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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Neonatal seizures typically indicate significant underlying disease.They are poorly classified, under-recognized, and often difficult to treat. Recognition of etiology is often helpful in prognosis and treatment; the most common is hypoxic-ischemic encephalopathy. Patients generally have a poor prognosis, with most developing a severe encephalopathy and epilepsy. Studies suggest that neonatal seizures and their etiology have a significant impact on the developing brain; it is critical to recognize seizures early and initiate immediate antiepileptic therapy. Continuous computerized simultaneous video electroencephalograph monitoring is imperative;at-risk infants will frequently have electrographic seizures without clinical manifestations. Although there are antiepileptic therapies for neonatal seizures, they are ineffective in over 35% of cases. The goal of research should be the development of more effective therapies for neonatal seizures, regardless of etiology.
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PMID:Neonatal seizures. 1527 83

Neonatal seizures are difficult to detect, diagnose, and manage. Infants with a history of seizures often have long-term neurologic sequelae. Controversy exists as to whether neonatal seizures themselves cause damage to the developing brain, and thus, subsequent sequelae; or if these sequelae are due primarily to the underlying cause of the seizures. Treatment of seizures involves identifying and treating the underlying etiology of the seizure and appropriate use of pharmacologic interventions. To provide the context for pharmacological management of seizures in newborns, this article examines the pathophysiology and etiology of seizures and discusses pharmacological agents and issues, short- and long-term outcomes, clinical implications, and directions for future research. Understanding pharmacological issues within this context provides a comprehensive foundation for decision making and management of neonatal seizures.
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PMID:Neonatal seizures: diagnosis, pharmacologic interventions, and outcomes. 1547 77

Neonatal seizures may increase neuronal vulnerability later in life. Therefore, status epilepticus was induced with kainate (KA) during the first and second postnatal (P) weeks to determine whether early seizures shift the window of neuronal vulnerability to a younger age. KA was injected (i.p.) once (1x KA) on P13, P20 or P30 or three times (3 x KA), once on P6 and P9, and then either on P13, P20 or P30. After 1x KA, onset to behavioral seizures increased with age. Electroencephalography (EEG) showed interictal events appeared with maturation. After 3 x KA, spike number, frequency, spike amplitude, and high-frequency synchronous events and duration were increased at P13 when compared to age-matched controls. In contrast, P20 and P30 rats had decreases in EEG parameters relative to P20 and P30 rats with 1x KA despite that these animals had the same history of perinatal seizures on P6 and P9. In P13 rats with 1x KA, silver impregnation, hematoxylin/eosin and TUNEL methods showed no significant hippocampal injury and damage was minimal with 3 x KA. In contrast, P20 and P30 rats with 1x KA had robust eosinophilic or TUNEL positive labeling and preferential accumulation of silver ions within inner layer CA1 neurons. After 3 x KA, the CA1 but not CA3 of P20 and P30 rats was preferentially protected following 3 or 6 days. Although paradoxical changes occur in the EEG with maturation, the results indicate that early perinatal seizures do not significantly shift the window of hippocampal vulnerability to an earlier age but induce a tolerance that leads to long-term neuroprotection that differentially affects endogenous properties of CA1 versus CA3 neurons.
Seizure 2006 Jan
PMID:Perinatal seizures preferentially protect CA1 neurons from seizure-induced damage in prepubescent rats. 1630 25

