Introduction: Near-death experiences (NDE), reported as extremely vivid imagery, have long fascinated scientists and theologians. Recent quantitative electroencephalogram (EEG) studies suggest that the brain transiently becomes highly active during the immediate post-cardiac arrest (CA) period despite raw EEG showing progressive suppression. Additionally, the occipital lobes, harboring the visual cortices, appear to become the most active during NDE. Methods: Fifteen adult Wistar Rats (Male, 300-350gms) were implanted with EEG leads (L/R frontal lobes and L/R occipital lobes). One week later, rats underwent 7-minute asphyxial CA while undergoing continuous EEG. EEG sub-band analysis was done using Information Quantity (IQ), a well-established entropy based nonlinear calculation of the statistical variability and information content of EEG. Results: During CA induction, we find that EEG IQ in the R occipital lobe is significantly resistant to suppression at the EEG alpha sub-bands (8-12Hz; slope of EEG decrement = -0.086 IQ/min ±0.0028 [Std Dev]) and slow gamma sub-bands (30-50Hz; -0.0085 ± 0.0027 IQ/min) in comparison to either L frontal lobe (-0.0203 ± 0.0040 [alpha], -0.0261 ± 0.0044 [slow gamma]), R frontal lobe (-0.0193 ± 0.0043 [alpha], -0.0236 ± 0.0054[slow gamma]) or the L occipital lobe (-0.0198 ± 0.0045 [alpha], -0.0227 ± 0.0055 [slow gamma]). All p-values<0.001. Conclusions: In a rodent model of asphyxial CA, these data show that the R occipital lobe has profound resistance to loss of EEG entropy, most robustly in the alpha and slow gamma EEG sub-bands. In humans, gamma range EEG and its coherence with slower bands are associated with waking consciousness and higher cortical processing. While the R occipital region’s role and connectivity with surrounding temporo-parietal regions is established in imagery, our data is the first to demonstrate a critical role for the R occipital lobe during death. Upon further validation in humans, these data may better elucidate mechanisms of NDE-related vivid imagery.
© 2013 by the Society of Critical Care Medicine and Lippincott Williams & Wilkins