Apr 23 2010
Back in 2008 I wrote on Near Death Experiences (NDE’s). I have an interest in this topic as I have frequent exposure to near death; my wife has a predilection for watching Judge Judy. Since 2008 there have been a few studies on the topic of NDEs as researchers try and find evidence that consciousness transcends the brain, if that is what a NDE represents. I have also been ill for most of the last week and have not had the usual time to spend generating typos to drive some readers to distraction. Fortunately, I have a miracle cure that is 100% effective in resolving all my self-limited illnesses: time. It passed and with it the illness. As a result I am about 10 days behind in the commitments in my life, so this will be a shorter than usual post.
As will come as no surprise to anyone who reads this blog regularly, I am of the opinion that NDEs are almost certainly physiologic in origin. I see no reason why consciousness should exist beyond physiologic brain function. I am not sympathetic to the whole mind-brain dichotomy and see no reason why the mind is not the result of brain function. No one ever speaks of the lung-gas exchange dichotomy or the kidney-urine production dichotomy. But that is my bias, and I mention it at the beginning of the post in the interest of openness.
There is an enormous popular literature on NDEs, but little in the way of science, probably, I would guess, is that it is difficult to prospectively find subjects upon which to do studies.
There are people, however, who are going to die and it is nice to allow them to go gentle into that good night. I appreciate the efforts of palliative care specialists, as while I have never particularly worried about being dead, the process of getting there has never seemed particularly inviting. Part of ensuring that patients are comfortable is to monitor their cerebral function to make sure the remain unaware. This technique was developed by anesthesiologists who did not want their patients to become conscious during surgery yet have no ability to communicate that they were now aware that their appendix was being removed.
Dying patients had their brain function monitored to make sure they remained unconscious as they died. If you decide to remove a patient from the ventilator as an example, you do not want them to be aware.
As the brain dies, there appears to be a last, short, burst of a of electrical activity.
…loss of blood pressure, as monitored by indwelling arterial line, was followed by a decline is BIS/PSI activity followed by a transient spike in BIS/PSI activity that approached levels normally associated with consciousness. This spike in electroencephalogram (EEG) activity had short duration and the activity then declined to a level of activity associated with burst suppression.
A last gasp of activity before the void. What is happening? What does this burst represent? Is the world being observed one last time? Does the patient see themselves from afar? Are they going to the light? Are memories reviewed or being formed? No one knows. Everyone died and are unable to report what they thought or experienced with the burst of activity. But one could speculate. And one does
We speculate that this level of BIS/SEDline activity is related to the cellular loss of membrane polarization due to hypoxemia. We further speculate that since this increase in electrical activity occurred when there wash no blood pressure, patients who suffer “near death” experiences may be recalling the aggregate memory of the synaptic activity associated with this terminal but potentially reversible hypoxemia.
So perhaps the NDE is the last flurry of electrical activity by the brain and, if the patient were brought back from the grave, they would recall this activity as a NDE. Or not. Like most of what occurs in the minds of the dying, it is lost to death.
NDEs can be induced by drugs. Ketamine, an anesthetic drug, can also cause a reaction similar to an NDE. Ketamine can cause visual distortions and a lost sense of time, sense, and identity. Ketamine works as a NMDA receptor antagonist, similar to the action the more familiar drugs dextromethorphan, phencyclidine (PCP), and nitrous oxide. All these drugs can cause a dissociative state. I remember when I had nitrous oxide for my wisdom teeth extractions, I became convinced that I was not in the dental chair, but was somehow outside looking in on the oral surgery. To ‘prove’ I was in the chair, I kept lifting my hands up and waving them, to the distraction of the oral surgeon. I had a similar reaction to indomethacin, a sense that I was in the corner of the room looking down at me. It is most odd.
We aimed here at assessing, in a sample of ketamine misusers, concordance between the typical near-death experience (NDE) features and the on-drug psychoactive effects the subjects experienced. In 2003-2005, a sample of previous ketamine misusers recollecting a ketamine-related NDE were recruited through snowballing and screened with the means of the Greyson NDE Scale; 125 participants made an initial contact with the researcher and 50 reported a minimum score of seven at the “Greyson NDE Scale”. Interviewees were in the range 21-66 years old; 27 participants (54%) were educated at BA level, 18 (36%) had an MSc, and 5 (10%) a PhD. Eight (16%) interviewees had a definite religious background. An average lifetime ketamine intake of 140 occasions was reported by the interviewees, who typically presented with a polydrug, including cannabis and MDMA/ecstasy, misuse history. In 45 (90%) cases, the NDE occurred during the first few occasions of intake. Most frequent features of reported NDE states included: altered perception of time (90%), strong sense of detaching from own physical body (88%), and a sense of peace/joy (76% of subjects). Although results here described were elicited from a self-selected, nonrandomized, limited size sample of misusers, we suggest that recreational ketamine intake may be associated with occurrence of near-death related states.
