RESUMO
BACKGROUND: Neonatal seizures (NS) are the most common form of neurological dysfunction observed in newborns. PURPOSE: The purpose of this study in newborn piglets was to determine the effect of cerebral hypothermia (CH) on neural activity during pharmacologically induced NS. We hypothesized that the neuroprotective effects of CH would preserve higher frequencies observed in electrocorticogram (ECoG) recordings. METHODS: Power spectral density was employed to determine the levels of brain activity in ECoGs to quantitatively assess the power of each frequency observed in neurological brain states of delta, theta, alpha, and beta-gamma frequencies. RESULT: The most significant reduction of power occurs in the lower frequency band of delta-theta-alpha of CH cohorts, while t score probabilities imply that high-frequency brain activity in the beta-gamma range is preserved in the CH population. CONCLUSION: While the overall power density decreases over time in both groups, the decrease is to a lesser degree in the CH population.
RESUMO
Epileptic seizures in neonates cause cerebrovascular injury and impairment of cerebral blood flow (CBF) regulation. In the bicuculline model of seizures in newborn pigs, we tested the hypothesis that selective head cooling prevents deleterious effects of seizures on cerebral vascular functions. Preventive or therapeutic ictal head cooling was achieved by placing two head ice packs during the preictal and/or ictal states, respectively, for the â¼2-h period of seizures. Head cooling lowered the brain and core temperatures to 25.6 ± 0.3 and 33.5 ± 0.1°C, respectively. Head cooling had no anticonvulsant effects, as it did not affect the bicuculline-evoked electroencephalogram parameters, including amplitude, duration, spectral power, and spike frequency distribution. Acute and long-term cerebral vascular effects of seizures in the normothermic and head-cooled groups were tested during the immediate (2-4 h) and delayed (48 h) postictal periods. Seizure-induced cerebral vascular injury during the immediate postictal period was detected as terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling-positive staining of cerebral arterioles and a surge of brain-derived circulating endothelial cells in peripheral blood in the normothermic group, but not in the head-cooled groups. During the delayed postictal period, endothelium-dependent cerebral vasodilator responses were greatly reduced in the normothermic group, indicating impaired CBF regulation. Preventive or therapeutic ictal head cooling mitigated the endothelial injury and greatly reduced loss of postictal cerebral vasodilator functions. Overall, head cooling during seizures is a clinically relevant approach to protecting the neonatal brain by preventing cerebrovascular injury and the loss of the endothelium-dependent control of CBF without reducing epileptiform activity.