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1 tent postoperative seizures in patients with temporal lobe epilepsy.
2 l circuits in experimental models of chronic temporal lobe epilepsy.
3 lications for restraining SE-induced chronic temporal lobe epilepsy.
4 namics before spontaneous seizures in medial temporal lobe epilepsy.
5 of hippocampal seizures in a mouse model of temporal lobe epilepsy.
6 uring spontaneous seizures in a rat model of temporal lobe epilepsy.
7 ation processing remain poorly understood in temporal lobe epilepsy.
8 ethylation sensitive non-coding RNA in human temporal lobe epilepsy.
9 on cardiovascular function in a rat model of temporal lobe epilepsy.
10 ory function, which is typically impaired in temporal lobe epilepsy.
11 ound in hippocampectomies from patients with temporal lobe epilepsy.
12 ns is similar to that of human patients with temporal lobe epilepsy.
13 4 (TLR4) pathway is known to be involved in temporal lobe epilepsy.
14 ology similar to that of human patients with temporal lobe epilepsy.
15 reported previously for human patients with temporal lobe epilepsy.
16 cial cognitive function that is disrupted in temporal lobe epilepsy.
17 wever, none of these children have developed temporal lobe epilepsy.
18 al lobe resection than verbal memory in left temporal lobe epilepsy.
19 and in vivo optogenetics in a mouse model of temporal lobe epilepsy.
20 gions of the brain and pharmacoresistance in temporal lobe epilepsy.
21 rat model is used frequently to investigate temporal lobe epilepsy.
22 ppocampal network in a mouse model of mesial temporal lobe epilepsy.
23 thesized to contribute to the development of temporal lobe epilepsy.
24 ycoprotein activity in vivo in patients with temporal lobe epilepsy.
25 seizures in patients with intractable mesial temporal lobe epilepsy.
26 tate gyrus in the mouse pilocarpine model of temporal lobe epilepsy.
27 ncy is important in the amnestic symptoms of temporal lobe epilepsy.
28 h multiple sclerosis, Alzheimer's disease or temporal lobe epilepsy.
29 YP) seizures in the rat pilocarpine model of temporal lobe epilepsy.
30 cuits might contribute to epileptogenesis in temporal lobe epilepsy.
31 n schizophrenia, major depression and mesial temporal lobe epilepsy.
32 were associated with febrile seizures and/or temporal lobe epilepsy.
33 mine the clinical utility of imaging TSPO in temporal lobe epilepsy.
34 vitro in surgical samples from patients with temporal lobe epilepsy.
35 l-dependent learning in patients with mesial temporal lobe epilepsy.
36 lzheimer's disease, Parkinson's disease, and temporal lobe epilepsy.
37 excitability including neuropathic pain and temporal lobe epilepsy.
38 ateral to the seizure focus in patients with temporal lobe epilepsy.
39 ylase (GAD) have been found in patients with temporal lobe epilepsy.
40 ial sequence that resembles neuronal loss in temporal lobe epilepsy.
41 nounced neuronal remodeling is a hallmark of temporal lobe epilepsy.
42 e seizure-onset zone of patients with mesial temporal lobe epilepsy.
43 heir fates in the mouse pilocarpine model of temporal lobe epilepsy.
44 rain region in the pathophysiology of mesial temporal lobe epilepsy.
45 ion is an effective treatment for refractory temporal lobe epilepsy.
46 e in the pre-surgical workup of non-lesional temporal lobe epilepsy.
47 26 patients with surgically confirmed mesial temporal lobe epilepsy.
48 event this important negative consequence of temporal lobe epilepsy.
49 usual mode of inheritance in familial mesial temporal lobe epilepsy.
50 current seizures in the pilocarpine model of temporal lobe epilepsy.
51 ing is a common abnormality in patients with temporal lobe epilepsy.
52 eizures may contribute to the development of temporal lobe epilepsy.
53 native to open surgery for unilateral mesial temporal lobe epilepsy.
54 Deletion of beta 4 in mice causes temporal lobe epilepsy.
55 ed in hippocampal slices from a rat model of temporal lobe epilepsy.
56 eatment option for some patients with mesial temporal lobe epilepsy.
57 endent in vivo rat model systems relevant to temporal lobe epilepsy.
58 for further testing as a potential cause of temporal lobe epilepsy.
59 roximately one-third of patients with mesial temporal lobe epilepsy.
60 ucture of BC-->GC synapses in a rat model of temporal lobe epilepsy.
61 t seizures on the model of pharmacoresistant temporal lobe epilepsy.
62 ntrol seizures in up to 80% of patients with temporal lobe epilepsy.
