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1 eizures and a long history of drug-resistant focal epilepsy.
2 al neuronal activity, especially intractable focal epilepsy.
3 ppealing for selected people with refractory focal epilepsy.
4  mechanisms generating these events in human focal epilepsy.
5 guage function for presurgical evaluation of focal epilepsy.
6 ith localized pathology, such as intractable focal epilepsy.
7 table epilepsy may be delayed, especially in focal epilepsy.
8  in 63 consecutively recruited patients with focal epilepsy.
9 al development often suffer from intractable focal epilepsy.
10 surgical outcome in patients with refractory focal epilepsy.
11 ribute to the development and maintenance of focal epilepsy.
12 is valuable for understanding drug-resistant focal epilepsy.
13 tical circuits and may lead to generation of focal epilepsy.
14 s in the electroencephalogram of people with focal epilepsy.
15 NPRL2 and NPRL3, also contribute to cases of focal epilepsy.
16 h FCD or magnetic resonance imaging-negative focal epilepsy.
17 ing reveals most cerebral lesions underlying focal epilepsy.
18 is an effective treatment for drug-resistant focal epilepsy.
19 ality in patients with medically intractable focal epilepsy.
20                   Of these, 46,995 (47%) had focal epilepsy.
21  of structural and functional disruptions in focal epilepsy.
22 ncing to analyze 404 unrelated probands with focal epilepsy.
23 d mutations in DEPDC5 as a cause of familial focal epilepsy.
24 ery is an effective treatment for refractory focal epilepsy.
25 al treatments or therapies for some forms of focal epilepsy.
26 tients, with difficult to localise and treat focal epilepsy.
27 s in >10% of small families with nonlesional focal epilepsy.
28 was restricted to offspring of probands with focal epilepsy.
29 al delay as well as 1 individual with ID and focal epilepsy.
30 epilepsy and 27% (standard deviation 5%) for focal epilepsy.
31 ampled at 2,048 Hz in people with refractory focal epilepsy.
32  2.6 (95% confidence interval 1.19-4.26) for focal epilepsy.
33  2.5 (95% confidence interval 0.92-4.00) for focal epilepsy.
34  delay as well as of ID with childhood onset focal epilepsy.
35 e lateralization in children with left-sided focal epilepsy.
36 ment, most of whom were newly diagnosed with focal epilepsy.
37 ortant risk factors for both generalized and focal epilepsies.
38 tudy in epilepsy has been published, for the focal epilepsies.
39  emerged as a major gene mutated in familial focal epilepsies.
40 3 patients (mean age 25 +/- 11 years); (iii) focal epilepsy, 15 patients (mean age 25 +/- 9 years).
41 obands with either generalized (2.5-fold) or focal epilepsy (2.6-fold) may reflect some coexisting sh
42 ve seizures from 48 subjects with refractory focal epilepsy (20 females, age range 15-61 years).
43              All patients had drug-resistant focal epilepsy, 5 of them underwent surgery, and 1 had a
44 ysed data from 612 consecutive patients with focal epilepsy admitted to a video-EEG Telemetry Unit fo
45 nance in patients with medically intractable focal epilepsies against the results of an intracarotid
46    However, the similar increase in risk for focal epilepsy among relatives of probands with either g
47  epilepsy (TLE) is the most frequent form of focal epilepsies and is generally associated with malfun
48 es, were a prominent feature of MRI-negative focal epilepsies and may represent neuronal migration di
49                 We studied 220 patients with focal epilepsy and 118 healthy volunteers who performed
50  recordings during sleep in 15 patients with focal epilepsy and 15 control subjects.
51 ay have a role in preoperative evaluation of focal epilepsy and can be extended to identify GM pathol
52 ce imaging was performed in 51 children with focal epilepsy and left-sided lesions and 36 healthy con
53 families with multiple members affected with focal epilepsy and linkage analysis on one of these.
54 d in 44 patients with refractory neocortical focal epilepsy and normal optimal MRI.
55 tudy both long-range network disturbances in focal epilepsy and regional connectivity at the epilepto
56 ptimal use and interpretation of EEG-fMRI in focal epilepsy and suggest a possible role for EEG-fMRI
57  these pathways play a central role in human focal epilepsy and that they are important currently une
58 ng pathways) are genetically associated with focal epilepsy and, hence, likely causal.
59 UK patients with epilepsy, of which 958 have focal epilepsy, and 5129 population control subjects, wi
60 l connectivity are observed in patients with focal epilepsy, and may reflect deleterious long-term ef
61 of the genetic influences on generalized and focal epilepsies are distinct.
62                                              Focal epilepsies are the most common form observed and h
63                                Children with focal epilepsy are at increased risk of language impairm
64 e molecular mechanisms underlying refractory focal epilepsy are poorly defined, we performed transcri
65                            Some patients had focal epilepsy associated with brain malformations.
66 ts from 4 families with DEPDC5 mutations and focal epilepsy associated with FCD were recruited and in
67 t can bring seizure remission in people with focal epilepsy but requires careful selection of candida
68 ion effects can be detected in patients with focal epilepsy by using a phase-cycled stimulus-induced
69 oral lobe epilepsy, the most common cause of focal epilepsy, can control seizures and improve quality
70               Seizure patterns identified in focal epilepsies caused by diverse etiologies are likely
71  in humans and in different animal models of focal epilepsy correlates with reduction of neuronal fir
72 ing that although the clinical definition of focal epilepsy does identify a genetically distinct epil
73                                Patients with focal epilepsy due to malformations of cortical developm
74  treatment of drug-resistant DEPDC5-positive focal epilepsies, even if the MRI is unremarkable.
