APPENDIX B
Neuroscientific Hypotheses I Considered to Explain My Experience
In reviewing my recollections with several other neurosurgeons and
scientists, I entertained several hypotheses that might explain my
memories. Cutting right to the chase, they all failed to explain the rich,
robust, intricate interactivity of the Gateway and Core experiences (the
“ultra-reality”). These included:
- A primitive brainstem program to ease terminal pain and suffering
(“evolutionary argument”—possibly as a remnant of “feigned-death”
strategies from lower mammals?). This did not explain the robust,
richly interactive nature of the recollections. - The distorted recall of memories from deeper parts of the limbic
system (for example, the lateral amygdala) that have enough overlying
brain to be relatively protected from the meningitic inflammation,
which occurs mainly at the brain’s surface. This did not explain the
robust, richly interactive nature of the recollections. - Endogenous glutamate blockade with excitotoxicity, mimicking the
hallucinatory anesthetic, ketamine (occasionally used to explain NDEs
in general). I occasionally saw the effects of ketamine used as an
anesthetic during the earlier part of my neurosurgical career at
Harvard Medical School. The hallucinatory state it induced was most
chaotic and unpleasant, and bore no resemblance whatsoever to my
experience in coma. - N,N-dimethyltryptamine (DMT) “dump” (from the pineal, or
elsewhere in the brain). DMT, a naturally occurring serotonin agonist
(specifically at the 5-HT1A, 5-HT2A and 5-HT2C receptors), causes
vivid hallucinations and a dreamlike state. I am personally familiar
with drug experiences related to serotonin agonist/antagonists (that is,