Introduction Neonatal seizures following hypoxic-ischaemic insults at birth are common. Additional exposure to endotoxins (LPS) prior to ischaemia has been shown to be able to increase or decrease neural injury, though whether this is achieved through altering seizure activity is unknown.
Methods Fetal sheep (aged 103–104 days gestation) were given a 5-day infusion of normal saline (n=9) or 250 ng/kg/24 h of lipopolysaccharide (a gram negative endotoxin) (n=10) prior to 15 min of umbilical cord ischaemia. Fetal EEG activity was recorded from 6 h before infusion to 5 days post ischaemia and analysed through visual and quantitative spectral methods.
Result Neural injury was lower in the group given LPS prior to ischaemia (p<0.05), though paradoxically seizure activity was significantly higher in this group (p<0.05). Quantitative EEG parameters reflected the degree of injury with power in all EEG bands returning to baseline more quickly in the LPS group (p<0.05). Subanalysis also showed that seizures correlated to activated microglial cell counts in the LPS group (p=0.0036) but not in the saline group (p=0.29).
Discussion LPS appears to ‘pre-condition’ the brain to subsequent hypoxic-ischaemic insults, whilst paradoxically increasing seizure activity. Whether exposure to in utero infection confers long-term seizure susceptibility and long-term ability to withstand hypoxic-ischaemic insults remains unclear but may be a promising area of future research.
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