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1 inguishing between epileptic and psychogenic convulsive seizures.
2 ng of treatment relative to the cessation of convulsive seizures.
3 acute group I mGluR-dependent propensity for convulsive seizures.
4 gy through blood-brain barrier breakdown and convulsive seizures.
5 lsant pentylenetetrazole-induced generalized convulsive seizures.
6 rosis), a history of secondarily generalised convulsive seizures (2.3; 95% CI 1.7 to 3.0 for these se
7 1) a strong IEGP response to kainate-induced convulsive seizures, (2) no IEGP response after prolonga
8 arlier were video-monitored for spontaneous, convulsive seizures 9 hr/day every day for 24-36 days.
9 e hypersynchronization and nonconvulsive and convulsive seizures, accompanied by expression changes i
10 se is a strain that is highly susceptible to convulsive seizures after repeated sensory stimulation.
12 ctal arrhythmias were mostly found following convulsive seizures and often associated with (near) SUD
13 eizure phenotype associated with spontaneous convulsive seizures and profound deficits in hippocampus
14 on of consciousness occurs after generalized convulsive seizures, and includes analgesia, lasting for
15 sorder that includes both convulsive and non-convulsive seizures, and is dependent upon Celf4 gene do
16 seizures (lightning-like jerks), generalized convulsive seizures, and varying degrees of neurological
17 esults suggest that local anesthetic-induced convulsive seizures are mediated by excitatory glutamate
19 milial Alzheimer's disease transgene-induced convulsive seizures did not occur in mice lacking PrP(C)
22 nnabidiol resulted in a greater reduction in convulsive-seizure frequency than placebo and was associ
23 patients who had at least a 50% reduction in convulsive-seizure frequency was 43% with cannabidiol an
24 that were validated in EEG recordings of 48 convulsive seizures from 48 subjects with refractory foc
25 (SUDEP) that exhibit audiogenic generalized convulsive seizures (GCS), ending in death due to respir
26 One serious adverse effect of these drugs is convulsive seizures; however, the mechanisms underlying
27 Certain anti-convulsant drugs, as well as convulsive seizures impede recovery when administered du
28 l symptoms, as well as spontaneous recurrent convulsive seizures in 45% and epileptiform spikes in 10
29 umented to exert a protective action against convulsive seizures in animal models, when administered
31 5-year seizure freedom (eg, a normal MRI and convulsive seizures in the previous year has a probabili
32 spinal cord in several forms of generalized convulsive seizures, including audiogenic seizures (AGS)
35 all animals as did the total duration of non-convulsive seizures (NCS) in the alpha-chloralose-anesth
36 was to elucidate the effects of generalized convulsive seizures on distinct and separate corticotrop
37 ce (n = 9) had increased numbers of observed convulsive seizures (P = 0.004), a higher total seizure
39 e minutes or more) or repetitive generalized convulsive seizures received intravenous diazepam (5 mg)
40 poexcitation of cortical circuits leading to convulsive seizure resistance, and (2) hyperexcitation o
41 FPI-treated rats developed nonconvulsive or convulsive seizures that could be distinguished electrog
44 es, with or without progression to bilateral convulsive seizures, was the most common seizure type.
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