We Need Your Help -- NDE Skepticism

#21
This is not exactly what you are asking for but it might help indirectly:

Materialist explanations of NDEs fail to explain the phenomenon.
http://ncu9nc.blogspot.com/2013/07/materialist-explanations-of-ndes-fail.html

Click on the hypothesis to see the refutation below, click on the sources to go to the original articles.

Lack of oxygen: Hogan, Tymn, Prescott (including acceleration induced hypoxia in pilots training under high g forces.), Facco and Christian, Beauregard, Greyson, near-death.com
Dying Brain: Hogan, Tymn, Beauregard, Greyson, near-death.com
Hallucinations: Hogan, near-death.com, Long
Religious Expectations: Hogan, Tymn, Long
Cultural Expectations: Hogan, Tymn, Long
Hearing about medical procedures after the fact: Hogan, Tymn
Hearing during resuscitation: Hogan, Prescott, Long
Brain Dysfunction (such as temporal lobe dysfunction): Tymn, Prescott, Facco and Christian, Beauregard, Greyson, near-death.com
Retinal dysfunction causing an image of the tunnel: Facco and Christian
Visual cortex dysinhibition associated with anoxia causing an image of the tunnel: Facco and Christian
Brain chemicals such as ketamine, DMT, etc.: Prescott (ketamine), Facco and Christian (endogenous opioids, neurotransmitter imbalance and hallucinogens including DMT), Beauregard (ketamine), Long
REM Intrusions: Facco and Christian, Long
Epilepsy or seizures: Beauregard
Psychopathology: Hogan, Tymn, Greyson
Unique Personality Traits: Greyson
Residual brain activity during unconsciousness: Greyson
The experience occurred before or after brain activity stopped: Greyson
The experience occurred during CPR: Long
Evolutionary Adaptation: near-death.com
Depersonalization: Hogan, near-death.com
Memory of birth: near-death.com
Medication: Hogan, Tymn, Facco and Christian
Defense against dying: Tymn
Partial anesthesia: Prescott, Long
Misuse of anecdotes: Long
Selective reporting: Long​
I just noticed that Appendix B from Proof of Heaven by Eben Alexander has been posted to several places on the internet:


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:

1. 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.

2. 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.

3. 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.

4. 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, LSD, mescaline) from my teen years in the early 1970s. I have had no
personal experience with DMT but have seen patients under its influence. The rich
ultra-reality would still require fairly intact auditory and visual neocortex as target
regions in which to generate such a rich audiovisual experience as I had in coma.
Prolonged coma due to bacterial meningitis had badly damaged my neocortex, which
is where all of that serotonin from the raphe nuclei in the brainstem (or DMT, a
serotonin agonist) would have had effects on visual/auditory experience. But my
cortex was off, and the DMT would have had no place in the brain to act. The DMT
hypothesis failed on the basis of the ultra-reality of the audiovisual experience, and
lack of cortex on which to act.

5. Isolated preservation of cortical regions might have explained some of my
experience, but were most unlikely, given the severity of my meningitis and its
refractoriness to therapy for a week: peripheral white blood cell (WBC) count over
27,000 per mm3, 31 percent bands with toxic granulations, CSF WBC count over
4,300 per mm3, CSF glucose down to 1.0 mg/dl, CSF protein 1,340 mg/dl, diffuse
meningeal involvement with associated brain abnormalities revealed on my enhanced
CT scan, and neurological exams showing severe alterations in cortical function and
dysfunction of extraocular motility, indicative of brainstem damage.

6. In an effort to explain the “ultra-reality” of the experience, I examined this
hypothesis: Was it possible that networks of inhibitory neurons might have been
predominantly affected, allowing for unusually high levels of activity among the
excitatory neuronal networks to generate the apparent “ultra-reality
” of my
experience? One would expect meningitis to preferentially disturb the superficial
cortex, possibly leaving deeper layers partially functional. The computing unit of the
neocortex is the six-layered “functionalcolumn,” each with a lateral diameter of 0.2–
0.3 mm. There is significant interwiring laterally to immediately adjacent columns in
response to modulatory control signals that originate largely from subcortical regions
(the thalamus, basal ganglia, and brainstem). Each functional column has a
component at the surface (layers 1–3), so that meningitis effectively disrupts the
function of each column just by damaging the surface layers of the cortex. The
anatomical distribution of inhibitory and excitatory cells, which have a fairly
balanced distribution within the six layers, does not support this hypothesis. Diffuse
meningitis over the brain’s surface effectively disables the entire neocortex due to
this columnar architecture. Full-thickness destruction is unnecessary for total
functional disruption. Given the prolonged course of my poor neurological function
(seven days) and the severity of my infection, it is unlikely that even deeper layers of
the cortex were still functioning.

7. The thalamus, basal ganglia, and brainstem are deeper brain structures (“subcortical
regions”)
that some colleagues postulated might have contributed to the processing
of such hyperrealexperiences
. In fact, none of those structures could play any such
role without having at least some regions of the neocortex still intact. All agreed in
the end that such subcortical structures alone could not have handled the intense
neuralcalculations required for such a richly interactive experiential tapestry.

8. A “reboot phenomenon”—a random dump of bizarre disjointed memories due to old
memories in the damaged neocortex, which might occur on restarting the cortex
into consciousness after a prolonged system-wide failure, as in my diffuse
meningitis. Especially given the intricacies of my elaborate recollections, this seems
most unlikely.

9. Unusual memory generation through an archaic visual pathway through the
midbrai
n, prominently used in birds but only rarely identifiable in humans. It can be
demonstrated in humans who are cortically blind, due to damaged occipitalcortex. It
provided no clue as to the ultra-reality I witnessed, and failed to explain the auditoryvisual
interleaving.
 
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#22
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 concept of a creature evolving a brain process to ease terminal pain makes absolutely no sense from a materialistic perspective (the perspective it is designed to support)!
How could the 'normal' concept of evolution by natural selection work in such a case? Are those dying in less pain more likely to pass on their genes than those in greater pain? I think this absurd suggestion illustrates just how bankrupt conventional ideas in this area have become.

David
 
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