Abstracts

Neurological injury following seizures has been shown to involve both neuronal cell death as well as astrocytic gliosis. Although there is evidence of seizure-induced neuronal injury in adults, as measured by neuron specific enolase (NSE), most studies in children have not documented elevated NSE, except in rare cases of children with acute symptomatic etiologies. Markers of astrocytic injury may potentially be a more sensitive indicator of cerebral damage during acute seizure activity. The goal of this study is to evaluate pediatric seizure patients for astrocytic injury by measuring cerebrospinal fluid (CSF) glial fibrillary acidic protein (GFAP), determine risk factors for GFAP elevation following seizures, and compare seizure-induced astrocyte injury with neuronal injury by concurrent measurement of CSF NSE.
CSF was obtained from 52 pediatric patients within 24 hours of seizure and assayed for GFAP and NSE. Retrospective chart review was performed for seizure type (partial or generalized), etiology (febrile, cryptogenic, or symptomatic), and duration. CSF levels of GFAP and NSE were compared to control patients (n=33) who presented with an indication for lumbar puncture, but had no underlying neurological or systemic disease.
Overall, children with seizures had elevated CSF GFAP compared to controls (p=0.0075), but no elevation of NSE (p=0.1437). There was no effect of seizure type or etiology, but there was a significant positive effect of seizure duration (p=0.0010) and status epilepticus (p=0.0296) on CSF GFAP. Individually, seven children (13%) had elevated GFAP ([gt]440 pg/ml); in five children the increased GFAP was not accompanied by elevations in NSE ([lt]12 ng/ml). Five children with elevated GFAP had symptomatic etiologies for their seizures, but the etiology of one child with elevated GFAP was cryptogenic, and one had febrile seizures.
Elevation of CSF GFAP following seizures suggests that astrocytic injury may occur in children. The incidence of elevated CSF GFAP is low, but increases with prolonged seizures. Increased GFAP levels may occur in patients with normal NSE, suggesting that GFAP may be a more sensitive marker of brain injury in some cases. While many patients with elevated GFAP had a symptomatic etiology, two patients did not have underlying neurological diagnoses, suggesting that seizures may directly cause astrocytic injury.
[Supported by: NIH 5K12NS0169004 (MW) and P60-DK20579 (ML)]