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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
34              Serious adverse events included seizure (18 [5%] vs 22 [6%]) and brain oedema (seven [2%
35  video-monitored for spontaneous, convulsive seizures 9 hr/day every day for 24-36 days.
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.
42                                              Seizure activity, in particular status epilepticus, incr
43  and [Cl(-)]i in response to hypercapnia and seizure activity.
44 r fMRI responses are much less predictive of seizure activity.
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
47 ntal delay, intellectual disability, ataxia, seizures and a happy affect.
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
53     In parallel, it reduced the incidence of seizures and delayed their occurrence.
54 llectual disability syndrome associated with seizures and dysmorphic features.
55 impairment, as well as generalized and focal seizures and EEG abnormalities for patients with gain- a
56 ost presented in the first week of life with seizures and encephalopathy.
57               These individuals are prone to seizures and have high brain levels of the inflammatory
58 fects of toxic exposure in these animals are seizures and hippocampal damage, and they have been prop
59                      In animal studies, both seizures and interictal spikes induce synaptic potentiat
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
62 g countries, where it is a frequent cause of seizures and other neurological disease.
63 to consider redefining the continuum between seizures and PDs, suggesting that additional damage afte
64 d onset epilepsies with medication-resistant seizures and poor developmental outcomes.
65 res on CEEG is dependent on history of prior seizures and presence of coma.
66 thological phenotypes, including spontaneous seizures and sudden death.
67 those experiencing auras only, those with no seizures and those with continuing seizures.
68 r progression corresponded with the onset of seizures and tumor invasion.
69 atency period (and thus predict the onset of seizures) and with the power change of the high-gamma rh
70 ecorded: heart failure, neurological deficit/seizure, and hemorrhage.
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
78                Because recurrent intractable seizures are a common feature of FCDs, epileptogenic ele
79                                        Focal seizures are assumed to arise from a hypersynchronous ac
80                                        Focal seizures are episodes of pathological brain activity tha
81 ctivity patterns associated with spontaneous seizures are not fully understood.
82                                  While daily seizures are uncommon in Rett syndrome, prolonged remiss
83 resenting in infancy with pharmaco-resistant seizures; are often accompanied by debilitating neuropsy
84 nical or electroencephalographic evidence of seizure around the time of the event.
85             These effects were not caused by seizures as indicated by EEG recordings.
86 e UBE3A gene, with behavioral phenotypes and seizures as key features.
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
89 to the severity of hippocampal sclerosis and seizure burden in chronic epilepsy.
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.
93                                      Kainate seizures cause an immediate, but transient, vacuolizatio
94           Recurrent high-frequency epileptic seizures cause progressive hippocampal sclerosis, which
95 e identified that, similar to electrographic seizures, cause brain tissue hypoxia, a measure of ongoi
96  developmental delay, hypotonia, early-onset seizures, cerebellar atrophy, and osteopenia.
97                                   Similar to seizures, cerebral blood flow increases in patients with
98  last year of follow-up, suggesting enduring seizure control was not regained by this timepoint.
99 denosine levels, which might have effects on seizure control.
100  for SRSE requiring pharmacological coma for seizure control.
101 o been proposed as models of complex partial seizures (CPSs) following traumatic brain injury (post-t
102 d access to high-quality, expertly annotated seizure data from prolonged recordings.
103 geons using simulated and recorded epileptic seizure data to demonstrate our system's effectiveness.
104           We combined human encephalographic seizure data with data of a computational model of seizu
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
108 s a promising target for further research on seizure disorder therapeutics.
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
116  months, most TBI mice exhibited spontaneous seizures during a 7 d video-EEG recording period.
117 campus, we control the risk of temporal lobe seizures during a specific time period.
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
120 in deaths (23.5%), 85 stroke (19.9%), and 60 seizure events (14.1%).
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
125 n withdrawal of medications in those who are seizure free is propitious.
126                               Stg/+ mice are seizure free with normal baseline beta/gamma power and n
127 obe epilepsy will not be rendered completely seizure-free after temporal lobe surgery.
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
130                   Patients who were entirely seizure-free for 1, 2 and 3 years had COSY of 4.9%, 3.5%
131 ewly diagnosed epilepsy cases fail to become seizure-free in response to antiseizure drugs.