63 ide (LPS) administration in mice with mesial temporal lobe epilepsy.
64 ges 50 and 65 years to treat drug-refractory temporal lobe epilepsy.
65 ocampus from patients with pharmacoresistant temporal lobe epilepsy.
66 ion with mossy fibre sprouting, a feature of temporal lobe epilepsy.
67 ting of mossy fiber axons, both hallmarks of temporal lobe epilepsy.
68 h seizure susceptibility in mice with mesial temporal lobe epilepsy.
69 about the recurrent excitation hypothesis of temporal lobe epilepsy.
70 may provide a novel avenue for treatment of temporal lobe epilepsy.
71 echanism to study cognitive comorbidities of temporal lobe epilepsy.
72 e epilepsy, the remaining 15 cases for extra-temporal lobe epilepsies.
73 e studied 33 patients with unilateral medial temporal lobe epilepsy (16 left) before, 3 and 12 months
74 e studied 36 patients with unilateral medial temporal lobe epilepsy (19 right) before and 3 and 12 mo
75 e studied 46 patients with unilateral medial temporal lobe epilepsy (25/26 left hippocampal sclerosis
76 e studied 72 patients with unilateral medial temporal lobe epilepsy (41 left) and 20 healthy controls
77 erogeneous forms of epilepsy including human temporal lobe epilepsy, a mouse model of acquired tempor
78 -1 and mutated in autosomal dominant lateral temporal lobe epilepsy (ADLTE), mediates this process in
79 mutated in human autosomal dominant lateral temporal lobe epilepsy (ADLTE), regulates postnatal prun
82 ients were studied, including 30 with mesial temporal lobe epilepsy and 31 with focal neocortical epi
83 blish further parallels between human medial temporal lobe epilepsy and a naturally occurring conditi
84 ctroclinical findings that are suggestive of temporal lobe epilepsy and can be considered as another
85 Brain injury is an etiological factor for temporal lobe epilepsy and can lead to memory and cognit
86 logy is associated with cognitive decline in temporal lobe epilepsy and explored this through clinico
87 early and acute psychotic state, the aura of temporal lobe epilepsy and hallucinogenic drug states.
89 ion in hippocampal tissue from patients with temporal lobe epilepsy and in mice following pilocarpine
90 A levels in the hippocampus of patients with temporal lobe epilepsy and in neural tissues from animal
92 tes of spontaneous seizures in patients with temporal lobe epilepsy and pilocarpine-treated rats that
93 tify the transcriptomic signature of chornic temporal lobe epilepsy and the drugs that reverse it.
94 es in 50-80% of patients with drug-resistant temporal lobe epilepsy and the effect of surgery on work
95 nt clinical observations about resection for temporal lobe epilepsy and the expectations from semanti
96 on of memory encoding networks in refractory temporal lobe epilepsy and the neural correlates of succ
97 t semantic memory is intact in resection for temporal lobe epilepsy and thus casting doubt over the c
98 tigate reorganization of memory functions in temporal lobe epilepsy and to determine whether preopera
99 and UFRs were observed only in patients with temporal lobe epilepsy and were recorded exclusively fro
101 ral lobe epilepsy, a mouse model of acquired temporal lobe epilepsy, and a mouse model of monogenic D
102 t common neuropsychological effect of mesial temporal lobe epilepsy, and because the underlying neuro
103 ears spared or even increased in intractable temporal lobe epilepsy, and has been suggested to contri
104 e basolateral amygdala kindling rat model of temporal lobe epilepsy, and it led to prolongation of th
105 has clear clinical utility in patients with temporal lobe epilepsy, and its potential easily transla
107 n SOV and seizure onset in the TeTX model of temporal lobe epilepsy, as well as the first demonstrati
110 nization of memory function in patients with temporal lobe epilepsy before and after left or right an
111 zures in 50-60% of patients with intractable temporal lobe epilepsy but may impair memory function, t
112 LR) is an effective treatment for refractory temporal lobe epilepsy but may result in a contralateral
113 ffective treatment for medically intractable temporal lobe epilepsy, but can cause memory impairment.
