the network excitability in MTLE.

47 in normal artificial cerebrospinal fluid in MTLE granule cells cannot be solely explained by a decre

48 (P<0.01)] and NE occurred more frequently in MTLE in Granular Cells of DG and Pyramidal Layer [P=0.05

49 amate accumulation and seizure generation in MTLE.

50 NE concentrations were higher in MTLE vs. NTLE in each subparcellation [P=0.012, 0.067 an

51 lain the perturbed glutamate homoeostasis in MTLE.

52 a new focus for therapeutic interventions in MTLE.

53 showed an overall increase in AQP4 levels in MTLE compared with non-MTLE hippocampi, quantitative Imm

54 nthetase in the hippocampus was 40% lower in MTLE than in non-MTLE samples (median 44 [IQR 30-58] vs

55 tate specific shift in metabolic networks in MTLE may improve the understanding of epileptogenesis an

56 ynaptic and cellular alterations observed in MTLE induce aberrant temporal coding in the hippocampus,

57 emporal lobe is the focus of the seizures in MTLE, and surgical resection of this structure, includin

58 explore the role of glutamine synthetase in MTLE we created a novel animal model of hippocampal glut

59 Among 242 subjects interviewed, MTLE was diagnosed in 9 of 121 relatives versus 0 of 121

60 Seventeen patients had left MTLE and 15 patients had right MTLE.

61 were set at 6 of 17 (P = 0.042) for the left MTLE group, 6 of 15 (P = 0.022) for the right MTLE group

62 SCOM studies in patients with well-localized MTLE most commonly show a region of hyperperfusion in th

63 ve NTLE patients but in only one of the nine MTLE patients (chi-square P<0.05).

64 In non-MTLE hippocampus, dystrophin was preferentially localize

65 ippocampus was 40% lower in MTLE than in non-MTLE samples (median 44 [IQR 30-58] vs 69 [56-87]% of ma

66 yme activity was lower by 38% in MTLE vs non-MTLE (mean 0.0060 [SD 0.0031] vs 0.0097 [0.0042] U/mg pr

67 s reduced by 44% in area CA1 of MTLE vs. non-MTLE hippocampi.

68 ase in AQP4 levels in MTLE compared with non-MTLE hippocampi, quantitative ImmunoGold electron micros

69 d to what extent newly diagnosed nonlesional MTLE actually represents familial MTLE (FMTLE).

70 ost one-fifth of newly diagnosed nonlesional MTLE, and it is largely unrecognized without direct ques

71 astrocytes was reduced by 44% in area CA1 of MTLE vs. non-MTLE hippocampi.

72 These results corroborate the concept of MTLE as a network disease, and may contribute to the und

73 that were suspicious, but not diagnostic, of MTLE occurred in 6 additional relatives versus none of t

74 ic rats obtained by the pilocarpine model of MTLE.

75 QP4 might be involved in the pathogenesis of MTLE.

76 ts demonstrated typical seizure semiology of MTLE.

77 In contrast to prior studies of MTLE, only 1 NTLE patient had frequent independent, cont

78 immunity-related subgroup in the syndrome of MTLE-HS.

79 ts with unilateral MTLE (12 left and 8 right MTLE).

80 ents had left MTLE and 15 patients had right MTLE.

81 ocampal sclerosis (five left and seven right MTLE) and 26 healthy controls were studied.

82 TLE group, 6 of 15 (P = 0.022) for the right MTLE group, and 5 of 11 (P = 0.021) for the MTS subgroup

83 al lobe epilepsy with hippocampal sclerosis (MTLE-HS) and to elucidate the clinical and laboratory cl

84 , those with medial temporal lobe sclerosis (MTLE), and those with extrahippocampal masses (MaTLE) wh

85 These results suggest that MTLE is associated with a state specific perfusion and p

86 These results suggest that MTLE is associated with reorganisation of the limbic sys

87 However, in the MTLE hippocampus, the perivascular dystrophin was absent

88 and activity of glutamine synthetase in the MTLE hippocampus.

89 was particularly pronounced in areas of the MTLE hippocampus with astroglial proliferation, even tho

90 ortical TLE (NTLE) and nine with mesial TLE (MTLE) were immediately placed in Ringer's lactate; stear

91 epilepticus (SE), a condition that leads to MTLE.

92 sy (LTLE; n = 8), and a rat model similar to MTLE in which rats become epileptic after electrically i

93 graphy (VEEG) in 20 patients with unilateral MTLE (12 left and 8 right MTLE).

94 12 patients with unilateral MTLE and hippocampal sclerosis (five left and seven righ

95 he criteria for the diagnosis of NTLE versus MTLE was absence versus presence of HPC sclerosis, respe

96 5-HT concentrations were higher in NTLE vs. MTLE in the Granular Cells of DG and the Pyramidal Layer

97 While MTLE is related to static structural limbic compromise,

98 uropsychological impairments associated with MTLE.

99 the Austin Health First Seizure Clinic with MTLE and normal magnetic resonance imaging (MRI) or MRI

100 entrations were higher in NTLE compared with MTLE in each HPC subparcellation [P=0.037, 0.024 and 0.0

101 y occurred in NTLE patients as compared with MTLE patients.

102 Consecutive patients diagnosed with MTLE fulfilling the MRI criteria for HS were enrolled.

103 campal tissue resected from individuals with MTLE, a major neurological disorder characterized by sei

104 ients were diagnosed with NTLE and nine with MTLE.

105 neocortex while eight of nine patients with MTLE had high concentrations of NE (chi-square P<0.01).

106 Relatives of patients with MTLE may experience deja vu phenomena that clinically li

107 bic structural connectivity in patients with MTLE was investigated, using diffusion tensor MRI, proba

108 ntrols (age 7-79 years) and 50 patients with MTLE with normal MRI on a 1.5-Tesla scanner.

109 eficient in the hippocampus in patients with MTLE, and we postulated that this deficiency is critical

110 receptor A in 1 patient of 111 patients with MTLE-HS and none of the control subjects.

111 a large consecutive series of patients with MTLE-HS.

112 t there might be a subgroup of patients with MTLE-NMRI in which the enlarged amygdala could be relate

113 perfusional limbic networks in patients with MTLE.

114 ion of spontaneous seizures in patients with MTLE.

115 pocampal microelectrodes in 10 patients with MTLE.

116 In 30 subjects with MTLE and confirmed medial temporal lobe sclerosis (MTS),