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1 owing traumatic brain injury (post-traumatic epilepsy).
2 experimental models of chronic temporal lobe epilepsy.
3 and seizure-like hallmarks characteristic of epilepsy.
4 mmon than in other causes of childhood onset epilepsy.
5 of the most catastrophic forms of pediatric epilepsy.
6 riants can lead to various forms of neonatal epilepsy.
7 Risk of childhood epilepsy.
8 associated with autism spectrum disorder and epilepsy.
9 l circuits leading to non-convulsive absence epilepsy.
10 h as cystic fibrosis, Bartter's syndrome and epilepsy.
11 trategy to reduce the incidence of childhood epilepsy.
12 monotherapy for adults with newly diagnosed epilepsy.
13 dentifying the variants and genes underlying epilepsy.
14 encephalography from canines and humans with epilepsy.
15 dhood, Rapid-onset Dystonia Parkinsonism, or epilepsy.
16 itations and future applications of LITT for epilepsy.
17 comorbid memory impairments associated with epilepsy.
18 recessive mutations in SLC45A1 cause ID and epilepsy.
19 emerging role for synaptic dysregulation in epilepsy.
20 ibility variants associated with generalized epilepsy.
21 spontaneous seizures from four patients with epilepsy.
22 izures in a mouse model of pharmacoresistant epilepsy.
23 of mutations in children with SCN2A-related epilepsy.
24 an effective treatment for refractory focal epilepsy.
25 ted with higher odds of an individual having epilepsy.
26 n activity-dependent long non-coding RNA and epilepsy.
27 , months and years play an important role in epilepsy.
28 yhydramnios, megalencephaly, and symptomatic epilepsy.
29 in spatial navigation, memory, dementia and epilepsy.
30 mental epileptogenesis and observed in human epilepsy.
31 cognitive impairment, movement disorder, or epilepsy.
32 eonatal complications and risks of childhood epilepsy.
33 f life and improved safety for patients with epilepsy.
34 s been linked to intellectual disability and epilepsy.
35 es, including behavioral symptoms of ASD and epilepsy.
36 human participants with medically refractory epilepsy.
37 -third of patients with mesial temporal lobe epilepsy.
38 ly behaving genetic rodent models of absence epilepsy.
39 at 2,048 Hz in people with refractory focal epilepsy.
40 results in ASD, intellectual disability, and epilepsy.
41 is no existing animal model of postmalarial epilepsy.
42 ntribute to the development of temporal lobe epilepsy.
43 in many human diseases, including cancer and epilepsy.
44 ents undergoing treatment for drug-resistant epilepsy.
45 s and a long history of drug-resistant focal epilepsy.
46 non-pharmacological treatment for refractory epilepsy.
47 proposed as a natural animal model for human epilepsy.
48 n patients with both idiopathic and acquired epilepsy.
49 help to predict whether someone will develop epilepsy.
50 ched for genes with a genetic association to epilepsy.
51 tive seizures in patients with temporal lobe epilepsy.
52 ure activity in patients with photosensitive epilepsy.
53 and pharmaco!dynamics biomarker for acquired epilepsy.
54 7D is associated with idiopathic generalized epilepsy.
55 mpal sclerosis and seizure burden in chronic epilepsy.
56 diseases such as autism spectrum disorder or epilepsy.
57 fiber axons, both hallmarks of temporal lobe epilepsy.
58 eloped depression and 97177 (0.9%) developed epilepsy.
59 stic yield of genetic testing for early-life epilepsies.
60 in remodeling protein mutated to cause human epilepsies.
61 romising alternative to treat drug-resistant epilepsies.
62 tial anticonvulsant compounds for refractory epilepsies.
63 of LITT for a variety of extratemporal lobe epilepsies.
64 and atypical), and myoclonic and generalized epilepsies.
