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1 l mechanism for the early crescendo phase of neonatal seizures.
2 nic acid and flurothyl models of symptomatic neonatal seizures.
3 l and diazepam, two drugs in current use for neonatal seizures.
4 Q channels may be effective for treatment of neonatal seizures.
5 metanide might be an effective treatment for neonatal seizures.
6 etanide should be useful in the treatment of neonatal seizures.
7 ng the diagnosis, aetiology and treatment of neonatal seizures.
8 irth weight is a significant risk factor for neonatal seizures.
9 f these infants were diagnosed with clinical neonatal seizures.
10 charge after resolution of acute symptomatic neonatal seizures.
11  an add-on to phenobarbital for treatment of neonatal seizures.
12 tion could be a viable approach for treating neonatal seizures.
13 arge for most infants with acute symptomatic neonatal seizures.
14 0 minutes, meconium aspiration syndrome, and neonatal seizures, adjusted for maternal height, materna
15 maintained at the time of discharge from the neonatal seizure admission.
16             There were 207 cases of clinical neonatal seizures among 116,048 live births (an incidenc
17 is study estimated the incidence of clinical neonatal seizures among infants born between 1992 and 19
18 h, an Apgar score of 3 or less at 5 minutes, neonatal seizure, an umbilical-artery blood pH of 7.05 o
19 c encephalopathy is the most common cause of neonatal seizures and can lead to chronic epilepsy.
20  In one family, the phenotype extends beyond neonatal seizures and includes rolandic seizures, and a
21 le deleterious effects of GABAergic drugs on neonatal seizures and on excitotoxic neuronal injury in
22  a clinically relevant target for refractory neonatal seizures and provide insights for future drug d
23 ng mutations responsible for benign familial neonatal seizures and/or peripheral nerve hyperexcitabil
24 re often hypotensive, needed intubation, had neonatal seizures, and received a clinical diagnosis of
25                                              Neonatal seizures are a naturally occurring source of ne
26                                      Whereas neonatal seizures are a predictor of adverse neurologica
27                                              Neonatal seizures are most commonly the clinical finding
28                                     Although neonatal seizures are quite common, there is controversy
29   This is of particular concern for treating neonatal seizures, as early life exposure to drugs such
30      Finally, human hippocampal samples from neonatal seizure autopsy cases also showed an increase i
31  known to be responsible for benign familial neonatal seizures (BFNS).
32 nt compounds inhibit motor manifestations of neonatal seizures but not cortical seizure activity.
33 ear in understanding the basis for a form of neonatal seizures can be attributed to the successful po
34                                              Neonatal seizures can lead to epilepsy and long-term cog
35                                              Neonatal seizures can lead to later life epilepsy and ne
36                                              Neonatal seizures can permanently disrupt neuronal devel
37 GABAergic) drugs, the standard treatment for neonatal seizures, can have excitatory effects in the ne
38                                              Neonatal seizures caused by hypoxia can be refractory to
39 ificates, death certificates, and a study of neonatal seizures conducted concurrently with this study
40                                              Neonatal seizures continue to present a diagnostic and t
41 nked lethal disorder involving cleft palate, neonatal seizures, contractures, central nervous system
42 nfant with ISOD who initially presented with neonatal seizures, diffusion restriction noted on magnet
43                   Approximately one-third of neonatal seizures do not respond to first-line anticonvu
44                                    Rats with neonatal seizures had a significant reduction in the num
45    Compared with controls, rats subjected to neonatal seizures had impaired learning and decreased ac
46 e absence of controlled trials, treatment of neonatal seizures has changed minimally despite poor dru
47                    Although the treatment of neonatal seizures has not significantly changed in the p
48 odent model of the most common form of human neonatal seizures, hypoxia-induced seizures (HS), we aim
49 approaches to the diagnosis and treatment of neonatal seizures, identifies some of the critical facto
50                             The incidence of neonatal seizures in Harris County was lower than the in
51 d bumetanide added to phenobarbital to treat neonatal seizures in the first trial to include a standa
52 iventricular leukomalacia in the preterm and neonatal seizures in the term infant.
53 s 0-3 at 5 minutes, meconium aspiration, and neonatal seizures increased similarly with maternal BMI.
54 echanism for phenobarbital inefficacy during neonatal seizures is the reduced abundance and function
55 SM) treatment duration for acute symptomatic neonatal seizures is variable.
56 lifetime is found in the neonatal period and neonatal seizures lead to a propensity for epilepsy and
57                    Whether better control of neonatal seizures leads to a reduction in neurodisabilit
58 d KV 7.3, are known to cause benign familial neonatal seizures mainly by haploinsufficiency.
59 y pH <7.0), hypoxic ischemic encephalopathy, neonatal seizures, neonatal respiratory support for grea
60                                              Neonatal seizures occur frequently, are often refractory
61 luded in the diagnostic workup of refractory neonatal seizures of unknown origin.
62 se to antidepressant exposure; the impact of neonatal seizures on dentate gyrus neurogenesis; and the
63 e onset in the first year of life, including neonatal seizure onset in 47%.
64        Genetic diagnosis was associated with neonatal seizure onset versus infantile seizure onset (1
65               We found that individuals with neonatal seizures or early infantile seizures followed b
66 ted channelopathies, such as benign familial neonatal seizures or peripheral nerve hyperexcitability
67 of an unknown prior diagnosis of epilepsy or neonatal seizures) or classified as not having epilepsy
68 pothesis that neonatal encephalopathy, early neonatal seizures, or both result from early antenatal i
69                                              Neonatal seizures pose a clinical challenge in their ear
70 nd in children affected with benign familial neonatal seizures (R213W mutation) or with neonatal epil
71                Electroclinical uncoupling of neonatal seizures refers to electrographic seizure activ
72  with the primary outcome measure) from 9 US Neonatal Seizure Registry centers, born from July 2015 t
73  [corrected] and need for resuscitation, and neonatal seizures-signs commonly attributed to birth asp
74 sted the hypothesis that a single episode of neonatal seizures (sNS) on rat postnatal day (P) 7 perma
75 ing that KCC2 phosphorylation regulates both neonatal seizure susceptibility and CLP290-mediated KCC2
76 recent insights about the pathophysiology of neonatal seizures that may provide the foundation for be
77      Using a rodent model of hypoxia-induced neonatal seizures that results in a persistent increase
78 eptic disorders ranging from benign familial neonatal seizures to severe epileptic encephalopathies.
79 In a CD-1 mouse model of refractory ischemic neonatal seizures, treatment with the KCC2 functional en
80 piration) scores less than 7 or less than 4; neonatal seizure; ventilator support; neonatal intensive
81                         In a rodent model of neonatal seizures, we have shown previously that adminis
82                                 The odds for neonatal seizure were higher and the odds for admission
83                                 Infants with neonatal seizures were ascertained from four sources: ho
84                             Risk factors for neonatal seizures were evaluated in 116,048 infants born
85 ve mutation in KCNQ2 that has a phenotype of neonatal seizures without permanent clinical CNS impairm