Of course, just because James Randi can bend a spoon using prestidigitation doesn’t mean that Uri Geller isn’t bending spoons with his mind. Similarly, just because NDEs can be mimicked in ketamine abusers, er, I mean misusers, doesn’t mean that ‘real’ NDEs are not the consciousness going towards the hereafter. But I am an Occam kind of guy; why should entities be multiplied beyond what is necessary?
Numerous physiologic parameters go awry as you die and all your body functions fail. Many tightly controlled parameters become progressively deranged: pH, C02, sodium, etc. Could these derangement’s have something to do with the physiology of NDEs?
In a recent study they evaluated 52 patients who survived an out of hospital cardiac arrest, of whom 11, or 21% had an NDE. As a group, the NDEs had both higher CO2 levels and lower O2 levels in the blood. They also found increased potassium in those with NDEs.
They note prior studies that demonstrate that low levels of oxygen can result in NDEs, perhaps by way of the NMDA receptor as well. Low oxygen and high CO2 may be a plausible physiologic partial explanation for NDEs. Whether some brains are predisposed to NDEs (since some patients had more than one, poor guys, nearly dying more than once) or there are other factors has yet to be elucidated.
The high potassium? In the discussion they comment,
“Alternative theories found the explanation for NDEs in quantum theory, which suggests that consciousness may arise from quantum processes within neuronal microtubules. The recent work of Bernroider and Roy suggests that quantum entanglement in the ion channels (especially in the potassium channel) of brain cells underlies information processing in the brain and, ultimately, also consciousness. Although untenable and purely theoretic, this possible connection between potassium channels in the brain and the mechanism of consciousness (and therefore the possible mechanism of NDEs) deserves further investigation.”
Once you invoke quantum mechanics for any process macroscopic process in medicine (except, perhaps, MRIs), you lose credibility. Exactly why an untenable explanation deserves further investigation is not explained.
Potentially psychologic factors were not associated with NDEs in this study. “Sex, level of education, fear of death, time until ROSC, and religious belief” were not associated with an NDE, lending credence to that idea that NDEs are a physiologic response rather than spiritual response, although I suspect the authors lean towards the spiritual side.
“Clearly, the presence of NDEs pushes the current knowledge of human consciousness and mind-brain relation to the edge of our understanding.”
To my mechanistic, reductionist way of thinking, NDEs are the last gasp of activity of a dying brain. Like a cramp in an ischemic leg, it does not push the muscle-contraction relation to the edge of out understanding.
Again, association is not causation, but there is an interesting rat study that suggests that both low pH and increase C02 combine to inhibit NMDA receptors, just like ketamine.
BACKGROUND: Carbon dioxide (CO2) dose-dependently decreases minimum alveolar concentration (MAC) of anaesthetics in rats. CO2 also dose-dependently decreases cerebrospinal fluid pH. N-methyl-D-aspartate (NMDA) channels exhibit pH sensitivity and are putative targets for inhaled anaesthetics. We hypothesized that CO2 dose-dependently decreases rat NMDA channel current via an acidifying effect at concentrations relevant to CO2 MAC.
METHODS: To test this hypothesis, we studied rat NR1/NR2A glutamate receptors expressed in voltage-clamped Xenopus oocytes. To measure pH effects, we used perfusates adjusted between 7.3 and 5.3 with HCl. To measure CO2 effects, we used equimolar sodium perfusates containing either 0 or 24 mM NaHCO3 and CO2 between 0% and 87% atm. Solution compositions were measured using a blood gas analyser with values corrected using a calibrated pH meter and gas chromatograph with solutions at 37 degrees C.
RESULTS: We found that decreasing pH decreased NMDA current. Moreover, pH effects produced by adding CO2 to NaHCO3-containing perfusates were identical to those produced by adding HCl to normal perfusates. The pH inhibiting 50% of NMDA current was 6.52. The CO2 concentration inhibiting 50% of rat NMDA current was 63% for solutions with 24 mM NaHCO3. CO2 exhibited a linear dose-dependent NMDA response analogous to that observed for in vivo CO2 anaesthetic potency in rats.
CONCLUSIONS: CO2 and hydrogen ions act via the same mechanism to inhibit NMDA receptors. Moreover, CO2 inhibits rat NMDA receptors in a manner that is consistent with CO2 MAC-sparing effects in rats.”
NDEs will unlikely be an area of research that will ever lead to definitive conclusions. Dead men tell no tales and those that survive are unlikely to volunteer their brains for further evaluation, and most patients to survive a cardiac arrest are in no condition to be used in acute clinical studies.
NDEs appear to be reproducible by medications and are probably the response of the dying brain to an inhospitable metabolic milieu. However, like Houdini, when I die, if I can come back, I will come back and tell you about my dying. In the meantime, if I see the light, I’m not going towards it, no matter how inviting.
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