66 omen, and 84791 [37%] were men; P < .001) or epilepsy (54419 [56%] were women, and 42758 [44%] were m
68 and Charlson Comorbidity Index with incident epilepsy, accounting for 4.6%, 7.1%, and 20.6% of the to
69 utcome defined as presence of one or more of epilepsy (active or in remission), motor disability, int
70 tcome and Measures: The hazard of developing epilepsy after incident depression and vice versa was ca
74 exclusively seen in patients with late onset epilepsies and lack of response to sodium channel blocke
76 al evaluation of newly presenting early-life epilepsies and not just reserved for those with severe p
77 parallels between human medial temporal lobe epilepsy and a naturally occurring condition in wild sea
78 rapeutic target for treatment of progressive epilepsy and a potential biomarker for epilepsy progress
79 to investigate the familial coaggregation of epilepsy and ADHD and to estimate the contribution of ge
81 gression to estimate the association between epilepsy and ADHD within individual and across relatives
83 is, deficits in the activity of KCC2 lead to epilepsy and are also implicated in neurodevelopmental d
84 highly associated with medication-resistant epilepsy and are the most common cause of neocortical ep
86 preclinical evidence supporting treatment of epilepsy and autistic-like behaviors linked to DS with C
87 ate intellectual disability, with or without epilepsy and behavioural disorders, and 14 patients with
89 phenotypes, occasionally with neonatal onset epilepsy and developmental impairment, as well as genera
90 y mass index (BMI) and the risk of childhood epilepsy and examine associations between obesity-relate
91 y implicate PPP3CA in early-onset refractory epilepsy and further support the emerging role for synap
92 es are implicated in synaptic dysfunction in epilepsy and in an array of degenerative and autoimmune
93 143 adults with unexplained childhood-onset epilepsy and intellectual disability who were recruited
104 observed only in patients with temporal lobe epilepsy and were recorded exclusively from mesiotempora
105 intellectual disability with absent speech, epilepsy, and hypotonia was observed in all affected ind
106 lfide HMGB1 in patients with newly diagnosed epilepsy, and its persistence was associated with subseq
108 between depression severity and the risk of epilepsy, and the degree to which depression mediates th
112 on people worldwide currently suffering with epilepsy are resistant to antiepileptic drugs (AEDs).
114 ll patients free of prevalent depression and epilepsy at 18-90 years of age who were active after the
115 , including schizophrenia, bipolar disorder, epilepsy, autism, Alzheimer's disease, and Parkinson's d
117 mbination significantly delayed the onset of epilepsy, blocked disease progression between 2 and 5 mo
118 des not only a candidate for human myoclonic epilepsy but also insights into the disease etiology, wh
119 bring seizure remission in people with focal epilepsy but requires careful selection of candidates.
120 children and adolescents with drug-resistant epilepsy, but additional data are needed from randomized
122 Approximately one-third of newly diagnosed epilepsy cases fail to become seizure-free in response t
124 y abnormal brain development and intractable epilepsy, caused similar defects in Golgi localization a
125 show that epilepsy eQTLs are enriched within epilepsy-causing genes: an epilepsy cis-gene is signific
126 yhydramnios, megalencephaly, and symptomatic epilepsy, characterized by abnormal brain development an
127 e enriched within epilepsy-causing genes: an epilepsy cis-gene is significantly more likely to be a c
129 mans and in different animal models of focal epilepsy correlates with reduction of neuronal firing an
130 ward chloride transport had no effect during epilepsy development, and significantly increased granul
132 loss-of-function mutations; (ii) more severe epilepsy, developmental problems and ataxia, and atrophy
133 However, a limited understanding of how epilepsy develops, particularly in the immature brain, l
135 endent predictors of seizure recurrence were epilepsy duration before remission, seizure-free interva
136 seizures in the last year of follow-up were epilepsy duration before remission, seizure-free interva
