Views on Eben Alexander III, M.D. Near Death Experience
Dr. Alexander's Views on his NDE:
"My story offers compelling proof that the conscious awareness of our
spirit thrives when freed from the limitations of the brain and body,
joins with an unimaginably grander Being of infinite love, engendering
our very existence with far more purpose -- that stories related to the
afterlife told through millennia, including the relatively recent
literature on near-death experiences, have a solid foundation in a realm
far richer than our physical realm, one that is truly eternal. My
conclusions are based on my rich experience during a severe and rare
case of meningitis that should have totally extinguished any experience
at all, should have been fatal, and certainly never should have allowed
my full recovery to tell the tale. My realization took months to evolve,
and is solidly based on the cutting edge of neuroscience, consciousness
studies (specifically "The Hard Problem of Consciousness"), and quantum
physics.
One can bicker about one's own version of "Heaven," all I can
say with certainty is that that glorious realm truly exists. The
variations in its description are related to the filtering or veiling
function of the brain, which taint recollections with a
cultural/personal flavor. The underlying reality is undeniable, fully
supported by the wealth of material on all manner of spiritually
transformative experiences, and on phenomena of extended consciousness
(as shown in Irreducible Mind: Toward a Psychology for the 21st Century,
by Edward Kelly et al)."
The followThe following is excerpted from the appendicies of
Dr. Alexanders
best selling book "Proof of Heaven: A Neurosurgeon's Near Death
Experience and Journey into the Afterlife"
Statement by Scott Wade, M.D.
As an Infectious infectious diseases specialist I was asked to see
Dr. Eben Alexander when he presented to the hospital on November 10,
2008, and was found to have bacterial meningitis. Dr. Alexander had
become ill quickly with flu-like symptoms, back pain, and a headache.
He was promptly transported to the Emergency Room, where he had a CT
scan of his head and then a lumbar puncture with spinal fluid suggesting
a gram-negative meningitis. He was immediately begun on
intravenous antibiotics targeting that and placed on a ventilator
machine because of his critical condition and coma. Within
twenty-four hours the gram-negative bacteria in the spinal fluid was
confirmed as E.coli. An infection more common in infants, E. coli
meningitis is very rare in adults (less than one in 10 million annual
incidence in the United States), especially in the absence of any head
trauma, neurosurgery, or other medical conditions such as diabetes.
Dr. Alexander was very healthy at the time of his diagnosis and no
underlying cause for his meningitis could be identified.
The mortality rate for gram-negative meningitis in children and
adults ranges from 40 to 80 percent. Dr. Alexander presented to
the hospital with seizures and a markedly altered mental status, both of
which are risk factors for neurological complications or death
(mortality over 90 percent). Despite prompt and aggressive
antibiotic treatment for his E.coli meningitis as well as continued care
in the medical intensive care unit, he remained in a coma six days and
hope for a quick recovery faded (mortality over 97 percent). Then,
on the sixth day, the miraculous happened—he opened his eyes, became
alert, and was quickly weaned from the ventilator. The fact that
he went on to have a full recovery from this illness after being in a
coma for nearly a week is truly remarkable.
—Scott Wade, M.D.
~~~~~~~~~~~~~~~~
Neuroscientific Hypotheses I Considered to
Explain My Experience
Dr. Eben Alexander III, MD
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 “functional
column,” 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 hyperreal
experiences. 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 neural calculations required for such a richly
interactive experiential tapestry.
8. A “Reboot Phenomenon” – 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 midbrain, prominently used in birds but only
rarely identifiable in humans. It can be demonstrated in humans who are
cortically blind, due to damaged occipital cortex. It provided no clue
as to the ultra-reality I witnessed, and failed to explain the
auditory-visual interleaving.