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1 al model with 3 states (entry, EEG risk, and seizure).
2 l risk factors) and 36% (coma and history of seizures).
3 l risk factors) and 64% (coma and history of seizures).
4 ross interneuron subtypes or evolve during a seizure.
5 and remission, and those who had relentless seizures.
6 owers the threshold for triggering epileptic seizures.
7 higher in CD rats that developed spontaneous seizures.
8 icits in conditions accompanied by recurrent seizures.
9 oupling to local field potential even before seizures.
10 es, implicating this miR in the avoidance of seizures.
11 neurodevelopmental disorders with or without seizures.
12 hesis, exaggerated mGluR-LTD, and audiogenic seizures.
13 mocortical phasic firing would treat absence seizures.
14 l neuronal injury during prolonged epileptic seizures.
15 ng sleep disorders, motor hyperactivity, and seizures.
16 mice but induced neither acute nor recurrent seizures.
17 atterns were reproducible across consecutive seizures.
18 disease, manifested in unprovoked recurrent seizures.
19 nterneurons ultimately help maintain ongoing seizures.
20 e with no seizures and those with continuing seizures.
21 intellectual disability, hyperactivity, and seizures.
22 imulation-induced patterns, and the risk for seizures.
23 thought to be crucial for the generation of seizures.
24 Scn1a (+/-) mice and suppressed spontaneous seizures.
25 as no significant reduction in nonconvulsive seizures.
26 clinical sequela of brain injury: edema and seizures.
27 tients with stroke, and 50% in patients with seizures.
28 anxiety-like behaviour and susceptibility to seizures.
29 metabolic conditions that could explain the seizures.
30 taxia, myokymia, and increased prevalence of seizures.
31 er (ASD), developmental delay, and infantile seizures.
32 ent periodic discharges (1 point); (3) prior seizure (1 point); (4) sporadic epileptiform discharges
33 was lower in patients with prolonged febrile seizures (14.3%, 6.3-29.4) and survivors of acute sympto
36 lectrocorticography-documented nonconvulsive seizures, accompanied by forebrain accumulation of the c
37 the SCN1A homologue recapitulate spontaneous seizure activity and mimic the convulsive behavioural mo
38 ere (1) pediatric seizure onset with ongoing seizure activity in adulthood, (2) intellectual disabili
39 also more likely to provoke seizures or pre-seizure activity in patients with photosensitive epileps
40 for 6 weeks and has the potential to control seizure activity up to 4 months (longest periods examine
41 these same mice, an 84% to 88% reduction in seizure activity was observed between 180 and 210 DAT.
45 D98 amino acid transporters was performed in seizure-affected cortex (n = 2) and compared with glioma
46 or spontaneous and pharmacologically induced seizures alongside changes in the cholinergic pathway ge
48 ssue obtained from 20 patients with frequent seizures and a long history of drug-resistant focal epil
49 a significantly higher rate of freedom from seizures and better scores with respect to behavior and
50 ptic encephalopathy (EIEE) experience severe seizures and cognitive impairment and are at increased r
51 f a new class of drugs for treatment of both seizures and comorbid memory impairments associated with
52 ction) versus generalized (gain-of-function) seizures and corresponding epileptic discharges with pro
55 impairment, as well as generalized and focal seizures and EEG abnormalities for patients with gain- a
58 fects of toxic exposure in these animals are seizures and hippocampal damage, and they have been prop
60 s and calcium sensitive exocytosis underlies seizures and large body size associated with 16p11.2 hom
61 ften accompanied by intellectual disability, seizures and other features is a severe, clinically and
63 to consider redefining the continuum between seizures and PDs, suggesting that additional damage afte
69 atency period (and thus predict the onset of seizures) and with the power change of the high-gamma rh
71 ech, a history of febrile and/or non-febrile seizures, and a wide-based, spastic, and/or stiff-legged
72 inhibition of mGluR5 corrects hyperactivity, seizures, and elevated de novo synaptic protein synthesi
73 , number of seizures before remission, focal seizures, and epileptiform abnormality on EEG before wit
74 TATION: Underlying pathology, repeated focal seizures, and global insults each contribute to atrophy
75 her incidence of pharmacoresistant epileptic seizures, and more severe neuropsychiatric disorders.
76 ts, a more severe phenotype with intractable seizures, and the potential for sudden unexpected death
77 epileptic mice correlated with frequency of seizures, and the set of genes differentially RNA-edited
83 resenting in infancy with pharmaco-resistant seizures; are often accompanied by debilitating neuropsy
87 epsy, history of febrile seizures, number of seizures before remission, absence of a self-limiting ep
88 e sex, family history of epilepsy, number of seizures before remission, focal seizures, and epileptif
90 ABAergic interneurons play critical roles in seizures, but it remains unknown whether these vary acro
91 brain amino acid metabolism during epileptic seizures by (18)F-FET PET and to elucidate the pathophys
92 iece of evidence to the proposal that limbic seizures can be supported by GABAergic hyperactivity.