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
134        The percentage of patients who became seizure-free was 5% with cannabidiol and 0% with placebo
135 ent and a consistent definition of long-term seizure freedom.
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 (+
138 n hyperthermia-induced seizures, spontaneous seizure frequency and survival.
139 imary end point was the change in convulsive-seizure frequency over a 14-week treatment period, as co
140                                              Seizure frequency ranged from an average of one every 3.
141                                              Seizure frequency significantly correlated with the loss
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
146 d eight multiscale recordings of spontaneous seizures from four patients with epilepsy.
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
150 ed in human visual cortex may play a role in seizure generation [1,2].
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
154 thy, encephalitis, meningitis, myelitis, and seizures have also been reported.
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
157                 To calculate the chance of a seizure in the next year (COSY) for seizures with impair
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
161          Neurosurgical treatment may improve seizures in children and adolescents with drug-resistant
162 tool to aid clinical judgment of the risk of seizures in critically ill patients.
163 lence was associated with increased risk for seizures in LPDs and GPDs.
164                        Treatment of clinical seizures in patients with Alzheimer's disease with selec
165            We propose that a risk factor for seizures in patients with photosensitive epilepsy is eng
166  into the causes of persistent postoperative seizures in patients with temporal lobe epilepsy.
167           We pharmacologically induced focal seizures in primary visual cortex (V1) of awake mice, an
168 y that viewing particular images can trigger seizures in some individuals.
169 ade, a treatment that paradoxically enhances seizures in stg/stg mice.
170                                              Seizures in temporal lobe epilepsy (TLE) disturb brain n
171  generation and propagation of temporal lobe seizures in temporal lobe epilepsy, using diffusion tens
172 ith the frequency of secondarily generalized seizures in the 3-5 days preceding the recordings.
173 metanide reduced rMF sprouting and recurrent seizures in the chronic epileptic phase.
174 nabidiol for the treatment of drug-resistant seizures in the Dravet syndrome.
175                    Independent predictors of seizures in the last year of follow-up were epilepsy dur
176 9%) of 1455 for whom data were available had seizures in their last year of follow-up, suggesting end
177                                    Recurrent seizures in TLE are associated with disturbances in ARAS
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
180 cts in normal conditions, while it prevented seizure-induced alterations of both STP and LTP.
181 have clinical implications for mechanisms of seizure-induced astrocyte injury and potential therapeut
182 ng the mTOR pathway is involved in mediating seizure-induced astrocyte injury.
183                     Our data also indicate a seizure-induced upregulation of neuronal, endothelial, a
184 e memory, the mechanisms by which early-life seizures influence them, and the means to abrogate the e
185                 Neuronal spiking activity at seizure initiation was highly heterogeneous and not hype
186                          We show that during seizure large-scale neural populations spanning centimet
187                                  Distinctive seizure-like events (SLEs) are induced in the olfactory
188 nel blocker 4-aminopyridine reliably induces seizure-like events in temporal lobe structures.
189 vity consistently preceded the initiation of seizure-like events.
190  brain reproduces many neuropathological and seizure-like hallmarks characteristic of epilepsy.
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
194  by forebrain accumulation of the convulsive seizures mediating miR-134.
195                  Complete remission off anti-seizure medications is possible, but future efforts shou
196 veness in two of the most widely used animal seizure models, namely, the maximal electroshock (MES) t
197  (MES) test and the psychomotor 6 Hz (32 mA) seizure models.
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
203                                      Febrile seizures occurred after dose 1 of MMR vaccine at a known
204                                 The onset of seizures occurred before 18 years of age in 75.9% of pat
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
207                       The frequency of total seizures of all types was significantly reduced with can
208          INTERPRETATION: The initial risk of seizures on CEEG is dependent on history of prior seizur
209  acute structural effects of kainate-induced seizures on cortical astrocytes.
210 cids rather than ketones are likely to block seizure onset and raise seizure threshold.
211 dinal course of epilepsy nor the patterns of seizure onset and remission have been described in Rett
212 gest that network mechanisms responsible for seizure onset can be region specific.
213 were compared at 3 weeks of age, the time of seizure onset for homozygous mice.
214 ozygotes, consistent with the earlier age of seizure onset in homozygotes.
215 le mechanisms underlying the different focal seizure onset patterns in the model.