114 pathological finding in patients with mesial temporal lobe epilepsy, but its role in epileptogenesis
115 ncoding networks within the temporal lobe in temporal lobe epilepsy, but little is known of the extra
116 th transcriptional regulation was evident in temporal lobe epilepsy, but overall few genes previously
117 excitatory neurons is frequently observed in temporal lobe epilepsy, but the extent to which inhibito
118 ibute to the pathogenesis and maintenance of temporal lobe epilepsy, but the underlying cell and mole
119 ties are thought to play a causative role in temporal lobe epilepsy, but their precise contribution h
120 mage have been implicated in the etiology of temporal lobe epilepsy, but whether or not they have a f
122 n the generation of epileptic seizures, with temporal lobe epilepsy constituting the most prevalent f
123 vide new insights for why some patients with temporal lobe epilepsy continue to experience postoperat
127 neurophysiological features of 20 new mesial temporal lobe epilepsy families including 51 affected in
128 ed in these families, together with 19 other temporal lobe epilepsy families previously reported by u
129 onsiderable neuropsychological literature on temporal lobe epilepsy, few studies have probed semantic
130 clinical trials enrolling 118 patients with temporal lobe epilepsy found greater freedom from seizur
131 proved verbal learning in patients with left temporal lobe epilepsy from preoperatively to 12 months
132 different patient groups (semantic dementia, temporal lobe epilepsy, glioma and stroke) as well as se
133 nance imaging analysis revealed that in left temporal lobe epilepsy, greater left hippocampal activat
138 ed analysis revealed that patients with left temporal lobe epilepsy had greater activation in the lef
142 for medication-resistant and well-localized temporal lobe epilepsy has good prognosis for seizure fr
144 g genes exhibited altered DNA methylation in temporal lobe epilepsy hippocampus (n = 9) when compared
147 ting in a status epilepticus model of mesial temporal lobe epilepsy in rats, which is associated with
148 Transient epileptic amnesia is a form of temporal lobe epilepsy in which sufferers often complain
149 lation-sensitive microRNA were identified in temporal lobe epilepsy including MIR27A, miR-193a-5p (MI
150 ranule cells from control rats and rats with temporal lobe epilepsy induced by pilocarpine hydrochlor
151 the potential role of mTOR in a rat model of temporal lobe epilepsy initiated by status epilepticus.
155 suggest that visual memory function in right temporal lobe epilepsy is affected differently by right
166 ory formation (e.g., pattern separation) and temporal lobe epilepsy, little is known about activity-d
167 s been suggested that the pathophysiology of temporal lobe epilepsy may relate to abnormalities in va
169 pocampi from mice with epilepsy (pilocarpine-temporal lobe epilepsy model) and 100 healthy control hi
170 more, despite induction of MF sprouting in a temporal lobe epilepsy model, KARs were not recruited to
173 n and 20 women; aged >/=12 years) had mesial temporal lobe epilepsy (MTLE) and disabling seizues for
174 ls (DGCs) are altered in experimental mesial temporal lobe epilepsy (mTLE) and whether their integrat
175 chronically lost in a mouse model of mesial temporal lobe epilepsy (MTLE) as well as in hippocampal
176 that 1 or more particular subtypes of mesial temporal lobe epilepsy (mTLE) exist that are particularl
182 ed neuronal loss and axonal damage in medial temporal lobe epilepsy (MTLE) may lead to the developmen
185 eatment for patients with intractable mesial temporal lobe epilepsy (mTLE), a third of patients will
186 pocampus of rodents and patients with mesial temporal lobe epilepsy (MTLE), but recently pHFOs have a
191 1738 European epilepsy patients with either temporal lobe epilepsy (n = 330) and genetic generalized
192 nt in neuroinflammation, aggravating stroke, temporal lobe epilepsy, neuropathic pain, and various ne
197 ectroencephalography for medically resistant temporal lobe epilepsy participated in a visual recognit
198 mory-encoding network in both left and right temporal lobe epilepsy patients across both verbal and v
200 usion tensor imaging in 26 left and 20 right temporal lobe epilepsy patients before and a mean of 4.5
201 ia invasive methods may not be necessary for temporal lobe epilepsy patients in whom a tailored resec
206 ileptic amnesia is a distinctive syndrome of temporal lobe epilepsy principally affecting middle-aged
207 l activity in human patients with unilateral temporal lobe epilepsy relative to age-matched healthy c
212 in a series of 100 consecutive patients with temporal lobe epilepsy submitted to epilepsy surgery.
214 ateral to the seizure focus in patients with temporal lobe epilepsy, suggesting increased expression
215 fast ripples, using a non-lesional model of temporal lobe epilepsy that lacks hippocampal sclerosis.
216 genome-wide DNA methylation changes in human temporal lobe epilepsy that may contribute to the molecu
220 FOR A SCIENTIFIC COMMENTARY ON THIS ARTICLE: Temporal lobe epilepsy, the most prevalent form of chron
221 Fifty-one patients (77%) had surgery for temporal lobe epilepsy, the remaining 15 cases for extra
223 more than 65,000,000 people worldwide, with temporal lobe epilepsy (TLE) being the most common form.
