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1                                              MTLE has been well characterised and can usually be iden
2                                              MTLE mice with GABAergic iNs show a significant reductio
3                                              MTLE was associated with a regional reduction in fibre d
4 cordings, SPECT studies, and MR images of 32 MTLE patients and of a subgroup of 11 patients with path
5                                      Using a MTLE mouse model, we show that retrovirus-driven express
6 e epilepsy (MTLE) without MRI abnormalities (MTLE-NMRI) represent a challenge for diagnosis of the un
7 etwork excitability dynamics in epilepsy and MTLE.
8 as present in the neocortex of both NTLE and MTLE patients in similar concentrations.
9 dies, we tested the hypothesis that NTLE and MTLE subtypes of human epilepsy might differ in regards
10 ined with western blots and compared between MTLE-HS patients who were showing (n = 06) or not showin
11 nd synaptic reorganization that characterize MTLE are not seen.
12 the interneurons in a mouse model of chronic MTLE resulted in consistent mesiotemporal seizure suppre
13                               At the Clinic, MTLE had been recognized to be familial in 2 patients on
14             Historically, we have considered MTLE a single disorder, but it may be time to view it as
15                  Compared to 8,718 controls, MTLE cases carried a higher burden of ultrarare missense
16 pocampal neuronal loss and gliosis), defines MTLE.
17 ng patients with newly intractable disabling MTLE, resective surgery plus AED treatment resulted in a
18 12 years) had mesial temporal lobe epilepsy (MTLE) and disabling seizues for no more than 2 consecuti
19 patients with mesial temporal lobe epilepsy (MTLE) and hippocampal sclerosis.
20 ouse model of mesial temporal lobe epilepsy (MTLE) as well as in hippocampal tissue resected from ind
21 rug-resistant mesial temporal lobe epilepsy (MTLE) following anterior temporal lobe (TL) resection.
22               Mesial temporal lobe epilepsy (MTLE) is a chronic neurological disorder affecting almos
23               Mesial temporal lobe epilepsy (MTLE) is a common medically refractory neurological dise
24               Mesial temporal lobe epilepsy (MTLE) is a syndromic disorder presenting with seizures a
25               Medial temporal lobe epilepsy (MTLE) is associated with limbic atrophy involving the hi
26  knowledge of mesial-temporal-lobe epilepsy (MTLE) is extensive, yet still insufficient to draw final
27  The cause of mesial temporal lobe epilepsy (MTLE) is often unknown.
28 s of LITT for mesial temporal lobe epilepsy (MTLE) is relevant to clinicians and patients.
29               Mesial temporal lobe epilepsy (MTLE) is the most common focal epilepsy.
30               Mesial temporal lobe epilepsy (MTLE) is the most common form of focal, pharmacoresistan
31 nal damage in medial temporal lobe epilepsy (MTLE) may lead to the development of aberrant connection
32 s in acquired mesial temporal lobe epilepsy (MTLE) remains unknown.
33 patients with mesial temporal lobe epilepsy (MTLE) show abnormalities in tissue concentrations of met
34 rast to prior mesial temporal lobe epilepsy (MTLE) studies, seizure-free intervals between the initia
35 izures in the mesial temporal lobe epilepsy (MTLE) syndrome.
36 patients with mesial temporal lobe epilepsy (MTLE) using the technique of composite subtraction ictal
37 progresses to mesial-temporal lobe epilepsy (MTLE) with dual pathology.
38 Patients with mesial temporal lobe epilepsy (MTLE) without MRI abnormalities (MTLE-NMRI) represent a
39 imal model of mesial temporal lobe epilepsy (MTLE), a disease accompanied with cognitive impairment.
40 patients with mesial temporal lobe epilepsy (MTLE), but recently pHFOs have also been recorded with c
41 c seizures in mesial temporal lobe epilepsy (MTLE), but the underlying mechanism remains unclear.
42 iagnosed with mesial temporal lobe epilepsy (MTLE), e.g., in hippocampal (HPC) pathology.
43 sections from mesial temporal lobe epilepsy (MTLE), plus neural stem-cell cultures and multi-electrod
44 apy-resistant mesial temporal lobe epilepsy (MTLE), which is associated with hippocampal seizures and
45 f surgery for mesial temporal lobe epilepsy (MTLE).
46 ouse model of mesial temporal lobe epilepsy (MTLE).
47 patients with mesial temporal lobe epilepsy (MTLE).
48 y intractable mesial temporal lobe epilepsy (MTLE).
49 patients with mesial temporal lobe epilepsy (MTLE).
50 patients with mesial temporal lobe epilepsy (MTLE; n = 64), those with extratemporal lobe (XTLE; n =
51 ver, immature astroglia are present in every MTLE case and their location and activity are dependent
52 onlesional MTLE actually represents familial MTLE (FMTLE).
