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1 tal delay and an intractable infantile-onset seizure disorder.
2 additional subjects, including one without a seizure disorder.
3 al disability, gastroesophageal reflux and a seizure disorder.
4 pharmacologic and surgical treatment of the seizure disorder.
5 relation has on the management of the actual seizure disorder.
6 pharmacologic and surgical treatment of the seizure disorder.
7 suggest that the deaths were related to the seizure disorder.
8 y could help identify novel therapeutics for seizure disorder.
9 sychoses to supernatural causes, followed by seizure disorder.
10 ndicating functional interactions leading to seizure disorder.
11 lepsy is a common and frequently intractable seizure disorder.
12 ted with a two-fold elevated risk for a late seizure disorder.
13 motor and cognitive impairment severity and seizure disorder.
14 f phenytoin, which had been administered for seizure disorder.
15 chiatric symptoms that are concurrent with a seizure disorder.
16 (neurocysticercosis) is a frequent cause of seizure disorders.
17 telemetry of epileptic events in humans with seizure disorders.
18 y prescribed to treat anxiety, insomnia, and seizure disorders.
19 se suggest that SCN8A may also contribute to seizure disorders.
20 interactions in the genomes of patients with seizure disorders.
21 e a therapeutic benefit for the treatment of seizure disorders.
22 cularly vulnerable to dysfunction leading to seizure disorders.
23 her therapeutic approach to the treatment of seizure disorders.
24 some spastic quadriplegic cerebral palsy and seizure disorders.
25 e of the pump in human neurodegenerative and seizure disorders.
26 genetic involvement of GABA(A) receptors in seizure disorders.
27 in investigations of the pathophysiology of seizure disorders.
28 nderstanding of the pathophysiology of human seizure disorders.
29 of therapeutic potential in the treatment of seizure disorders.
30 epileptic drugs have been developed to treat seizure disorders.
31 ion of structural abnormalities that underly seizure disorders.
32 , perinatal complications (4.34, 3.21-5.81), seizure disorders (2.90, 2.24-3.77), and house status (0
35 ific neurodevelopmental delay with co-morbid seizure disorder accounting for 33.3%, 14.8%, 18.5%, 7.4
38 isations was 0.89 (95% CI, 0.86 to 0.93) for seizure disorder and 0.32 (95% CI 0.31 to 0.34) for TGA.
39 articipants, one with a pre-existing complex seizure disorder and another who experienced oral surger
40 nsporter KCC2 generates mice with a profound seizure disorder and confirms the central role of this t
44 could be a novel therapeutic target to treat seizure disorders and epilepsy.SIGNIFICANCE STATEMENT We
45 intervention in obesity, metabolic syndrome, seizure disorders and other neurodegenerative diseases,
46 identified pathway in the pathophysiology of seizure disorders and provide evidence for a more genera
47 activity disorder, autism spectrum disorder, seizure disorder) and neurodegenerative (fragile X-assoc
48 d ventriculoperitoneal shunts, 36% developed seizure disorders, and 20% developed severe ototoxicity.
51 vere myoclonic epilepsy of infancy, a severe seizure disorder associated with mutations of the sodium
52 that underlie the M-channel cause the human seizure disorder benign familial neonatal convulsions (B
54 Temporal lobe epilepsy (TLE) is a common seizure disorder, but the underlying molecular mechanism
58 syndromes, traumatic nerve/muscle injuries, seizure disorders, decreased cognitive ability, poor pul
60 Developmental epilepsies are age-dependent seizure disorders for which genetic causes have been inc
62 le spasms, which comprise a severe infantile seizure disorder, have a high morbidity and are difficul
67 tifying the gene associated with a monogenic seizure disorder in mice, which may ultimately lead to a
72 al effects caused by cerebral hemorrhages or seizure disorders, keeps clinicians alert to any improve
73 luding low birth weight, maternal education, seizure disorder, kidney disease duration, and genetical
75 ible to unravel whether CVI is caused by the seizure disorder or increased intracranial pressure or b
76 of the tumour leads to focal or generalised seizure disorders or neurological deficits caused by com
78 nsory perception, behavioural abnormalities, seizure disorders, or a combination of these features.
82 nts (1 day-25 years), 13 children with other seizure disorders receiving B6 supplementation (1 month-
84 n pathogenesis is suggested by high rates of seizure disorder; research has highlighted the role of s
85 neurologic dysfunction in association with a seizure disorder, resulting in a 1-y period of behaviora
86 gical evidence from several animal models of seizure disorder that adenosine possesses endogenous ant
87 double knock-out mice display a progressive seizure disorder that dramatically reduces their median
88 neuronal RNA-binding protein, have a complex seizure disorder that includes both convulsive and non-c
91 been associated with a poor response of the seizure disorder to pharmacotherapy and epilepsy surgery
96 7.4, and in serum samples from patients with seizure disorders who were treated with phenytoin or car
97 oside biosynthesis, result in an early-onset seizure disorder with profound motor and cognitive decay
98 most Spnb3(-/-) animals develop a myoclonic seizure disorder with significant reductions of EAAT4, E
99 epilepsies are a heterogeneous collection of seizure disorders with a lifetime expectancy risk rate o
100 ts (n=19) who were in good health except for seizure disorder, with stable anticonvulsant drug levels
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