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| title | chunk | source | category | tags | date_saved | instance |
|---|---|---|---|---|---|---|
| Near-death experience | 7/8 | https://en.wikipedia.org/wiki/Near-death_experience | reference | science, encyclopedia | 2026-05-05T04:18:06.795176+00:00 | kb-cron |
==== Neurochemical models ==== Some theories explain reported NDE experiences as resulting from drugs used during resuscitation (in the case of resuscitation-induced NDEs) ─ for example, ketamine ─ or from endogenous chemicals (neurotransmitters) that transmit signals between brain cells:
In the early 1980s, Daniel Carr wrote that the NDE has characteristics that are suggestive of a limbic lobe syndrome and that the NDE can be explained by the release of endorphins and enkephalins in the brain. Endorphins are endogenous molecules "released in times of stress and lead to a reduction in pain perception and a pleasant, even blissful, emotional state." Judson and Wiltshaw (1983) noted how the administration of endorphin-blocking agents such as naloxone had been occasionally reported to produce "hellish" NDEs. This would be coherent with endorphins' role in causing a "positive emotional tone of most NDEs". Morse et al. (1989) proposed a model arguing that serotonin played a more important role than endorphins in generating NDEs, "at least with respect to mystical hallucinations and OBEs". A 2019 large-scale study found that ketamine, Salvia divinorum, and DMT (and other classical psychedelic substances) are linked to near-death experiences. While ketamine, and other endogenous chemicals can be a source for NDE, it can also mimic these NDE and simulate that out-of-body experiences linked to NDE.
==== Criticism ==== According to Parnia, neurochemical models are not backed by data. This is true for "NMDA receptor activation, serotonin, and endorphin release" models. Parnia writes that no data has been collected via thorough and careful experimentation to back "a possible causal relationship or even an association" between neurochemical agents and NDE experiences.
==== Multi-factorial models ==== The first formal neurobiological model for NDEs in 1989 included endorphins, neurotransmitters of the limbic system, the temporal lobe and other parts of the brain. Extensions and variations of their model came from other scientists such as Louis Appleby (1989). Other authors suggest that all components of near-death experiences can be explained in their entirety via psychological or neurophysiological mechanisms, although the authors admit that these hypotheses have to be tested by science.
==== Low oxygen levels (and G-LOC) model ==== Low oxygen levels in the blood (hypoxia or anoxia) have been hypothesized to induce hallucinations and hence possibly explain NDEs. This is because low oxygen levels characterize life-threatening situations and also the apparent similarities between NDEs and G-force-induced loss of consciousness (G-LOC) episodes. These episodes are observed with fighter pilots experiencing very rapid and intense acceleration that results in lack of sufficient blood supply to the brain. Whinnery studied almost 1000 cases and noted how the experiences often involved "tunnel vision and bright lights, floating sensations, automatic movement, autoscopy, OBEs, not wanting to be disturbed, paralysis, vivid dreamlets of beautiful places, pleasurable sensations, psychological alterations of euphoria and dissociation, inclusion of friends and family, inclusion of prior memories and thoughts, the experience being very memorable (when it can be remembered), confabulation, and a strong urge to understand the experience." Acceleration-induced hypoxia's primary characteristics are "rhythmic jerking of the limbs, compromised memory of events just prior to the onset of unconsciousness, tingling of extremities ..." that are not observed during NDEs. G-LOC episodes do not feature life reviews, mystical experiences and "long-lasting transformational aftereffects", although this may be due to the fact that subjects have no expectation of dying. Hypoxic hallucinations are characterized by "distress and agitation", and this is very different from near-death experiences, which subjects usually report as being pleasant.
==== Altered blood gas levels models ==== Some investigators have studied whether hypercarbia or higher than normal carbon dioxide levels, could explain the occurrence of NDEs. However, studies are difficult to interpret since NDEs have been observed both with increased levels as well as decreased levels of carbon dioxide, and other studies have observed NDEs when levels had not changed, but there is insufficient data on these factors.
==== Other models ==== French said that at least some reports of NDEs might be based upon false memories. According to Engmann (2008), near-death experiences of people who are clinically dead are psychopathological symptoms caused by a severe malfunction of the brain resulting from the cessation of cerebral blood circulation. An important question is whether it is possible to "translate" the bloomy experiences of the reanimated survivors into psychopathologically basic phenomena, e.g., acoasms (nonverbal auditory hallucinations), central narrowing of the visual field, autoscopia, visual hallucinations, activation of limbic and memory structures (according to Moody's stages). The symptoms suppose a primary affliction of the occipital and temporal cortices under clinical death. This basis could be congruent with the thesis of pathoclisis – the inclination of special parts of the brain to be the first to be damaged in case of disease, lack of oxygen, or malnutrition – established in 1922 by Cécile Vogt-Mugnier and Oskar Vogt. Professor of neurology Terence Hines (2003) claimed that near-death experiences are hallucinations caused by cerebral anoxia, drugs, or brain damage. Greyson has called into question the adequacy of the materialist, mind-brain identity model for explaining NDEs. An NDE often involves vivid and complex mentation, sensation and memory-formation under circumstances of completely disabled brain function during general anesthesia, or near-complete cessation of cerebral blood flow and oxygen uptake during cardiac arrest. Materialist models predict that such conscious experiences should be impossible under these conditions. The mind-brain identity model of classic materialist psychology may need to be expanded to adequately explain an NDE.
== See also ==