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
218 rlap with those identified clinically as the seizure onset zone.
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
221  associated with classically defined absence seizures or CPSs.
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
224 of 70 to 84 and either GMFCS level 2, active seizures, or hearing with amplification.
225  often arise before the onset of spontaneous seizures, or independent from them, yet the mechanisms i
226 emotely or related to acute illness (34% had seizures; OR = 3.0, p < 0.001).
227 e, lamotrigine, and valproate had short-term seizure outcome determined.
228                                   We audited seizure outcome of 693 adults who had resective epilepsy
229 ng the International League Against Epilepsy seizure outcome scale.
230 re Ab positive were more likely to have good seizure outcome than were patients with epilepsy of unkn
231 peratively identifiable risk factors of poor seizure outcome.
232 edictors of seizure recurrence and long-term seizure outcomes and to produce nomograms for estimation
233 nor allele frequency >/= 15%) in 4 genes and seizure outcomes were assessed.
234 ct of depression on the risk of epilepsy and seizure outcomes.
235                                    The novel seizure pattern here described is not observed in other
236 s.SIGNIFICANCE STATEMENT We describe a novel seizure pattern peculiar of the olfactory cortex that re
237                                              Seizure patterns identified in focal epilepsies caused b
238           The median frequency of convulsive seizures per month decreased from 12.4 to 5.9 with canna
239 ated cells mediate epileptogenesis, but that seizures per se are initiated elsewhere in the circuit.
240                        During the latent pre-seizure period, epileptiform spikes were more frequent i
241    Following this common beginning, however, seizures persist and propagate both locally and into hom
242     By contrast, lamotrigine exacerbated the seizure phenotype.
243 VGSC gene, Scn8a, contribute to two distinct seizure phenotypes: (1) hypoexcitation of cortical circu
244                                    Epileptic seizures potently modulate hippocampal adult neurogenesi
245                       The ability to improve seizure prediction algorithms through straightforward, p
246        For all subjects, clinically relevant seizure prediction results were significant, and the add
247 es of Dravet syndrome, including spontaneous seizures, premature death and seizures triggered by hype
248                   Three distinct patterns of seizure prevalence emerged in classic Rett syndrome, inc
249 ere not significantly associated with either seizure prevalence or seizure severity.
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
253                    Independent predictors of seizure recurrence were epilepsy duration before remissi
254       The risk with this action, however, is seizure recurrence.
255 es also had to contain information regarding seizure recurrences during and after withdrawal.
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
258                 Surgical treatment can bring seizure remission in people with focal epilepsy but requ
259                                    Epileptic seizures represent altered neuronal network dynamics, bu
260 n of cortical circuits leading to convulsive seizure resistance, and (2) hyperexcitation of thalamoco
261                       It is characterised by seizures resulting from aberrant hypersynchronous neural
262 ce of LPDs and GPDs also conferred increased seizure risk (37% frequent vs 45% abundant/continuous, O
263 owever, specific features that confer higher seizure risk remain unclear.
264 sk factors and guide clinicians in assessing seizure risk.
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
268 associated with either seizure prevalence or seizure severity.
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
272 tability and is associated with pathological seizure states.
273 no common polymorphisms were associated with seizure status.
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
276                     IL-1Ra treatment reduced seizure susceptibility 2 weeks after TBI compared with v
277 pairments, the degree of neuropathology, and seizure susceptibility, after pediatric brain injury in
278 stored normal synaptic responses and reduced seizure susceptibility.
279 neurons, which could explain how AE3 reduces seizure susceptibility.
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
282  applications, such as preventing audiogenic seizures that originate in the auditory midbrain.
283 t-unilateral, and frontomedial) and magnetic seizure therapy (MST) with cap coil on vertex.
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)
286                      Here we show that SZT2 (seizure threshold 2), a metazoan-specific protein mutate
287 V-containing neurons transiently reduced the seizure threshold of the mice but induced neither acute
288  are likely to block seizure onset and raise seizure threshold.
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
291 ng spontaneous seizures, premature death and seizures triggered by hyperthermia.
292 onset epileptic encephalopathy with multiple seizure types that are often refractory to conventional
293                                              Seizure was the most common symptom, but almost 30% of e
294                                  The induced seizures were qualitatively and quantitatively indisting
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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