According to some scientists, the NDE can be explained by physiological and psychological manifestations.
Clinical circumstances which may lead to NDE include the following conditions: cardiac arrest, post-traumatic shock after significant blood loss or perioperative complications, anaphylaxis, shock, coma, intracerebral hemorrhage or cerebral infarction, attempted suicide, quasi- drowning or asphyxia, apnea, and severe depression.
Physiological explanation
Several neuroscientists explain the near-death experience with an altered consciousness, the latter being due to the disturbance of brain chemistry occurring during the process of death or may result from a psychological response to the perceived threat of death. The brain is supposed to be hypoactive during cardiac arrest. However neurophysiology at the time of cardiac arrest has not been systematically studied in survivors of cardiac arrest, clues would point that this is not the case at the start of cardiac arrest, outbreaks of electroencephalographic activity (measured by the bispectral index) have been reported in humans undergoing organ donation after cardiac death. An animal model was established to analyze the state of consciousness in mammals during the first ten seconds of clinical death. Experimental results allow to observe a general increase and transient brain activity associated with a strong cerebral excitement. At the beginning of clinical death, many electrical signatures already known to consciousness exceed the levels identified in the waking state, suggesting that the brain is capable of organized electrical activity during the early phase of clinical death . Furthermore, it was shown that hypercapnia and hyperkalemia are indicators for the occurrence of NDE when the levels reach a certain threshold. Physiological factors that may be important in triggering the NDE are anoxia, the presence of endorphins, dopamine and serotonin. These factors can induce abnormal activity of the temporal lobe or the limbic system. The temporal lobe is probably crucial in NDE due to its sensitivity to anoxia whose stimuli are known to induce hallucinations, retrospective memory, and output of body experiences. Deprivation of oxygen, or anoxia, is known to cause many symptoms of NDE. This process involves the NMDA receptor. These receptors are abundant in levels of synapses in the cortex of the frontal and temporal lobes. These lobes are involved in cognitive processes such as thinking, memory and perception. NMDA receptors are activated by glutamate, a neurotransmitter, but if glutamate release is too high, eg during anoxia, it can cause neuronal death by a process known as “excitotoxicity”. The brain has mechanisms to protect against excitotoxicity due to anoxia. To inhibit excitotoxicity, a competitive inhibitor may bind at a site allosteric near NMDA receptor steric hindrance physically prevents access of glutamate to the NMDA receptor. The blocking of NMDA receptors has the side effect of blocking the activity of neurons. However, a decrease in activity of neurons in the right temporal lobe, especially the angular gyrus, can induce output body experience (autoscopic phenomenon). Indeed, in 2002, Olaf Blanke, Stephanie Ortigue, Theodor Landis and Margitta Seeck, Department of Neurology of the University Hospital of Geneva, published in Nature an article describing a disembodiment of experience caused by electrical stimulation of the angular gyrus in an epileptic patient. According Blanke and Christina Mohr77 the autoscopic phenomena include the body of the out of body experiences (OBE), the autoscopic hallucinations (also called: external autoscopy, and specular deuteroscopy or hallucination) and autoscopy.
- Out of body experiments are defined as a impression to see his environment, and hence often the physical body, from the outside of his body. The outside view most frequently cited is the one who is over his own body. Incidentally, when the OBE phenomenon occurs during sleep, the splitting body takes different denominations following authors: gorgeous body, defined by Frederik van Eeden, whose description can not be distinguished from dual astral, but that he considers a product of his imagination, me imaginary body defined by Frétigny and Viral, that explain it as an experience where the subject projects two imaginary body: one who acts and one who remains stationary.
- The autoscopic hallucinations are defined as the vision itself from his actual physical body. There aren’t actually a splitting phenomenon in the strict sense. Catherine Lemaire asks why the vision is described as semi-transparent in autoscopic hallucinations, while it seems very in the out of body experiences. Anyway, the autoscopic hallucinations seem to match the phenomena of the doppelgänger and bilocation.
- The autoscopy experience is an intermediate between OBE and autoscopic hallucination where the subject does not always know if he is disembodied or whether his view is from his body or hid double.
According to Susan Blackmore, anoxia will be also involved in the visual cortex by inducing cortical disinhibition and would be at the origin of tunnel vision. The visual cortex is organized with numerous cells dedicated to the vision in the center of the field, and little on the outskirts. The random excitation produces a bright light effect in the center of the visual field and fade to obscurity in the periphery, in other words, a tunnel effect.
Moreover, some-have a reconciliation with the REM intrusions in wakefulness observed in some pathologies. It is an activation of the occipital cortex, regulated by several brainstem structures like pedunculopontine nucleus, the lateral tegmentum, the dorsal raphe, locus coeruleus (cholinergic mechanism that would counterbalance the reaction of noradrenergic alert locus involving the locus cœruleus). Kevin Nelson continued His research and established the role of the brain stem in triggering the visual phenomena of NDE.
Psychological explanation
In 1976, Dr. in psychiatry Russell Noyes Jr speculated that NDE would consist of a form of depersonalization, characterized by the loss of the sense of reality and which would act as a defense against death threat.
NDE can also be explained in terms of dissociation, reactivation of birth memories and regression.
In a theory developed by Kinseher in 2006, the current knowledge of the autonomic nervous system are applied in search of NDE phenomenon. His theory explains that the experience of imminent death is a paradox of extreme strangeness for a living organism, which in turn triggers a NDE: during it, the individual becomes able to “see” the brain full analysis of all episodic memory (including prenatal experiences) to find a similar experience to the imminent death situation. All these pieces of information analyzed and recovered are continuously evaluated by the brain, as if searching for a mechanism to copy a way to avoid this potentially fatal situation. Kinseher think that’s why a near-death experience is so unusual. According to this theory, extracorporeal experiences that “accompany” the NDE would be an attempt by the brain to re-create a mental representation of the situation and the stage. The brain then draw on the information of the sensory collectors and stored experience (knowledge), producing a sort of “dream” about the self and the environment. Anyway, physiological or psychological explanations do not explain, in the present state of knowledge, the NDE with a flat EEG, therefore no electrical brain activity.
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