Background: The activation synchrony index (ASI) is new measure of interhemispheric connectivity from the electroencephalogram (EEG). It may be of value to identify high-risk infants after hypoxic-ischemic (HI) injury, but the impact of HI or therapeutic hypothermia are unknown.
Methods: Instrumented 0.85 gestation fetal sheep received sham-ischemia (n = 9) or 30 min cerebral ischemia, then either normothermia (n = 8), or hypothermia from 3 to 72 h followed by rapid rewarming over ~1 h (n = 8) or slow rewarming over ~10 h (n = 9). Changes in neurophysiological parameters were assessed for 7 days after ischemia.
Results: Cerebral ischemia suppressed EEG power, and increased ASI. After reperfusion, EEG power gradually increased over approximately the first ~8 h, followed by delayed onset of evolving seizures. From 48 h onwards, EEG power became suppressed. By contrast, the increase in ASI after ischemia was sustained for the first 24h, with a very transient fall from 24 to 36 h to near sham control values. From 48 h ASI significantly increased, and remained elevated to the end of the experimental period. Hypothermia did not significantly affect either EEG power or ASI in the first ~24 h. Both hypothermia protocols attenuated the fall in ASI from 24 to 48 h. From 48 h both hypothermia protocols were associated with similarly improved EEG power and a reciprocal progressive suppression of ASI to baseline values from ~96 h.
Conclusions: These data suggest that rate of rewarming is not an important determinant of outcome. The substantial elevation of ASI after cerebral ischemia, in principle, reflects prolonged impaired cortical synchronization. It may have clinical utility for early recruitment but further investigation of its relationship with seizures and background activity is essential. Its delayed recovery during hypothermia could underlie the known delayed neural recovery during therapeutic hypothermia.