95 e identified that, similar to electrographic seizures, cause brain tissue hypoxia, a measure of ongoi
101 o been proposed as models of complex partial seizures (CPSs) following traumatic brain injury (post-t
103 geons using simulated and recorded epileptic seizure data to demonstrate our system's effectiveness.
105 ompetition to crowdsource the development of seizure detection algorithms using intracranial electroe
106 eveloping accurate, validated algorithms for seizure detection is limited access to high-quality, exp
107 Affected individuals suffer from refractory seizures, developmental delay, cognitive disability, and
109 luding low birth weight, maternal education, seizure disorder, kidney disease duration, and genetical
110 could be a novel therapeutic target to treat seizure disorders and epilepsy.SIGNIFICANCE STATEMENT We
111 nts (1 day-25 years), 13 children with other seizure disorders receiving B6 supplementation (1 month-
112 any other neurological impairments including seizures, disrupted cortical lamination, and widespread
113 is one mechanism through which intermittent seizures drive persistent cognitive deficits in conditio
114 43 expression by shRNA significantly reduced seizure duration and severity in CD rats after acute sei
115 ed at 5 months without modifying the average seizure duration or the incidence of epilepsy in animals
118 iate early gene induced by electroconvulsive seizures (ECS), blocks its antidepressant efficacy.
119 s ratio [OR] = 1.8, p < 0.01) and history of seizures, either remotely or related to acute illness (3
121 is study aimed to clarify how DHA suppresses seizures, focusing on the regulation of 17beta-estradiol
122 lformations (CCMs) are a cause of stroke and seizure for which no effective medical therapies yet exi
123 e proportion of patients remaining free from seizures for 6 consecutive months after stabilisation at
124 -loop TES in rats can consistently interrupt seizures for 6 weeks and has the potential to control se
128 n cohorts of patients with epilepsy who were seizure-free and had started withdrawal of antiepileptic
129 completed 6 months of treatment and remained seizure-free entered a 6-month maintenance period on the
132 nce were epilepsy duration before remission, seizure-free interval before antiepileptic drug withdraw
133 -up were epilepsy duration before remission, seizure-free interval before antiepileptic drug withdraw
136 changes in the dentate gyrus correlate with seizure frequency and help prioritize potential mechanis
137 hermia-induced seizures, reduced spontaneous seizure frequency and prolonged survival in the Scn1a (+
139 imary end point was the change in convulsive-seizure frequency over a 14-week treatment period, as co
142 o had at least a 50% reduction in convulsive-seizure frequency was 43% with cannabidiol and 27% with
143 patients who were seropositive, reduction in seizure frequency was associated with use of immunomodul
144 iol group and the placebo group in change in seizure frequency, -22.8 percentage points; 95% confiden
145 GABA-mediated inhibition, reduce spontaneous seizure frequency, and rescue behavioral deficits in a c
147 mulation did not show an additional risk for seizures from the underlying pattern risk (P > .10).
148 an epilepsy GWAS meta-analysis and a febrile seizures (FS) GWAS are significantly more enriched with
149 d to intellectual disability with or without seizures, gait abnormalities, problems of social behavio
151 tive contribution of regions of the brain to seizure generation and consequently which brain regions
152 epilepsy, including "neuron projection" and "seizures." Genes with differential RNA editing were pref
153 nt (2.9%, 0.5-14.5) in the prolonged febrile seizures group developed temporal lobe epilepsy with mes
155 tive problems.SIGNIFICANCE STATEMENT Whereas seizures have been the central focus of epilepsy researc
156 osahexaenoic acid (DHA) attenuates epileptic seizures; however, the molecular mechanism by which it a
158 nderwent epilepsy surgery for drug-resistant seizures in 36 centers from 12 European countries over 2
159 ptin, produces a dose-dependent reduction in seizures in a mouse model of pharmacoresistant epilepsy.
