A follow‐up study of intractable seizures in childhood

Huttenlocher, Peter R.; Hapke, Ronald

doi:10.1002/ana.410280516

Cited by 181 publications

(119 citation statements)

References 47 publications

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“…In a previous study of the same childhood population (17), we reported that SE did not imply an increased risk of SMR or other additional major neuroimpairments, but SE occurred significantly more frequently in children with intractable epilepsy than in those with controlled epilepsy. Tonic, myoclonic, and atonic seizures and atypical absences are commonly reported to be frequent in intractable epilepsy, as is a low level of partial seizures (34,48). This was also the case in the univariate comparison.…”

Section: Discussionsupporting

confidence: 59%

Intractable Epilepsy in a Population‐Based Series of Mentally Retarded Children

et al. 1998

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Summary: Purpose:The characteristics of intractable epilepsy were analyzed in a population-based study of active epilepsy in mentally retarded children aged 6-13 years.Methods: Diagnostic registers, EEG laboratory registers, and registers for the Education of the Subnormal were searched. Medical files were scrutinized. Clinical examinations and interviews with parents and caregivers or both were performed. EEG recordings, computed tomography (CT) and magnetic resonance imaging (MRI) of the CNS were reevaluated.Results: Forty-five percent (44 of 98) of the children with mental retardation (MR) and active epilepsy had intractable seizures, defined as one or more seizures every day or week. The median age at onset was 0.8 years, as compared with 3.0 years for those with controlled epilepsy. Predictive factors for frequent seizures were the number of seizure types, severe MR, status epilepticus (SE) and tonic seizures. Epileptiform EEG activity was present in 91%, and focal activity in 65%. Brain lesions were detected on CT and MRI in 70%, with generalized lesions in 60%. Concurrent focal epileptiform activity and focal brain lesions on CTIMRI were detected in 26%. The percentages and prevalence rates for infantile spasms (IS) and LennoxGastaut syndrome (LGS) were 18% (0.25 in 1,OOO) and 7% (0.06 in 1,000), respectively. One of 8 children with IS had had previous neonatal seizures, 3 had SE and 1 later developedLGS . Conclusions:Children with MR and intractable epilepsy have a high frequency of severe MR and additional major neuroimpairments. EEG recordings frequently showed focal changes despite generalized lesions in neuroradiology.

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Section: Discussionsupporting

confidence: 59%

Intractable Epilepsy in a Population‐Based Series of Mentally Retarded Children

et al. 1998

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“…Medically intractable epilepsy is a common condition among children. The tragic consequence of this condition is its effect on the brain, causing recurring seizures throughout the person's life (Huttenlocher and Hapke, 1990;Berg et al, 2006). Neonates and infants are at the highest risk of developing seizures.…”

Section: Introductionmentioning

confidence: 99%

Silencing miR-181a produces neuroprotection against hippocampus neuron cell apoptosis post-status epilepticus in a rat model and in children with temporal lobe epilepsy

Ren

Zhu

2016

Genet. Mol. Res.

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ABSTRACT. Epilepsy is one of the most frequent neurological disorders. Recently, the regulation of microRNAs was found to be associated with epilepsy, but the molecular mechanism by which microRNA influences epilepsy process remains to be unveiled and the development of microRNA-based therapy requires more intensive research. In this study, five microRNAs with potential relevance to epilepsy were initially chosen: miR-132, miR-146a, miR-181a, miR-34a, and miR-124. Twenty-five children who were patients with epilepsy were selected as subjects to obtain tissue samples for the study. The miRNA-181a, which represented the most increased fold-changes in clinical samples, were then selected for further function study in mouse model. The temporal lobe epilepsy (TLE) model, along with lithium-pilocarpine-induced status epilepticus (SE), was established in Sprague-Dawley rats. The antagomir of miR-181a was used to determine the role of miR-181a in cell apoptosis. Analyses were conducted to determine the expression levels of miR-181a, neuronal apoptosis in post-SE, and activated caspase-3. We found evidence of significant time dependent up-regulation of miR-181a amongst post-SE rats and TLE on 24 h (4.47 ± 0.35), 7 days (4.85 ± 0.53), and 2 weeks (5.66 ± 0.64). Experiments with the miR-181a antagomir showed that this particular miRNA led to the inhibition of the protein expression of caspase-3, and was up-regulated in the course of seizure-induced neuronal apoptosis. This study provided evidence that targeting miR-181a leads to a neuroprotective response and is linked to an increase in the activation of the caspase-3 protein. These findings suggest that miR-181a may serve as a promising therapeutic target for epilepsy.

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“…Neonatal brain injury following acute neurological disorders such as status epilepticus, encephalopathy and stroke often leads to excitotoxicity and long-term neurological perturbations, including motor and mental deficits, learning disabilities, mental retardation and/ or epilepsy (Huttenlocher and Hapke, 1990;Ferriero, 2004). While the effects of brain injury, especially from excitotoxicity, have been well studied in mature neurons in vivo and in vitro (Lipton, 1999;Sattler and Tymianski, 2001;Contestabile, 2002), the mechanisms mediating responses to excitotoxic challenge in immature neurons remain poorly understood.…”

Section: Introductionmentioning

confidence: 99%

“…Nonetheless, despite increased spontaneous excitability, the immature brain undergoes less cell death than the mature brain after seizures of identical magnitude (Rennie, 1997;Sperber et al, 1997). It is unclear how immature neurons survive concentrations of excitatory compounds that are lethal to mature neurons, and whether in the absence of cell death, neuronal differentiation is impaired by the changes in the developmental patterns of activity, which could in turn result in later cognitive or motor neurological deficits (Huttenlocher and Hapke, 1990;Holmes et al, 2002;Ferriero, 2004).…”

Section: Introductionmentioning

confidence: 99%

Differential effects of AMPA receptor activation on survival and neurite integrity during neuronal development

Manzini

Joseph

MacDermott

et al. 2007

Molecular and Cellular Neuroscience

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While neuronal cultures are an established model for analyzing excitotoxic brain injury in the adult, in vitro systems have not been extensively employed to study how developing neurons respond to levels of excitatory compounds that are lethal to mature neurons. Recently, we reported that the in vivo differentiation programs of cerebellar granule cells (CGNs) are recapitulated in purified CGN cultures (Manzini et al, 2006). Here, we have used this model system to compare the response of immature and mature neurons to excitotoxic compounds. We found that immature CGNs are less sensitive to AMPA receptor (AMPA-R) activation than mature cells and that levels of AMPA-Rs expression on the plasma membrane are critical in regulating the balance between death and survival during maturation of these neurons. However, the majority of immature cells that survive excitotoxic treatment bear a degenerating neurite, suggesting that AMPA-R activation can still cause damage in the absence of cell death.

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A follow‐up study of intractable seizures in childhood

Cited by 181 publications

References 47 publications

Intractable Epilepsy in a Population‐Based Series of Mentally Retarded Children

Intractable Epilepsy in a Population‐Based Series of Mentally Retarded Children

Silencing miR-181a produces neuroprotection against hippocampus neuron cell apoptosis post-status epilepticus in a rat model and in children with temporal lobe epilepsy

Differential effects of AMPA receptor activation on survival and neurite integrity during neuronal development

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