137 asive, potentially lifelong TES treatment of epilepsy either alone or as a complement to drug treatme
140 S) GWAS are significantly more enriched with epilepsy-eQTLs than with normal hippocampal eQTLs from t
142 her adults with a history of childhood-onset epilepsy exhibit increased brain amyloid accumulation, p
145 rios identifies synonymous variants in known epilepsy genes, thus pinpointing risk factors of disease
147 ephalopathies with infantile/childhood onset epilepsies (>/=3 months of age) occur almost as often as
148 ate that disease-associated variants from an epilepsy GWAS meta-analysis and a febrile seizures (FS)
151 us work in monogenic mouse models of absence epilepsy have shown that the interictal EEG displays aug
152 tiepileptic drug withdrawal, age at onset of epilepsy, history of febrile seizures, number of seizure
153 the treatment regimen and the course of the epilepsy in 66 patients for which well-documented medica
154 s study aimed to characterize post-traumatic epilepsy in a mouse model of pediatric brain injury, and
157 EEG were performed in people with suspected epilepsy in Bhutan (2014-2015), and recordings were inte
161 ed significantly to evaluate the etiology of epilepsy in clinic and lay the foundation to develop mol
162 tions in KCC2 are a known cause of infantile epilepsy in humans and KCC2 dysfunction is present in pa
164 heritable absence epilepsy or post-traumatic epilepsy in humans, and may instead reflect typical rode
165 rkers for epileptogenesis and drug-resistant epilepsy in humans, necessitating evaluation in larger-s
166 d cohort of individuals with childhood-onset epilepsy in southwestern Finland, together with 46 match
168 ched for functional terms highly relevant to epilepsy, including "neuron projection" and "seizures."
172 ppocampal cholinergic system in experimental epilepsy, involving fiber sprouting into the dentate mol
173 eizure susceptibility.SIGNIFICANCE STATEMENT Epilepsy is a common cause of morbidity after traumatic
177 s seizures.SIGNIFICANCE STATEMENT Postinjury epilepsy is an unpreventable and devastating disorder th
182 for seizures in patients with photosensitive epilepsy is engagement of the circuitry that produces ga
185 , such as Fragile X syndrome, Rett syndrome, epilepsy, major depressive disorder, and autism spectrum
186 sodium channel (VGSC) mutations cause severe epilepsies marked by intermittent, pathological hypersyn
187 ons that cause neurological diseases such as epilepsy may affect a surprising range of connection typ
188 sample, 5373 births were in 3586 women with epilepsy; mean (SD) age at first delivery of the epileps
189 ice with epilepsy (pilocarpine-temporal lobe epilepsy model) and 100 healthy control hippocampi, we i
191 altered in experimental mesial temporal lobe epilepsy (mTLE) and whether their integration differs fr
194 l morbidity, but primarily in those who have epilepsy, neurological abnormalities, or both before the
195 nal membrane contribute to the generation of epilepsy, neuropathic pain, and autism spectrum disorder
196 However, neither the longitudinal course of epilepsy nor the patterns of seizure onset and remission
197 re withdrawal, female sex, family history of epilepsy, number of seizures before remission, focal sei
198 nd parasite strain combinations, so that the epilepsy observed retained universality with respect to
201 good seizure outcome than were patients with epilepsy of unknown etiology (15 of 23 [65.2%] vs 24 of
203 seizure control, in cases of drug-resistant epilepsy, often requires neurosurgical intervention targ
205 form progressively increased in blood before epilepsy onset and prospectively identified animals that
206 of Pafah1b1(+/-) mice that may contribute to epilepsy or cognitive impairments associated with lissen
207 nd, non-inferiority trial, patients from 185 epilepsy or general neurology centres in Europe, North A
208 nomena do not always model heritable absence epilepsy or post-traumatic epilepsy in humans, and may i
209 recruited from the Toronto Western Hospital epilepsy outpatient clinic from January 1, 2012, through
212 ed electric potentials intracranially in ten epilepsy patients and estimated electric fields across t
213 e analyzed iEEG recordings obtained from 215 epilepsy patients as they performed a free recall task.
