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1 in approximately one-third of patients with mesial temporal lobe epilepsy.
2 saccharide (LPS) administration in mice with mesial temporal lobe epilepsy.
3 ion with seizure susceptibility in mice with mesial temporal lobe epilepsy.
4 the hippocampal network in a mouse model of mesial temporal lobe epilepsy.
5 es and seizures in patients with intractable mesial temporal lobe epilepsy.
6 duced in schizophrenia, major depression and mesial temporal lobe epilepsy.
7 pocampal-dependent learning in patients with mesial temporal lobe epilepsy.
8 d in the seizure-onset zone of patients with mesial temporal lobe epilepsy.
9 a key brain region in the pathophysiology of mesial temporal lobe epilepsy.
10 res in 26 patients with surgically confirmed mesial temporal lobe epilepsy.
11 is the usual mode of inheritance in familial mesial temporal lobe epilepsy.
12 n alternative to open surgery for unilateral mesial temporal lobe epilepsy.
13 be a treatment option for some patients with mesial temporal lobe epilepsy.
14 to the hypothesis that TEA is a syndrome of mesial temporal lobe epilepsy.
15 sprouting in both clinical and experimental mesial temporal lobe epilepsy.
16 y underlie other disorders of homeostasis in mesial temporal lobe epilepsy.
17 ostictal secretion of luteinizing hormone in mesial temporal lobe epilepsy.
18 s altered minimally by severe neuron loss in mesial temporal lobe epilepsy.
19 jection of kainic acid, and in patients with mesial temporal lobe epilepsy.
20 l subjects and nine patients with unilateral mesial temporal lobe epilepsy.
21 can be present in up to 50% of patients with mesial temporal lobe epilepsy.
22 is not the sole determinant of cBZR loss in mesial temporal lobe epilepsy.
24 one patients were studied, including 30 with mesial temporal lobe epilepsy and 31 with focal neocorti
25 olume effect in six patients with refractory mesial temporal lobe epilepsy and a quantitative MRI dia
26 es in MRIs from 62 patients with intractable mesial temporal lobe epilepsy and in 20 normal controls.
27 on" within a well-characterized patient with mesial temporal lobe epilepsy and thus has potential med
28 ients), and in nine patients with refractory mesial temporal lobe epilepsy and unilateral hippocampal
29 the most common neuropsychological effect of mesial temporal lobe epilepsy, and because the underlyin
30 eurologic disorders, including encephalitis, mesial temporal lobe epilepsy, and multiple sclerosis.
32 n neuropathological finding in patients with mesial temporal lobe epilepsy, but its role in epileptog
33 order to detect bilateral changes of cBZR in mesial temporal lobe epilepsy due to hippocampal scleros
34 ZR) binding restricted to the hippocampus in mesial temporal lobe epilepsy due to unilateral hippocam
35 teinizing hormone secretion in patients with mesial temporal lobe epilepsy during two 24-hour epochs:
36 al and neurophysiological features of 20 new mesial temporal lobe epilepsy families including 51 affe
38 (rather than chance aggregation) in familial mesial temporal lobe epilepsy has come from twin studies
39 hood, the majority of people with refractory mesial temporal lobe epilepsy have their initial onset i
41 derstanding of the processes associated with mesial temporal lobe epilepsy in humans and in experimen
42 forgetting in a status epilepticus model of mesial temporal lobe epilepsy in rats, which is associat
49 (18 men and 20 women; aged >/=12 years) had mesial temporal lobe epilepsy (MTLE) and disabling seizu
50 the generation of seizures in patients with mesial temporal lobe epilepsy (MTLE) and hippocampal scl
51 ule cells (DGCs) are altered in experimental mesial temporal lobe epilepsy (mTLE) and whether their i
52 ing was chronically lost in a mouse model of mesial temporal lobe epilepsy (MTLE) as well as in hippo
53 (cBZRs) are restricted to the hippocampus in mesial temporal lobe epilepsy (mTLE) caused by unilatera
54 One is that 1 or more particular subtypes of mesial temporal lobe epilepsy (mTLE) exist that are part
60 However, the role of BK channels in acquired mesial temporal lobe epilepsy (MTLE) remains unknown.
63 ood flow changes in a group of patients with mesial temporal lobe epilepsy (MTLE) using the technique
65 ell firing is affected in an animal model of mesial temporal lobe epilepsy (MTLE), a disease accompan
66 tive treatment for patients with intractable mesial temporal lobe epilepsy (mTLE), a third of patient
67 the hippocampus of rodents and patients with mesial temporal lobe epilepsy (MTLE), but recently pHFOs
68 as a likely trigger of epileptic seizures in mesial temporal lobe epilepsy (MTLE), but the underlying
69 psy (NTLE), differ from those diagnosed with mesial temporal lobe epilepsy (MTLE), e.g., in hippocamp
71 er left anterior temporal lobe resection for mesial temporal lobe epilepsy (mTLE), we tested for the
77 s electroencephalography among patients with mesial temporal lobe epilepsy (MTLE; n = 64), those with
78 rontal-parietal epilepsy (FPE) progresses to mesial-temporal lobe epilepsy (MTLE) with dual pathology
80 anial EEG recordings from five patients with mesial temporal lobe epilepsy obtained during evaluation
82 usefulness of the measure in a test case of mesial temporal lobe epilepsy: the SI can be readily cal
84 ed in the entorhinal cortex of patients with mesial temporal lobe epilepsy using local field potentia
86 6 patients with medically intractable, focal mesial temporal lobe epilepsy who had been screened for
88 ere we compared miRNA expression patterns in mesial temporal lobe epilepsy with and without hippocamp
89 new direction to biological understanding of mesial temporal lobe epilepsy with hippocampal sclerosis
90 ed a genome-wide significant association for mesial temporal lobe epilepsy with hippocampal sclerosis
92 sclerosis are typically drug-resistant, and mesial temporal lobe epilepsy with hippocampal sclerosis
94 ry of febrile seizures, we tested cases with mesial temporal lobe epilepsy with hippocampal sclerosis
95 ral syndromes, amongst the most common being mesial temporal lobe epilepsy with hippocampal sclerosis
96 e-wide association study in 1018 people with mesial temporal lobe epilepsy with hippocampal sclerosis
97 endent sample set comprising 959 people with mesial temporal lobe epilepsy with hippocampal sclerosis
98 ly reproduces the defining features of human mesial temporal lobe epilepsy with hippocampal sclerosis
99 es (NAbs) in a large consecutive series with mesial temporal lobe epilepsy with hippocampal sclerosis
100 rocyte dysfunction might be a prime cause of mesial temporal lobe epilepsy with sclerosis and identif
101 found that the hippocampus of patients with mesial temporal lobe epilepsy with sclerosis is complete
102 Fate mapping confirmed that in the course of mesial temporal lobe epilepsy with sclerosis, astrocytes
103 e glial changes represent cause or effect of mesial temporal lobe epilepsy with sclerosis, we develop
105 in hippocampal specimens from patients with mesial temporal lobe epilepsy without (n = 44) and with
106 es and seizures in patients with intractable mesial temporal lobe epilepsy, without affecting memory.
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