225 on 11 ([11C])-labeled PBR28 in patients with temporal lobe epilepsy (TLE) found increased TSPO ipsila
226 of TLE.SIGNIFICANCE STATEMENT Development of temporal lobe epilepsy (TLE) generally takes years after
227 FSE) produces hippocampal sclerosis (HS) and temporal lobe epilepsy (TLE) has long been debated.
230 ined whether a commonly used animal model of temporal lobe epilepsy (TLE) is characterized by behavio
236 ersely related in the DG of individuals with temporal lobe epilepsy (TLE) or AD and correlate with pe
238 similar network abnormalities are present in temporal lobe epilepsy (TLE) patients with a history of
240 ation of magnetic resonance imaging-negative temporal lobe epilepsy (TLE) undergoing standard anterio
244 itivity to localize hippocampal pathology in temporal lobe epilepsy (TLE), but has rarely been evalua
245 male adult rats in the pilocarpine model of temporal lobe epilepsy (TLE), exhibited gross expansion
248 y status epilepticus promotes development of temporal lobe epilepsy (TLE), revealing TrkB as a therap
258 or temporal lobe resection for long-standing temporal lobe epilepsy to be semantically impaired.
259 ppocampus and neocortex of rats with chronic temporal lobe epilepsy to demonstrate that subsets of ce
260 sequently, we utilized the kindling model of temporal lobe epilepsy to determine if intranasal admini
262 red in models of several diseases, including temporal lobe epilepsy, TRIP8b may play a role in both n
263 and propagation of temporal lobe seizures in temporal lobe epilepsy, using diffusion tensor imaging a
265 lohippocampectomy and temporal lobectomy for temporal lobe epilepsy were associated with subtle diffe
266 ngs suggest an epilepsy-related tauopathy in temporal lobe epilepsy, which contributes to accelerated
267 selected 16 patients with pharmacoresistant temporal lobe epilepsy who had seizures despite treatmen
268 3 mg/kg; in patients with pharmacoresistant temporal lobe epilepsy, whole-brain K1 increased by only
269 coordinating gene networks in patients with temporal lobe epilepsy will help to identify novel thera
270 in every two patients with pharmacoresistant temporal lobe epilepsy will not be rendered completely s
271 ce of 20 patients with resection for chronic temporal lobe epilepsy with a full battery of semantic a
272 compared miRNA expression patterns in mesial temporal lobe epilepsy with and without hippocampal scle
273 gene are responsible for autosomal dominant temporal lobe epilepsy with auditory features, whereas L
274 s) in a large consecutive series with mesial temporal lobe epilepsy with hippocampal sclerosis (MTLE-
275 sample set comprising 959 people with mesial temporal lobe epilepsy with hippocampal sclerosis and 35
276 association study in 1018 people with mesial temporal lobe epilepsy with hippocampal sclerosis and 75
278 sis are typically drug-resistant, and mesial temporal lobe epilepsy with hippocampal sclerosis is fre
280 ebrile seizures, we tested cases with mesial temporal lobe epilepsy with hippocampal sclerosis with (
281 ection to biological understanding of mesial temporal lobe epilepsy with hippocampal sclerosis with f
282 nome-wide significant association for mesial temporal lobe epilepsy with hippocampal sclerosis with f
286 e prolonged febrile seizures group developed temporal lobe epilepsy with mesial temporal sclerosis.
287 a pilot study of the methylation profiles of temporal lobe epilepsy with or without hippocampal scler
288 Unique methylation profiles were evident in temporal lobe epilepsy with or without hippocampal scler
289 dysfunction might be a prime cause of mesial temporal lobe epilepsy with sclerosis and identify novel
290 that the hippocampus of patients with mesial temporal lobe epilepsy with sclerosis is completely devo
291 pping confirmed that in the course of mesial temporal lobe epilepsy with sclerosis, astrocytes acquir
292 changes represent cause or effect of mesial temporal lobe epilepsy with sclerosis, we developed a mo
294 ontrols and kainate-treated rats, a model of temporal lobe epilepsy, with and without tariquidar pret
295 andard of care for patients with intractable temporal lobe epilepsy, with anterior temporal lobe rese
296 HT-1A receptor ligands have been reported in temporal lobe epilepsy, with controversial association w
297 acquired disorder, several forms of familial temporal lobe epilepsy, with mesial or lateral seizure s
298 pocampal specimens from patients with mesial temporal lobe epilepsy without (n = 44) and with scleros
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