215 wever, the molecular basis for a majority of epilepsy patients remains elusive, and furthermore, most
216 s in the amygdala and hippocampus from human epilepsy patients to examine oscillatory activity during
219 Scn2a(Q54) mouse model of epilepsy, a focal epilepsy phenotype is caused by transgenic expression of
220 t (Scn1a (+/-)) mice recapitulate the severe epilepsy phenotype of Dravet syndrome and are an accepte
221 s study, we evaluated activity of SGE-516 on epilepsy phenotypes in the Scn1a (+/-) mouse model that
223 cing data from 100 hippocampi from mice with epilepsy (pilocarpine-temporal lobe epilepsy model) and
224 apsin II (SynII) leads to the development of epilepsy, probably due to impairments in inhibitory syna
229 d 2), a metazoan-specific protein mutated in epilepsy, recruits a fraction of mammalian GATOR1 and GA
234 reas seizures have been the central focus of epilepsy research, they are commonly accompanied by cogn
236 h a similar phenotype, including early-onset epilepsy, severe intellectual disability, postnatal micr
238 peutic target to treat seizure disorders and epilepsy.SIGNIFICANCE STATEMENT We recently reported tha
240 enrolled in the Turku Adult Childhood Onset Epilepsy study at the mean (SD) age of 5.1 (4.5) years (
245 zure outcome of 693 adults who had resective epilepsy surgery between 1990 and 2010 and used survival
246 n specimens from 9523 patients who underwent epilepsy surgery for drug-resistant seizures in 36 cente
248 th drug-resistant epilepsy who had undergone epilepsy surgery had a significantly higher rate of free
253 se comprising 16 patients who have undergone epilepsy surgery, revealing rich-club structures within
255 epilepsy (CAE) is the most common paediatric epilepsy syndrome and is characterized by frequent and t
256 e likely to be a causal gene for a Mendelian epilepsy syndrome than to be a causal gene for another M
257 before remission, absence of a self-limiting epilepsy syndrome, developmental delay, and epileptiform
258 ishment might be impaired in a human genetic epilepsy syndrome, polyhydramnios, megalencephaly, and s
266 CANCE STATEMENT Development of temporal lobe epilepsy (TLE) generally takes years after an initial in
267 in the DG of individuals with temporal lobe epilepsy (TLE) or AD and correlate with performance on t
268 evance of herpes simplex encephalitis and of epilepsy to AD, the action of IFN, and the possible rele
269 neocortex of rats with chronic temporal lobe epilepsy to demonstrate that subsets of cells discharge
270 udy evaluated a mouse model of temporal lobe epilepsy to test which pathological changes in the denta
271 late onset group, including myoclonic-atonic epilepsy (two patients), Lennox-Gastaut not emerging fro
272 drome, including movement disorders, absence epilepsy (typical and atypical), and myoclonic and gener
273 ailure to thrive, dilated cardiomyopathy and epilepsy, ultimately leading to death in early childhood
275 n of temporal lobe seizures in temporal lobe epilepsy, using diffusion tensor imaging and automated f
277 ected, and cumulative lifetime prevalence of epilepsy was determined using the Kaplan-Meier estimator
280 from rare patients with medically resistant epilepsy, we find that theta oscillations are a distinct
281 nslation of closed-loop TES for treatment of epilepsy, we show here for the first time that unsupervi
283 with intellectual disability, autism, and/or epilepsy were identified: 2p16.1-p15 duplication, 6p25.3
285 d 16 years or older and with newly diagnosed epilepsy were randomly assigned in a 1:1 ratio, via a co
288 erviews with family members of patients with epilepsy who died suddenly without other identifiable ca
289 children and adolescents with drug-resistant epilepsy who had undergone epilepsy surgery had a signif
291 es had to report on cohorts of patients with epilepsy who were seizure-free and had started withdrawa
293 atients with pharmacoresistant temporal lobe epilepsy will not be rendered completely seizure-free af
294 from West syndrome (two patients), and focal epilepsies with an electrical status epilepticus during
295 devastating group of severe childhood onset epilepsies with medication-resistant seizures and poor d
299 ne associations between exposure to maternal epilepsy with or without antiepileptic drug (AED) therap
300 c features of a canine generalized myoclonic epilepsy with photosensitivity and onset in young Rhodes
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