Murals (2008) by PHANTAST - Graffiti - Cultural Music & Art Association inc. - 98 Milne St. Benleigh
"My experience showed me that the death of the body and brain is not the end of consciousness..."
When prominent US neurosurgeon Dr. Eben Alexander goes into a coma after contracting a severe brain infection, his doctors tell his family to prepare for the worst - death or, at best, survival in a vegetative state.. Remarkably, Dr. Alexander wakes seven days later with his faculties intact. Based on all that is known about how the brain works, Dr. Alexander had no capacity, while in the coma, to create thought; his neocortex, the part of the brain that makes us human, had effectively shut down. So how was it that he awoke with a coherent and profound set of memories?
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 - all failed to explain the rich, robust, intricate interactivity of the Gateway and Core experiences:
1. A primitive brainstem program to ease terminal pain and suffering ("evolutionary argument" - possibly 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 overlaying brain to be relatively protected from the meningitic inflammation, which occurs mainly at the brain's surface - again, did not explain the interactive nature of the recollections.
3. Endogenous glutamate blockade with excitotoxicity, mimicking the hallucinatory anesthetic, ketamine (occasionally used to explain near-death-experiences in general. I occasionally saw the effects of ketamine used as an anesthetic during the earlier part of my neurological career at Harvard Medical School. The hallucinatory state it induced was most chaotic and unpleasant, and bore no resemblance whatsoever to my experinece.
4. N,N-dimethyltryptamine (DMT) "dump" (form the pineal, or elsewhere in the brain). DMT, a naturally occurring serotonin agonist, causes vivid hallucinations and a dreamlike state. 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 would have had effects on visual/ auditory experience.
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 cell count (WBC)> 27,000 per mmc; 31% bands with toxic granulations, CSF WBC count > 4,300 per mmc; 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. Diffuse meningitis over the brain's surface effectively disable the entire neocortex due to this columnar architecture. Full- thickness destruction is unnecessary for total function 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" - 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 seem most unlikely.
9. Unusual memory generation through an archaic visual pathway through the midbrain, prominently used in birds but only rarely identifiable 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. (Proof of Heaven, Eben Alexander, M.D. First published 2012 in US by Simon & Schuster).