Mortality associated with neonatal seizures has declined although long-term neurodevelopmental morbidity remains unchanged. Seizure etiology and background EEG patterns remain powerful prognostic factors. Diagnostic advances have changed the etiologic distribution for neonatal seizures and improved accuracy of outcome prediction. Global cerebral hypoxia-ischemia, the most common etiology, is responsible for the large majority of infants with poor long-term outcome.

Our data suggest that all antiepileptic drugs studied except levetiracetam had varying degrees of deleterious effects on thyroid function.

Serum and CSF Zn levels are decreased in children with febrile seizures. Zinc deprivation may play a role in the pathogenesis of febrile seizures.

Because the rate of neurological problems is increased in children with CD, neurological abnormalities should be carefully investigated early after the diagnosis of CD is made.

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During the acute phase of FC, patients had significantly increased plasma IL-1 beta and prostaglandin levels and decreased serum Zn levels. These changes may be responsible for FC pathogenesis.

The aim of this study was to evaluate the correlative value of magnetic resonance imaging (MRI) in children with periventricular leukomalacia (PVL) for neurodevelopmental outcome. MRI examinations of 89 children (46 males, 43 females) with PVL (median age 4y, range 1 to 14y) were reevaluated. PVL was graded as follows: grade I, unilateral or bilateral areas of periventricular hyperintensity (1-3); grade II, hyperintensity more than 3; grade III, hyperintense lesions more than 3 and ventricular wall irregularity; grade IV, diffuse PVL and ventricular dilatation. Localizations of PVL and brain abnormalities associated with PVL were also noted. Assignment to PVL grades on MRI was as follows: PVL I (n=22), PVL II (n=18), PVL III (n=30), and PVL IV (n=19). Cerebral palsy was slightly less common in children with PVL I and II compared with PVL III to IV. Motor function was normal in 50% of children with PVL grade I, but severely impaired in 73.7% of children with PVL grade IV. Results of visual function were normal in all with PVL I, but pathological in 42.1% of patients with PVL IV. Developmental tests were appropriate for age in 75% of patients with PVL I, but significantly delayed in all patients with PVL IV. Thinning of the corpus callosum and presence of cortical atrophy were also correlated with neurological outcome. Significant risk factors associated with developmental delay were asphyxia at birth (odds ratio [OR] 4.3), PVL localization numbers over 3 (OR 4.4), PVL III to IV (OR 15), thinning of corpus callosum, and cortical atrophy.

No abstract