53 zures) was 1645 (95% CI = 1448,1830) and for MTLE subjects (774 seizures) was 1500 (95% CI = 1324,163
54 t randomised trial of surgical treatment for MTLE, questions remain about the neurological consequenc
55 ation (DBS) of grey matter has been used for MTLE with limited success.
56   The chronological similarity between human MTLE and PLS rat epilepsy suggests that limbic seizure o
57 le for mGluR5 as therapeutic target in human MTLE.
58  subject as follows: epilepsy, specifying if MTLE; manifestations suspicious for epilepsy; or unaffec
59                                           In MTLE, NE concentrations in the CA1 subfield of the Pyram
60      The enzyme activity was lower by 38% in MTLE vs non-MTLE (mean 0.0060 [SD 0.0031] vs 0.0097 [0.0
61 tulate that the loss of perivascular AQP4 in MTLE is likely to result in a perturbed flux of water th
62 d in vivo whole-brain mGluR5 availability in MTLE patients using positron emission tomography (PET) a
63  a promising approach for seizure control in MTLE.
64 campal neurogenesis dramatically declines in MTLE patients with increased disease duration.
65 efined pattern of hippocampal deformation in MTLE patients compared with matched controls.
66 chanism which results in glutamate excess in MTLE remains unknown.
67 hanism affecting the network excitability in MTLE.
68 PET provides a focal biomarker for the EZ in MTLE with higher spatial accuracy compared to [(18) F]FD
69     Taken together with previous findings in MTLE-HS patients with IF who were evaluated by stereotac
70  in normal artificial cerebrospinal fluid in MTLE granule cells cannot be solely explained by a decre
71 (P<0.01)] and NE occurred more frequently in MTLE in Granular Cells of DG and Pyramidal Layer [P=0.05
72 amate accumulation and seizure generation in MTLE.
73             NE concentrations were higher in MTLE vs. NTLE in each subparcellation [P=0.012, 0.067 an
74 lain the perturbed glutamate homoeostasis in MTLE.
75 a new focus for therapeutic interventions in MTLE.
76 showed an overall increase in AQP4 levels in MTLE compared with non-MTLE hippocampi, quantitative Imm
77 nthetase in the hippocampus was 40% lower in MTLE than in non-MTLE samples (median 44 [IQR 30-58] vs
78 tate specific shift in metabolic networks in MTLE may improve the understanding of epileptogenesis an
79                 Further, immature neurons in MTLE are mostly inactive, and are not observed in cases
80 ynaptic and cellular alterations observed in MTLE induce aberrant temporal coding in the hippocampus,
81 emporal lobe is the focus of the seizures in MTLE, and surgical resection of this structure, includin
82  explore the role of glutamine synthetase in MTLE we created a novel animal model of hippocampal glut
83              Among 242 subjects interviewed, MTLE was diagnosed in 9 of 121 relatives versus 0 of 121
84                  Seventeen patients had left MTLE and 15 patients had right MTLE.
85 ateral TLH was significantly greater in left MTLE patients (p < 0.001), whereas right MTLE patients h
86                                      In left MTLE patients, greater extent of resection of ipsilatera
87 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
88  networks in patients with right versus left MTLE, and can guide preoperative counseling and surgical
89 SCOM studies in patients with well-localized MTLE most commonly show a region of hyperperfusion in th
90       In the largest prospective multicenter MTLE LITT cohort, LITT was found to be well tolerated wi
91 ve NTLE patients but in only one of the nine MTLE patients (chi-square P<0.05).
92                                       In non-MTLE hippocampus, dystrophin was preferentially localize
93 ippocampus was 40% lower in MTLE than in non-MTLE samples (median 44 [IQR 30-58] vs 69 [56-87]% of ma
94 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
95 s reduced by 44% in area CA1 of MTLE vs. non-MTLE hippocampi.
96 ase in AQP4 levels in MTLE compared with non-MTLE hippocampi, quantitative ImmunoGold electron micros
97 d to what extent newly diagnosed nonlesional MTLE actually represents familial MTLE (FMTLE).
98 ost one-fifth of newly diagnosed nonlesional MTLE, and it is largely unrecognized without direct ques
99 n contributes to the genetic architecture of MTLE, but does not appear to have a major role in failur
100 astrocytes was reduced by 44% in area CA1 of MTLE vs. non-MTLE hippocampi.
101     These results corroborate the concept of MTLE as a network disease, and may contribute to the und
102 that were suspicious, but not diagnostic, of MTLE occurred in 6 additional relatives versus none of t
103 ot appear to have a major role in failure of MTLE surgery.
104  cell dispersion, a pathological hallmark of MTLE.
105  patterns depending on the lateralization of MTLE may represent distinct epileptic networks in patien
106 ic rats obtained by the pilocarpine model of MTLE.
107  with seizure generation in a mouse model of MTLE.
108 tic variation influences seizure outcomes of MTLE surgery.
109 QP4 might be involved in the pathogenesis of MTLE.
110 ts demonstrated typical seizure semiology of MTLE.