Endogenous PGE(2) dynamically regulates membrane excitability, synaptic transmission and plasticity. Neonatal seizures are associated with a number of activity-dependent changes in brain development including altered synaptogenesis and synaptic plasticity as well as reduction in neurogenesis. Thus, it is reasonable to hypothesize that alteration of cyclooxygenase-2 (COX-2) expression induced by neonatal seizure may influence brain development. We evaluated the expression of COX-2 and microsomal prostaglandin E synthase (mPGES) by Western blot analysis and immnohistochemistry in flurothyl-induced neonatal seizure and also studied the effect of celecoxib on seizure induction. Seven to 10 days old Sprague-Dawley rats were used for control (n = 18) and experimental group (n = 30). Recurrent seizure group showed more increased level of COX-2 expression than control group. However, the level of mPGES-2 expression was similar in both groups, and mPGES-1 was not detected. Hippocampus of control rats showed endogenous COX-2 expression, which was localized mainly in CA3 region. This localization pattern was similar in recurrent seizure rats, but intensity of COX-2 expression was more increased than in control rats. Celecoxib treatment significantly delayed the seizure attack and also reduced COX-2 expression. In conclusion, this study suggests that COX-2 expression is related to epileptogenesis in flurothyl-induced neonatal seizure model and shows the possibility that its inhibition lessens functional impairments that occurred in neonatal seizure.
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PMID:Cyclooxygenase-2 expression and effect of celecoxib in flurothyl-induced neonatal seizure. 1643 15

Neonatal seizures can result in long-term adverse consequences including alteration of seizure susceptibility and impairment in spatial memory. However, little is known about the effects of neonatal seizures on developmental changes occurring in synaptic transmission during the first postnatal weeks. The purpose of the present study was to examine the effect of neonatal seizures on several aspects of gamma-aminobutyric acid (GABA)ergic and glutamatergic synaptic transmission in the developing rat hippocampus. Flurothyl was used to induce multiple recurrent seizures in rat pups during the first postnatal days. Whole-cell patch-clamp recordings from the hippocampal CA3 pyramidal cell and extracellular recordings from the CA3 pyramidal cell layer were made in slice preparations. In rats that experienced neonatal seizures the amplitude of spontaneous inhibitory postsynaptic currents at P15-17 was decreased by 27% compared with controls, whereas neither frequency nor the kinetic properties were altered. Neonatal seizures did not affect the timing of the developmental switch in the GABAA signaling from excitatory to inhibitory. None of the studied parameters of glutamatergic postsynaptic currents was different between the flurothyl and control groups, including the amplitude and frequency of the spontaneous excitatory postsynaptic currents, the ratio of the amplitudes and frequencies of the alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) and N-methyl-D-aspartate (NMDA)-mediated spontaneous postsynaptic currents, and the kinetics of AMPA and NMDA mediated postsynaptic currents in the age groups P8-10 and P15-17. We suggest that the selective depression of the amplitude of GABAergic synaptic responses may contribute to the adverse neurological and behavioral consequences that occur following neonatal seizures.
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PMID:Selective impairment of GABAergic synaptic transmission in the flurothyl model of neonatal seizures. 1655 19

Neonatal seizures are markers for time-specific etiologies during antepartum, intrapartum and neonatal time periods. Seizures with or without encephalopathic signs can represent a continuum of maternal, placental, fetal and neonatal risk factors and disease states. A multi-dimensional classification scheme for neonatal seizures is suggested that will help strategize specific therapeutic interventions to optimize neurologic outcome and anticipate later neurological morbidities including epilepsy risk. This scheme combines "epileptic" and "non-epileptic" seizure descriptions which capture time-specific and brain region-specific mechanisms for seizures. Synchronized video electroencephalographic monitoring provides the most accurate start and endpoints for cortically generated seizures. However, subcortical sites of injury may also initiate abnormal clinical signs with or without the subsequent expression of electrographic seizures. Co-registration of digital neuroimaging techniques such as magnetic resonance imaging with computational electroencephalographic datasets will provide more precise structure-function correlates for neonatal seizures that address both cortical and subcortical sites of injury. Finally, more precise definitions of neonatal status epilepticus need to be established because of the long-term harmful effects on brain development by prolonged seizures expressed as epilepsy and cognitive-behavioral deficits. With this expanded classification scheme for neonatal seizures, novel pharmacologic and surgical strategies can be designed for disease-specific rescue, repair, and regeneration strategies of damaged brain tissue that occur during fetal and neonatal periods, and are later expressed during infancy and childhood. Clinical neuroscientists must strive to develop a classification scheme that bridges bench to bedside concepts of developmental neural plasticity research, recognizing both negative and positive consequences of brain remodeling and repair of the child and adolescent brain. Developmental neural plasticity also extends into adulthood when brain remodeling mechanisms further contribute to epileptogenesis and continues to impair quality of life.
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PMID:Neonatal seizure classification: a fetal perspective concerning childhood epilepsy. 1688 42