75 e have identified NPRL2 and NPRL3 as two new focal epilepsy genes that also play a role in the mTOR-s
76                      The patient with ID and focal epilepsy had a missense mutation in the extracellu
77 ncreasingly used as treatment for refractory focal epilepsy; however, few rigorous reports of long-te
78 can lead to seizure freedom in patients with focal epilepsy; however, sometimes it fails due to an in
79 ome sequencing analysis of two families with focal epilepsy identified NPRL2 and NPRL3 as the top can
80 s are the most significant cause of familial focal epilepsy identified to date, including cases with
81 oral lobe epilepsy (mTLE) is the most common focal epilepsy in adults and is often refractory to medi
82  Here we use a mouse cortical slice model of focal epilepsy in which the epileptogenic focus can be i
83          For patients with pharmacoresistant focal epilepsy in whom surgical resection of the epilept
84 f268 and c-fos, were investigated in chronic focal epilepsy induced by tetanus toxin (TT, 20-35 ng) i
85                                              Focal epilepsy involves excessive cortical activity that
86                                  Intractable focal epilepsy is a devastating disorder with profound e
87                                              Focal epilepsy is commonly pharmacoresistant, and resect
88 tifactorial model of white matter atrophy in focal epilepsy is proposed.
89 sess how similar the genetic architecture of focal epilepsy is to that of non-focal epilepsy; we demo
90 epilepsy, the most prevalent form of chronic focal epilepsy, is associated with a high prevalence of
91             Twenty children with intractable focal epilepsy (mean age +/- SD, 11 +/- 4 y; age range,
92 n 172 patients suffering from drug-resistant focal epilepsy (mean age 25.6, standard deviation 11.6;
93 8, 4-12 years, 24 females) and children with focal epilepsy (n = 21, 5-12 years, nine females) with l
94                   For people with refractory focal epilepsy, neurosurgical resection offers the possi
95     Individuals with left-sided, early-onset focal epilepsy often show atypical (i.e. bilateral or ri
96 rol seizures in patients with drug-resistant focal epilepsy, often leading to improvements in cogniti
97 onance imaging we investigated the impact of focal epilepsy on the developing language system using m
98  We describe first cousin sibling pairs with focal epilepsy, one of each pair having focal cortical d
99 lysed in 31 consecutive medically refractory focal epilepsy patients, evaluated by stereo-electroence
100               In our cohort of 404 unrelated focal epilepsy patients, we identified five mutations in
101        MRI-negative (MRI-) pharmacoresistant focal epilepsy (PFE) patients are most challenging for e
102  (MRI(-) or "nonlesional") pharmacoresistant focal epilepsy (PFE) patients, discovering a previously
103 In the Scn2a(Q54) mouse model of epilepsy, a focal epilepsy phenotype is caused by transgenic express
104 brile seizures-but included more adults with focal epilepsies (rather than the idiopathic generalised
105 rder Amish children with cortical dysplasia, focal epilepsy, relative macrocephaly, and diminished de
106              In patients with drug-resistant focal epilepsy requiring surgery, hippocampal sclerosis
107 otential surgical candidates with refractory focal epilepsy, standard MRI does not identify the cause
108                In relatives of probands with focal epilepsy, standardized incidence ratios were 1.0 (
109 PDC5 loss-of-function mutations in different focal epilepsy syndromes.
110 c zone in patients with medically refractory focal epilepsy than (18)F-FDG PET.
111 arges in patients with medically intractable focal epilepsy undergoing diagnostic workup for localiza
112                          Eight patients with focal epilepsy undergoing presurgical surface and intrac
113 -TLE, n = 26) was studied as an archetype of focal epilepsy, using fixel-based analysis of diffusion-
114                             In patients with focal epilepsies, we detected primarily global increases
115 t clinical examination of four subjects with focal epilepsy, we confirm a similar correlation of temp
116 itecture of focal epilepsy is to that of non-focal epilepsy; we demonstrate both significant differen
117 pilepsy women and women with generalized and focal epilepsy were investigated during ovulatory (n=11,
118 ta in 23 patients with medically intractable focal epilepsy were retrospectively analyzed.
119 ations in patients with febrile seizures and focal epilepsy, which encompasses the temporal lobe epil
120 ise as a novel approach to treat intractable focal epilepsy while minimizing disruption of normal cir
121 eciated in patients with treatment-resistant focal epilepsy who are treated with surgery, as some may
122                             In patients with focal epilepsy who can benefit from surgery, invasive EE
123                          Forty patients with focal epilepsy who underwent presurgical stereo-EEG (SEE
124   To investigate the spatiotemporal scale of focal epilepsy, wide-bandwidth electrophysiological reco
125 rging from West syndrome (two patients), and focal epilepsies with an electrical status epilepticus d
126 y identified DEPDC5 as the gene for familial focal epilepsy with variable foci and found mutations in

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