(Thanks to Michael from Aware of Aware blog)
I wanted to understand this issue more in depth so I reached out. Here is the response I got from Dr. Bruce Greyson. I think we can really put this to bed.
Michael,
Thank you for forwarding this new article to me. The mainstream media has gone wild the past couple of days with claims that that this single case report definitively proves NDEs are explained entirely by persistent brain electrical activity, but the authors of the article themselves are (justifiably) much more circumspect, writing only that “it is intriguing to speculate that such activity could support a last ‘recall of life’ that may take place in the near-death state.”
In fact, the data from this paper show NOT an increase in gamma activity that is claimed to be responsible for (at least) the life review, but actually show a reduction in absolute gamma waves after cardiac arrest. It is only the relative amount of gamma that is increased compared to alpha, beta, and delta.
That is, all brain activity falls off after cardiac arrest, but because alpha, beta, and delta decrease faster than gamma, the percent of residual activity that is in the gamma range is increased relative to the other frequencies. This hardly seems like an explanation of anything meaningful.
To further complicate the interpretation of these findings, the peak power of the gamma waves is in the upper gamma range, between 60 – 120 Hz, which is most typical of muscle activity, and it occurs primarily on the frontal and temporal electrodes, where muscle artifact is most often found. So this purported gamma activity may not be coming from the brain after all.
Furthermore, the EKG tracing in this paper clearly shows continued heart electrical activity past the point that they said the patient experienced cardiac arrest. The EKG tracing shows ventricular tachycardia, but not ventricular fibrillation or asystole, which are required to diagnose cardiac arrest. So at the time of the changes in brain electrical activity, the patient had not in fact experienced cardiac arrest but was still having some cardiac activity as well.
To their credit, the authors of this article appropriately ends with six reasons not to place too much importance on this one idiosyncratic case: the patient’s traumatic brain injury and subdural hematoma, the anesthesia-induced loss of consciousness, the dissociative drugs given to the patient, the anticonvulsant drugs given to control his seizures, and the patient’s asphyxia and hypercapnia – all of which are known to influence brain electrical activity, including gamma waves – and the lack of any normal brain electrical activity recorded from the patient that can serve as a baseline for comparison.
In summary, this paper, as the authors wrote, is intriguing enough to stimulate speculation, but hardly anything to write home about.
Best wishes,
Bruce
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