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1 vasive, non-pharmacological intervention for refractory epilepsy.
2 ng cause of premature death in patients with refractory epilepsy.
3 oop chemo-optogenetic strategy to treat drug-refractory epilepsy.
4 $135 million (95% CI $111-$159 million) for refractory epilepsy.
5 -surgical outcome in patients with medically refractory epilepsy.
6 novel microbiome-guided approaches to treat refractory epilepsy.
7 f ganaxolone in patients with CDD-associated refractory epilepsy.
8 leveraging big data in surgical planning for refractory epilepsy.
9 used as a non-pharmacological treatment for refractory epilepsy.
10 from nine human participants with medically refractory epilepsy.
11 s, during the presurgical evaluation of drug-refractory epilepsy.
12 orpus callosum in 22 patients with medically refractory epilepsy.
13 ort for patients with intractable, medically refractory epilepsy.
14 oglia was also reported in human cortex from refractory epilepsy.
15 n appear to be more prevalent in people with refractory epilepsy.
16 mmon cause of death in patients with chronic refractory epilepsy.
17 the leading cause of death in patients with refractory epilepsy.
18 ions of the epileptogenic zone for medically refractory epilepsy.
19 rmine the longer term outcome in people with refractory epilepsy.
20 focal cortical dysplasia (FCD) is early life refractory epilepsy.
21 ho underwent resective surgery for medically refractory epilepsy.
22 opment (MCDs) are a major cause of medically refractory epilepsy.
23 valuate patients treated with vigabatrin for refractory epilepsy.
24 ysiological monitoring for pharmacologically refractory epilepsy.
25 ical trials targeting Pgp expression in drug-refractory epilepsy.
26 rapy for selected individuals with medically refractory epilepsy.
27 drug (AED) treatment and those children with refractory epilepsy.
28 dult patients meeting a strict definition of refractory epilepsy.
29 may explain the relatively high incidence of refractory epilepsy.
30 markedly from that observed in patients with refractory epilepsy.
31 ) from interictal SPECT for 53 patients with refractory epilepsy.
32 er or lesser extent and is often manifest as refractory epilepsy.
33 ble seizure focus in pediatric patients with refractory epilepsy.
34 le in the diagnostic evaluation of medically refractory epilepsy.
35 iduals undergoing presurgical monitoring for refractory epilepsy.
36 e consistent with the hallmarks of medically refractory epilepsy.
37 ds as potential anticonvulsant compounds for refractory epilepsies.
39 cross 759 implantations in 724 patients with refractory epilepsy (368 male, 354 female, two unspecifi
40 For the large population of people with drug-refractory epilepsy, alternative treatment approaches ar
41 alysed the ECG recordings of 185 people with refractory epilepsy and 178 controls without epilepsy.
43 from the sensorimotor cortex of people with refractory epilepsy and classified five facial expressio
44 iets has been used for the treatment of drug-refractory epilepsy and for neurodegenerative diseases,
45 we securely implicate PPP3CA in early-onset refractory epilepsy and further support the emerging rol
46 s who were thereafter operated on because of refractory epilepsy and had a follow-up period of at lea
47 parently more severe clinical phenotype with refractory epilepsy and intellectual disability but a no
49 an effective and semi-invasive treatment for refractory epilepsy and other neurological disorders.
50 ion has also been reported in other types of refractory epilepsy and our understanding of how miRNA l
51 nt stimulation (ctDCS), has emerged to treat refractory epilepsy and seizures, although the cellular-
52 unctive treatment option for e.g. medication-refractory epilepsy and treatment-resistant depression.
53 shown to be up-regulated in animal models of refractory epilepsy, and adding a Pgp inhibitor to treat
54 essive spasticity, choreoathetoid movements, refractory epilepsy, and brain atrophy were part of the
55 et generalized hypotonia, psychomotor delay, refractory epilepsy, and elevated lactate in the blood a
56 e treatment of last resort for some cases of refractory epilepsy, and this has been among the stronge
57 ata from a cohort of patients with medically refractory epilepsy as they completed a visual recogniti
59 In 20% of potential surgical candidates with refractory epilepsy, current optimal MRI does not identi
60 dividuals had neurodegenerative disease with refractory epilepsy, developmental regression, and reduc
61 neurodevelopmental diseases characterized by refractory epilepsy, distinct electroencephalographic an
62 data from rare patients (Ps) with medically refractory epilepsy, enabling us to test the hypothesis
63 expressed in brain tissue from patients with refractory epilepsy; expression has been shown in glia a
64 the majority of TSC patients with medically refractory epilepsy following treatment with everolimus.
65 We examined expression of MDR1 and MRP1 in refractory epilepsy from three common causes, dysembryop
66 ically resected specimens from patients with refractory epilepsy have led to the development of two h
68 surgical planning in patients with medically refractory epilepsy; however, their spatial and temporal
69 ity with promising therapeutic potential for refractory epilepsy; however, tools for examining FUS ef
71 sy (mTLE), the most common form of medically refractory epilepsy in adults, is usually associated wit
73 which is the most common cause of medically refractory epilepsy in the pediatric population and the
76 ria, congenital macrocephaly and early-onset refractory epilepsy, in keeping with other mTOR-opathies
77 er characterized by cognitive disability and refractory epilepsy, is often caused by heterozygous mut
79 on the duration of seizures in patients with refractory epilepsy, little is known about the duration
83 Planning surgery for patients with medically refractory epilepsy often requires recording seizures us
84 lities, to heterogeneous, but generally more refractory epilepsies, often with a history of febrile s
85 timulation offers a therapeutic approach for refractory epilepsy patients ineligibles for resective s
87 onged PGES (>50 seconds) appears to identify refractory epilepsy patients who are at risk of SUDEP.
88 rolled epilepsy, patients with chronic, drug-refractory epilepsy persistently expressed the acetylate
90 ercent (approximately 5% per year) of a drug refractory epilepsy population obtained a 6-month termin
93 ation of epileptogenic foci in patients with refractory epilepsy remains a significant diagnostic cha
95 stance proteins in tissue from patients with refractory epilepsy suggests one possible mechanism for
96 gimen; its effectiveness in the treatment of refractory epilepsy suggests that the mechanisms underly
97 t syndrome (DS) is a devastating early-onset refractory epilepsy syndrome caused by variants in the S
100 nlikely to contribute to the pathogenesis of refractory epilepsy through transport of carbamazepine o
103 ed in ictal SPECT in pediatric patients with refractory epilepsy, to compare the patterns of ictal an
105 ing a memory task in patients with medically refractory epilepsy undergoing depth electrode monitorin
106 th malformations of cortical development and refractory epilepsy underwent five consecutive sessions
107 pileptic drug in a cohort of 155 people with refractory epilepsy was previously reported after a medi
109 6 years) who underwent surgery for medically refractory epilepsy were compared with histopathologic f
110 ith confirmed diagnosis of TSC and medically refractory epilepsy were treated for a total of 12 weeks
111 my is a neurosurgical procedure for treating refractory epilepsy, which entails disconnecting a signi
112 ctively recruited 52 patients with medically refractory epilepsy who underwent standard pre-surgical
114 18% (95% CI 0.316% to 0.320%) in people with refractory epilepsy who underwent video-EEG monitoring.