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      The evolutionary origin of near-death experiences: a systematic investigation

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          Abstract

          Near-death experiences are known from all parts of the world, various times and numerous cultural backgrounds. This universality suggests that near-death experiences may have a biological origin and purpose. Adhering to a preregistered protocol, we investigate the hypothesis that thanatosis, aka death-feigning, a last-resort defense mechanism in animals, is the evolutionary origin of near-death experiences. We first show that thanatosis is a highly preserved survival strategy occurring at all major nodes in a cladogram ranging from insects to humans. We then show that humans under attack by animal, human and ‘modern’ predators can experience both thanatosis and near-death experiences, and we further show that the phenomenology and the effects of the two overlap. In summary, we build a line of evidence suggesting that thanatosis is the evolutionary foundation of near-death experiences and that their shared biological purpose is the benefit of survival. We propose that the acquisition of language enabled humans to transform these events from relatively stereotyped death-feigning under predatory attacks into the rich perceptions that form near-death experiences and extend to non-predatory situations.

          Abstract

          Thanatosis, also known as death-feigning or tonic immobility, is a well-described and phylogenetically highly preserved survival strategy in the animal kingdom. Peinkhofer et al. investigate the hypothesis that thanatosis is the evolutionary origin of near-death experiences in humans.

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          Most cited references105

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          The role of spreading depression, spreading depolarization and spreading ischemia in neurological disease.

          The term spreading depolarization describes a wave in the gray matter of the central nervous system characterized by swelling of neurons, distortion of dendritic spines, a large change of the slow electrical potential and silencing of brain electrical activity (spreading depression). In the clinic, unequivocal electrophysiological evidence now exists that spreading depolarizations occur abundantly in individuals with aneurismal subarachnoid hemorrhage, delayed ischemic stroke after subarachnoid hemorrhage, malignant hemispheric stroke, spontaneous intracerebral hemorrhage or traumatic brain injury. Spreading depolarization is induced experimentally by various noxious conditions including chemicals such as potassium, glutamate, inhibitors of the sodium pump, status epilepticus, hypoxia, hypoglycemia and ischemia, but it can can also invade healthy, naive tissue. Resistance vessels respond to it with tone alterations, causing either transient hyperperfusion (physiological hemodynamic response) in healthy tissue or severe hypoperfusion (inverse hemodynamic response, or spreading ischemia) in tissue at risk for progressive damage, which contributes to lesion progression. Therapies that target spreading depolarization or the inverse hemodynamic response may potentially treat these neurological conditions.
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            Neural Circuitry of Wakefulness and Sleep.

            Sleep remains one of the most mysterious yet ubiquitous animal behaviors. We review current perspectives on the neural systems that regulate sleep/wake states in mammals and the circadian mechanisms that control their timing. We also outline key models for the regulation of rapid eye movement (REM) sleep and non-REM sleep, how mutual inhibition between specific pathways gives rise to these distinct states, and how dysfunction in these circuits can give rise to sleep disorders.
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              A putative flip-flop switch for control of REM sleep.

              Rapid eye movement (REM) sleep consists of a dreaming state in which there is activation of the cortical and hippocampal electroencephalogram (EEG), rapid eye movements, and loss of muscle tone. Although REM sleep was discovered more than 50 years ago, the neuronal circuits responsible for switching between REM and non-REM (NREM) sleep remain poorly understood. Here we propose a brainstem flip-flop switch, consisting of mutually inhibitory REM-off and REM-on areas in the mesopontine tegmentum. Each side contains GABA (gamma-aminobutyric acid)-ergic neurons that heavily innervate the other. The REM-on area also contains two populations of glutamatergic neurons. One set projects to the basal forebrain and regulates EEG components of REM sleep, whereas the other projects to the medulla and spinal cord and regulates atonia during REM sleep. The mutually inhibitory interactions of the REM-on and REM-off areas may form a flip-flop switch that sharpens state transitions and makes them vulnerable to sudden, unwanted transitions-for example, in narcolepsy.
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                Author and article information

                Contributors
                Journal
                Brain Commun
                Brain Commun
                braincomms
                Brain Communications
                Oxford University Press
                2632-1297
                July 2021
                22 June 2021
                22 June 2021
                : 3
                : 3
                : fcab132
                Affiliations
                Department of Neurology, Rigshospitalet, Copenhagen University Hospital , Copenhagen 2100, Denmark
                Department of Psychiatry, Frederiksberg Hospital, Copenhagen University Hospital , Copenhagen 2000, Denmark
                Coma Science Group, GIGA-Consciousness, University of Liège , Liège 4000, Belgium
                Centre du Cerveau2, University Hospital of Liège , Liège 4000, Belgium
                Coma Science Group, GIGA-Consciousness, University of Liège , Liège 4000, Belgium
                Coma Science Group, GIGA-Consciousness, University of Liège , Liège 4000, Belgium
                Centre du Cerveau2, University Hospital of Liège , Liège 4000, Belgium
                Department of Neurology, Rigshospitalet, Copenhagen University Hospital , Copenhagen 2100, Denmark
                Department of Clinical Medicine, University of Copenhagen , Copenhagen 2100, Denmark
                Author notes
                Correspondence to: Daniel Kondziella, MD, PhD, MSc, FEBN Department of Neurology, Rigshospitalet, Copenhagen University Hospital, DK-2100 Copenhagen, Denmark. E-mail: daniel_kondziella@ 123456yahoo.com

                Costanza Peinkhofer and Charlotte Martial contributed equally to this work.

                Author information
                https://orcid.org/0000-0001-5562-9808
                Article
                fcab132
                10.1093/braincomms/fcab132
                8260963
                34240053
                832b7331-ba61-453e-8d79-e3709ed4f94b
                © The Author(s) (2021). Published by Oxford University Press on behalf of the Guarantors of Brain.

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 22 March 2021
                : 18 April 2021
                : 05 May 2021
                Page count
                Pages: 13
                Funding
                Funded by: Lundbeck Foundation; Rigshospitalets forskningspuljer, Rigshospitalet, Copenhagen University Hospital; Region Hovedstaden; Jens Juhl Fonden; Jascha Fonden (D.K.); the University and University Hospital of Liege;
                Funded by: Belgian National Funds for Scientific Research;
                Funded by: European Union’s Horizon 2020 Framework Programme for Research and Innovation; the Bial Foundation, the Mind Science Foundation and the European Commission; the Fund Generet; the King Baudouin Foundation; the Mind-Care foundation;
                Categories
                Original Article
                AcademicSubjects/MED00310
                AcademicSubjects/SCI01870

                death,evolution,near-death experience,survival,tonic immobility

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