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1 used as a non-pharmacological treatment for refractory epilepsy.
2 oglia was also reported in human cortex from refractory epilepsy.
3 n appear to be more prevalent in people with refractory epilepsy.
4 mmon cause of death in patients with chronic refractory epilepsy.
5 the leading cause of death in patients with refractory epilepsy.
6 ions of the epileptogenic zone for medically refractory epilepsy.
7 from nine human participants with medically refractory epilepsy.
8 rmine the longer term outcome in people with refractory epilepsy.
9 focal cortical dysplasia (FCD) is early life refractory epilepsy.
10 ho underwent resective surgery for medically refractory epilepsy.
11 opment (MCDs) are a major cause of medically refractory epilepsy.
12 valuate patients treated with vigabatrin for refractory epilepsy.
13 ysiological monitoring for pharmacologically refractory epilepsy.
14 ical trials targeting Pgp expression in drug-refractory epilepsy.
15 rapy for selected individuals with medically refractory epilepsy.
16 drug (AED) treatment and those children with refractory epilepsy.
17 dult patients meeting a strict definition of refractory epilepsy.
18 s, during the presurgical evaluation of drug-refractory epilepsy.
19 may explain the relatively high incidence of refractory epilepsy.
20 orpus callosum in 22 patients with medically refractory epilepsy.
21 markedly from that observed in patients with refractory epilepsy.
22 ) from interictal SPECT for 53 patients with refractory epilepsy.
23 er or lesser extent and is often manifest as refractory epilepsy.
24 ble seizure focus in pediatric patients with refractory epilepsy.
25 le in the diagnostic evaluation of medically refractory epilepsy.
26 ort for patients with intractable, medically refractory epilepsy.
27 ds as potential anticonvulsant compounds for refractory epilepsies.
28 alysed the ECG recordings of 185 people with refractory epilepsy and 178 controls without epilepsy.
30 iets has been used for the treatment of drug-refractory epilepsy and for neurodegenerative diseases,
31 we securely implicate PPP3CA in early-onset refractory epilepsy and further support the emerging rol
32 s who were thereafter operated on because of refractory epilepsy and had a follow-up period of at lea
34 an effective and semi-invasive treatment for refractory epilepsy and other neurological disorders.
35 ion has also been reported in other types of refractory epilepsy and our understanding of how miRNA l
36 shown to be up-regulated in animal models of refractory epilepsy, and adding a Pgp inhibitor to treat
37 et generalized hypotonia, psychomotor delay, refractory epilepsy, and elevated lactate in the blood a
38 In 20% of potential surgical candidates with refractory epilepsy, current optimal MRI does not identi
39 data from rare patients (Ps) with medically refractory epilepsy, enabling us to test the hypothesis
40 expressed in brain tissue from patients with refractory epilepsy; expression has been shown in glia a
41 the majority of TSC patients with medically refractory epilepsy following treatment with everolimus.
42 We examined expression of MDR1 and MRP1 in refractory epilepsy from three common causes, dysembryop
43 ically resected specimens from patients with refractory epilepsy have led to the development of two h
46 which is the most common cause of medically refractory epilepsy in the pediatric population and the
49 er characterized by cognitive disability and refractory epilepsy, is often caused by heterozygous mut
51 on the duration of seizures in patients with refractory epilepsy, little is known about the duration
54 lities, to heterogeneous, but generally more refractory epilepsies, often with a history of febrile s
56 onged PGES (>50 seconds) appears to identify refractory epilepsy patients who are at risk of SUDEP.
57 rolled epilepsy, patients with chronic, drug-refractory epilepsy persistently expressed the acetylate
59 ercent (approximately 5% per year) of a drug refractory epilepsy population obtained a 6-month termin
62 ation of epileptogenic foci in patients with refractory epilepsy remains a significant diagnostic cha
63 stance proteins in tissue from patients with refractory epilepsy suggests one possible mechanism for
64 gimen; its effectiveness in the treatment of refractory epilepsy suggests that the mechanisms underly
66 nlikely to contribute to the pathogenesis of refractory epilepsy through transport of carbamazepine o
67 ed in ictal SPECT in pediatric patients with refractory epilepsy, to compare the patterns of ictal an
69 th malformations of cortical development and refractory epilepsy underwent five consecutive sessions
70 pileptic drug in a cohort of 155 people with refractory epilepsy was previously reported after a medi
72 6 years) who underwent surgery for medically refractory epilepsy were compared with histopathologic f
73 ith confirmed diagnosis of TSC and medically refractory epilepsy were treated for a total of 12 weeks
74 18% (95% CI 0.316% to 0.320%) in people with refractory epilepsy who underwent video-EEG monitoring.
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