We Need Your Help -- NDE Skepticism

Discussion in 'Skeptiko Shows' started by Jason NM, Nov 10, 2016.

  1. 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.
     
    Last edited: Apr 11, 2017
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  2. David Bailey

    David Bailey Administrator

    Joined:
    Oct 31, 2013
    Messages:
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    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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