111              In contrast to prior studies of MTLE, only 1 NTLE patient had frequent independent, cont
112 immunity-related subgroup in the syndrome of MTLE-HS.
113 enrollees undergoing LITT for drug-resistant MTLE with at least 6 months of follow-up were included.
114  cell therapy alternative for drug-resistant MTLE, which is derived from a human embryonic stem cell
115 red as a treatment option for drug-resistant MTLE.
116 nical trial (NCT05135091) for drug-resistant MTLE.
117 ts with unilateral MTLE (12 left and 8 right MTLE).
118 ents had left MTLE and 15 patients had right MTLE.
119                                     In right MTLE patients, CTL hypometabolism was the strongest pred
120 ocampal sclerosis (five left and seven right MTLE) and 26 healthy controls were studied.
121 TLE group, 6 of 15 (P = 0.022) for the right MTLE group, and 5 of 11 (P = 0.021) for the MTS subgroup
122 eft MTLE patients (p < 0.001), whereas right MTLE patients had significantly higher rates of contrala
123 al lobe epilepsy with hippocampal sclerosis (MTLE-HS) and to elucidate the clinical and laboratory cl
124 e epilepsy related to hippocampus sclerosis (MTLE-HS) have seizures with fear, which is called ictal
125 , those with medial temporal lobe sclerosis (MTLE), and those with extrahippocampal masses (MaTLE) wh
126                   These results suggest that MTLE is associated with a state specific perfusion and p
127                   These results suggest that MTLE is associated with reorganisation of the limbic sys
128                              However, in the MTLE hippocampus, the perivascular dystrophin was absent
129  and activity of glutamine synthetase in the MTLE hippocampus.
130  was particularly pronounced in areas of the MTLE hippocampus with astroglial proliferation, even tho
131 f interictal spikes and fast ripples in this MTLE model.
132 ortical TLE (NTLE) and nine with mesial TLE (MTLE) were immediately placed in Ringer's lactate; stear
133  epilepticus (SE), a condition that leads to MTLE.
134 sy (LTLE; n = 8), and a rat model similar to MTLE in which rats become epileptic after electrically i
135                        Thirty-one unilateral MTLE patients and 30 healthy controls underwent [(11) C]
136 ients operated for drug-resistant unilateral MTLE, of whom 196 (149 with favorable outcome and 47 wit
137 rwent surgery for drug-resistant, unilateral MTLE with normal magnetic resonance imaging (MRI) or MRI
138 graphy (VEEG) in 20 patients with unilateral MTLE (12 left and 8 right MTLE).
139                  12 patients with unilateral MTLE and hippocampal sclerosis (five left and seven righ
140 he criteria for the diagnosis of NTLE versus MTLE was absence versus presence of HPC sclerosis, respe
141  5-HT concentrations were higher in NTLE vs. MTLE in the Granular Cells of DG and the Pyramidal Layer
142                                        While MTLE is related to static structural limbic compromise,
143 uropsychological impairments associated with MTLE.
144  the Austin Health First Seizure Clinic with MTLE and normal magnetic resonance imaging (MRI) or MRI
145 entrations were higher in NTLE compared with MTLE in each HPC subparcellation [P=0.037, 0.024 and 0.0
146 y occurred in NTLE patients as compared with MTLE patients.
147          Consecutive patients diagnosed with MTLE fulfilling the MRI criteria for HS were enrolled.
148 rolled 145 patients (73 [50.3%] female) with MTLE undergoing LITT, with 77 reaching 2-year follow-up.
149 campal tissue resected from individuals with MTLE, a major neurological disorder characterized by sei
150 ients were diagnosed with NTLE and nine with MTLE.
151 ance regenerative medicine for patients with MTLE and other cognitive disorders.
152  neocortex while eight of nine patients with MTLE had high concentrations of NE (chi-square P<0.01).
153                   Relatives of patients with MTLE may experience deja vu phenomena that clinically li
154 bic structural connectivity in patients with MTLE was investigated, using diffusion tensor MRI, proba
155 ntrols (age 7-79 years) and 50 patients with MTLE with normal MRI on a 1.5-Tesla scanner.
156 eficient in the hippocampus in patients with MTLE, and we postulated that this deficiency is critical
157 receptor A in 1 patient of 111 patients with MTLE-HS and none of the control subjects.
158  a large consecutive series of patients with MTLE-HS.
159 t there might be a subgroup of patients with MTLE-NMRI in which the enlarged amygdala could be relate
160 amage similar to that found in patients with MTLE.
161 hological abnormality found in patients with MTLE.
162 perfusional limbic networks in patients with MTLE.
163 ion of spontaneous seizures in patients with MTLE.
164 pocampal microelectrodes in 10 patients with MTLE.
165                          In 30 subjects with MTLE and confirmed medial temporal lobe sclerosis (MTS),

 
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