The science behind near death experiences
Currently, there has been no significant evidence indicating the role of neurochemical processes in near-death experiences (NDEs). However, there have been several hypotheses and/or research regarding the role of physiology in near-death experiences.
Are they associated with decreased brain activity? In fact, evidence has witnessed an increase in brain activity right before death, which could possibly explain NDEs. Consequently, it has been proposed that this surge in activity reflects the active cognitive processing that occurs during near-death experiences. Similarly, electrical activity in the brain has shown to persist in patients in a coma, near-death state.
However, it has been shown that decreased activity in the locus cereleus(responsible for stress and panic responses) may contribute to NDEs.
There is evidence linking NDEs to the opioid system, as 88% of ketamine misusers felt the same ‘Out-Of-Body’ detachment experience.
Carr (1981) suggested that the release of endorphins under stress contributed to the NDE. There have also been suggestions regarding dopamine, serotonin and noradrenaline, but I could find little experimental research on the matter.
Yet, these are simply propositions and have been shown by multiple sources to not be backed by any data.
Brain region propositions:
For one, the ‘Out-Of-Body’ experience (when one’s mind feels detached from their body) is shown to arise from malfunction of the temporo-parietal junction (TPJ). Contrastingly however, stimulating the temporal lobe also evoked NDE symptoms.
Other brain regions that are suggested to be involved include the occipital lobe, frontal lobe (activity shows to persist and not decrease), hippocampus, basal ganglia, and amygdala . Moreover, there has been gray and white matter damage shown in patients experiencing NDEs.
It has also been suggested that bright light can induce NDEs, possibly due to the loss of oxygen to the eye: However, I have not found scientific data specifically measuring such a phenomenon. Moreover, Lommel P (2001)’s findings showed an opposite result, suggesting that hypoxia (loss of oxygen to the brain) may not necessarily be a factor causing NDEs.
Multifactorial models (i.e, comprising most/all of these reasons for NDEs) have also been proposed.
Thus although there are various models and theories to explain NDEs, the data on this is vague and very limited to outline an actual mechanism.