160 tment with ethosuximide significantly blocks seizures in both genotypes, but the abnormal phase-ampli
171 generation and propagation of temporal lobe seizures in temporal lobe epilepsy, using diffusion tens
176 9%) of 1455 for whom data were available had seizures in their last year of follow-up, suggesting end
178 If epileptiform findings developed, the seizure incidence was between 18% (no clinical risk fact
179 dation versus synthetic CB agonist on limbic seizures induced by maximal dentate activation (MDA) acu
181 have clinical implications for mechanisms of seizure-induced astrocyte injury and potential therapeut
184 e memory, the mechanisms by which early-life seizures influence them, and the means to abrogate the e
191 acterized by periodic dynamics that increase seizure likelihood at certain times of day, and which ar
192 reating this disease remains a challenge, as seizures manifest through mechanisms and features that s
193 tically reduced the frequency of spontaneous seizures measured at 5 months without modifying the aver
196 veness in two of the most widely used animal seizure models, namely, the maximal electroshock (MES) t
198 ute encephalopathy syndromes, simple febrile seizures (n = 14), other seizures (n = 16), acute ataxia
199 mes, simple febrile seizures (n = 14), other seizures (n = 16), acute ataxia (n = 4), and other subac
200 [5%]), brain oedema (eight [2%] vs 11 [3%]), seizure (nine [2%] vs eight [2%]), and headache (six [2%
201 no evidence of transient ischemic attack or seizure, no acute lesion on diffusion-weighted imaging,
202 age at onset of epilepsy, history of febrile seizures, number of seizures before remission, absence o
205 patients in the placebo group (P=0.001), and seizures occurred in 0.7% and 0.1%, respectively (P=0.00
206 greatest predictive value were coma (31% had seizures; odds ratio [OR] = 1.8, p < 0.01) and history o
211 dinal course of epilepsy nor the patterns of seizure onset and remission have been described in Rett
216 The inclusion criteria were (1) pediatric seizure onset with ongoing seizure activity in adulthood
217 al distribution of spikes in relation to the seizure onset zone as well as anatomical regions of the
219 esia, scoliosis, gastrostomy feeding, age of seizure onset, and late age of diagnosis were independen
220 g stimulation of hyperperfused areas outside seizure onset, positive significant correlations between
222 visual cortex is also more likely to provoke seizures or pre-seizure activity in patients with photos
223 Ten patients with 11 episodes of serial seizures or status epilepticus, who underwent MRI and (1
225 often arise before the onset of spontaneous seizures, or independent from them, yet the mechanisms i
230 re Ab positive were more likely to have good seizure outcome than were patients with epilepsy of unkn
232 edictors of seizure recurrence and long-term seizure outcomes and to produce nomograms for estimation
236 s.SIGNIFICANCE STATEMENT We describe a novel seizure pattern peculiar of the olfactory cortex that re
239 ated cells mediate epileptogenesis, but that seizures per se are initiated elsewhere in the circuit.
241 Following this common beginning, however, seizures persist and propagate both locally and into hom
243 VGSC gene, Scn8a, contribute to two distinct seizure phenotypes: (1) hypoexcitation of cortical circu
247 es of Dravet syndrome, including spontaneous seizures, premature death and seizures triggered by hype
250 many clinical features were associated with seizure prevalence; frequency of hospitalizations, inabi
251 Thus, while their roles may evolve during seizures, PV+ and SOM+ interneurons ultimately help main
252 of our study were to identify predictors of seizure recurrence and long-term seizure outcomes and to
256 tment protected against hyperthermia-induced seizures, reduced spontaneous seizure frequency and prol
257 the pathophysiology of epileptic disorders, seizures remain poorly controlled in approximately one-t
260 n of cortical circuits leading to convulsive seizure resistance, and (2) hyperexcitation of thalamoco
262 ce of LPDs and GPDs also conferred increased seizure risk (37% frequent vs 45% abundant/continuous, O
265 rface and cortical thickening that result in seizures, severe neurological impairment and development
266 rgery with respect to the score on the Hague Seizure Severity scale (difference, 19.4; 95% confidence
267 condary outcomes were the score on the Hague Seizure Severity scale, the Binet-Kamat intelligence quo
269 e to predict the future onset of spontaneous seizures.SIGNIFICANCE STATEMENT Postinjury epilepsy is a
270 effect of treatment on hyperthermia-induced seizures, spontaneous seizure frequency and survival.
271 mouse visual areas to demonstrate that these seizures start as local synchronous activation and then
274 eurologic injury was defined as brain death, seizures, stroke, and intracranial hemorrhage occurring
275 ot, however, cause an immediate reduction in seizures, suggesting that peri-insult generated cells me
277 pairments, the degree of neuropathology, and seizure susceptibility, after pediatric brain injury in
280 mediator of post-traumatic astrogliosis and seizure susceptibility.SIGNIFICANCE STATEMENT Epilepsy i
281 ate the neuronal network dynamics underlying seizure termination and the postictal generalized EEG su
284 These findings may guide the development of seizure therapy dosing paradigms with improved risk/bene
285 itude titrations of motor threshold (MT) and seizure threshold (ST) in four nonhuman primates (NHPs)
287 V-containing neurons transiently reduced the seizure threshold of the mice but induced neither acute
289 t syndrome, including those who did not have seizures throughout the study, those who had frequent re
290 e data with data of a computational model of seizures to elucidate the neuronal network dynamics unde
292 onset epileptic encephalopathy with multiple seizure types that are often refractory to conventional
295 characterized by brief (seconds) spontaneous seizures, which involve spike-wave discharges (SWDs) in
296 nce of a seizure in the next year (COSY) for seizures with impaired awareness in those experiencing a
297 of the olfactory cortex that resembles focal seizures with low-voltage fast activity at onset observe
298 duration and severity in CD rats after acute seizures with subsequent reduction in interictal spiking
299 no epileptiform findings on EEG, the risk of seizures within 72 hours was between 9% (no clinical ris
300 es, featuring early-onset ataxia and absence seizure without significant alterations in the basic pro
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