Neonatal seizures in term infants are rare but have important potential implications for brain development. Risk factors for neonatal seizures in term infants have been less well defined than those among preterm infants. To evaluate the relationship between maternal risk factors and neonatal seizures in the first 72 hours of life in term infants, a case-control study using the Colorado Birth Certificate Registry was conducted. Term neonates in all hospitals in Colorado with and without seizures in the first 72 hours were studied. After adjusting for vaginal delivery in the setting of herpes infection and post-term delivery, preexisting diabetes in the mother (odds ratio 4.30, 95% confidence interval 1.64-11.27, P < .01) and fetal distress (odds ratio 5.88, 95% confidence interval 4.60-7.13, P < .0001) were independent risk factors for neonatal seizures in term infants. These findings are confirmatory of previous reports that maternal preexisting diabetes and fetal distress increase the risk of neonatal seizure in term infants. Although we cannot establish the pathophysiology of neonatal seizures from this analysis, hypoxic-ischemic brain injury and hypoglycemia in infants of diabetic mothers are known causes of neonatal seizures that can be represented in this analysis by fetal distress and maternal preexisting diabetes, respectively. Maternal diabetic vasculopathy can also be a contributing factor.
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PMID:Maternal risk factors for term neonatal seizures: population-based study in Colorado, 1989-2003. 1697 Aug 88

Neonatal seizures are critical conditions because they are usually related to significant illnesses that require a specific therapy. Antepartum and peripartum seizures are very rare, and represent signs of prenatal-onset neurologic dysfunction. A review of the literature revealed that the main etiologies include severe brain malformations, multiple anomalies, and metabolic encephalopathy. A high incidence of early fatality and serious neurologic sequelae were noted. To our knowledge, this is the first case report of neonatal adrenoleukodystrophy presenting with seizure at birth. These very-early-onset seizures may require unique diagnostic and therapeutic considerations, in contrast with the later onset of seizures in neonates.
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PMID:Neonatal adrenoleukodystrophy presenting with seizure at birth: a case report and review of the literature. 1820 97

Seizures in the newborn period constitute a medical emergency. Subtle seizures are the commonest type of neonatal seizures, other types being clonic, tonic, and myoclonic. Myoclonic seizures carry the worst prognosis in terms of long-term neurodevelopmental outcome. Hypoxic-ischemic encephalopathy is the most common cause of neonatal seizures. Multiple etiologies often co-exist in neonates and hence it is essential to rule out conditions such as hypoglycemia, hypocalcemia, and meningitis before initiating specific therapy. A comprehensive approach for management of neonatal seizures has been described.
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PMID:Seizures in the newborn. 1833 96

Neonatal seizures are the most common neurological emergency in the neonatal period and are associated with a poor long-term outcome. Early detection and treatment may improve prognosis. This paper aims to develop an optimal set of parameters and a comprehensive scheme for patient-independent multi-channel EEG-based neonatal seizure detection. We employed a dataset containing 411 neonatal seizures. The dataset consists of multi-channel EEG recordings with a mean duration of 14.8 h from 17 neonatal patients. Early-integration and late-integration classifier architectures were considered for the combination of information across EEG channels. Three classifier models based on linear discriminants, quadratic discriminants and regularized discriminants were employed. Furthermore, the effect of electrode montage was considered. The best performing seizure detection system was found to be an early integration configuration employing a regularized discriminant classifier model. A referential EEG montage was found to outperform the more standard bipolar electrode montage for automated neonatal seizure detection. A cross-fold validation estimate of the classifier performance for the best performing system yielded 81.03% of seizures correctly detected with a false detection rate of 3.82%. With post-processing, the false detection rate was reduced to 1.30% with 59.49% of seizures correctly detected. These results represent a comprehensive illustration that robust reliable patient-independent neonatal seizure detection is possible using multi-channel EEG.
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PMID:Classifier models and architectures for EEG-based neonatal seizure detection. 1879 36


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