A Central Role for the NMDA Receptor
The Ketamine Model of the Near Death Experience:
Dr. Karl L. R. Jansen, MD, PhD, MRCPsych.
A Central Role for the NMDA Receptor
The Maudsley Hospital
London SE5 8AZ
Near-death experiences (NDE's) can be reproduced by ketamine via blockade
of receptors in the brain (the N-methyl-D-aspartate, NMDA receptors) for
the neurotransmitter glutamate. Conditions which precipitate NDE's
(hypoxia, ischaemia, hypoglycaemia, temporal lobe epilepsy etc.) have been
shown to release a flood of glutamate, overactivating NMDA receptors
resulting in neuro ('excito') toxicity. Ketamine prevents this
neurotoxicity. There are substances in the brain which bind to the same
receptor site as ketamine. Conditions which trigger a glutamate flood may
also trigger a flood of neuroprotective agents which bind to NMDA receptors
to protect cells, leading to an altered state of consciousness like that
produced by ketamine. This article extends and updates the theory proposed
in 1990 (Jansen, 1990b).
The near-death experience (NDE) is a phenomenon of considerable importance
to medicine, neuroscience, neurology, psychiatry, philosophy and religon
(Stevenson and Greyson, 1979; Greyson and Stevenson, 1980; Ring, 1980;
Sabom, 1982; Jansen, 1989a,b, 1990b). Unfortunately, some scientists have
been deterred from conducting research upon the NDE by claims that NDE's
are evidence for life after death, and sensationalist media reports which
impart the air of a pseudoscience to NDE studies. Irrespective of religous
beliefs, NDE's are not evidence for life after death on simple logical
grounds: death is defined as the final, irreversible end. Anyone who
'returned' did not, by definition, die - although their mind, brain and
body may have been in a very unusual state.
There is overwhelming evidence that 'mind' results from neuronal
activity. The dramatic effects on the mind of adding hallucinogenic drugs
to the brain, and the religous experiences which sometimes result, provide
further evidence for this (Grinspoon and Bakalar, 1981). One of the many
contradictions which 'after-lifers' can not resolve is that "the spirit
rises out of the body leaving the brain behind, but somehow still
incorporating neuronal functions such as sight, hearing, and
proprioception" (Morse, 1989, original italics).
All features of a classic NDE can be reproduced by the intravenous
administration of 50 - 100 mg of ketamine (Domino et al., 1965; Rumpf
,1969; Collier, 1972; Siegel,1978, 1980,1981; Stafford, 1977; Lilly, 1978;
Grinspoon and Bakalar, 1981; White, 1982; Ghoniem et al., 1985; Sputz,
1989; Jansen, 1989a,b, 1990b, 1993). There is increasing evidence which
suggests that the reproduction of NDE's by ketamine is unlikely to be a
coincidence. This evidence includes the discovery of the major neuronal
binding site for ketamine, known as the phencyclidine (PCP) binding site of
the NMDA receptor (Thomson et al., 1985), the importance of NMDA
receptors in the cerebral cortex, particularly in the temporal and frontal
lobes, the key role of these sites in cognitive processing, memory, and
perception, their role in epilepsy, psychoses, hypoxic/ischaemic and
epileptic cell damage (excitotoxicity), the prevention of this damage by
ketamine, the discovery of substances in the brain called 'endopsychosins'
which bind to the same site as ketamine, and the role of ions such as
magnesium and zinc in regulating the site (Anis et al., 1983; Quirion et
al., 1984; Simon et al., 1984; Benveniste et al., 1984; Ben-Ari,1985;
Thomson, 1986; Coan and Collingridge, 1987; Collingridge, 1987; Contreras
et al., 1987; Rothman et al., 1987; Mody et al., 1987; Quirion et al.,
1987; Westbrook and Mayer, 1987; Sonders et al., 1988; Barnes,1988;
Choi,1988; Monaghan et al., 1989; Jansen et al., 1989a,b,c, 1990a,b,c,
Characteristic Features of the Near-Death Experience
There is no internationally determined and agreed set of criteria which
define the NDE, no list of 'research diagnostic criteria' similar to those
provided by the American Psychiatric Association (APA) for psychiatric
disorders. This lack has allowed some critics of neurobiological models to
dismiss these models because some particular criterion which they believe
to be important may not have been fully accounted for by the model being
proposed, although it may well be that a consensus, statistical definition
of the key features of the NDE would not include those features - just as,
for example, the APA definition of schizophrenia (1980) represents an
international consensus and avoids the sectarian views of a few, or
inclusion of obscure cases which do not meet the general rule. For example,
Gabbard and Twemlow (1989) argued that Saavedra -Aguilar and Gomez-Jeria's
neurobiological hypothesis (1989), which was based on temporal lobe
electrical abnormalities, did not have general validity because Gabbard and
Twemlow had identified 5 cases in which hypoxia and stress did not appear
to be a triggering factor (temporal lobe epilepsy, and many acute
psychoses, can occur spontaneously without any apparent triggering
factors). These cases are certainly not adequate grounds for the dismissal
of neurobiological models.
Ketamine administered by intravenous injection, in appropriate dosage, is
capable of reproducing all of the features of the NDE which have been
commonly described in the most cited works in this field, and the following
account is based upon these (Domino et al., 1965; Rumpf, 1969; Collier,
1972; Siegel,1978, 1980, 1981; Stafford, 1977; Lilly, 1978; Grinspoon and
Bakalar, 1981; White, 1982; Ghoniem et al., 1985; Sputz, 1989; Jansen,
1989a, b,1990b, 1991c, 1993).
Important features of NDE's include a sense that what is experienced is
'real' and that one is actually dead, a sense of ineffability,
timelessness, and feelings of calm and peace, although some cases have been
frightening. There may be analgesia, apparent clarity of thought, a
perception of separation from the body, and hallucinations of landscapes,
beings such as 'angels', people including partners, parents, teachers and
friends (who may be alive at the time), and religous and mythical figures.
Transcendant mystical states are commonly described. Memories may emerge
into consciousness, and are rarely organised into a 'life review' (Greyson,
Hearing noises during the initial part of the NDE has also been described
(Noyes and Kletti, 1976a; Morse et al., 1985; Osis and Haraldsson, 1977;
Greyson and Stevenson, 1980; Ring, 1980; Sabom, 1982). Ring (1980)
classified NDE's on a 5 stage continuum: 1.feelings of peace and
contentment; 2.a sense of detachment from the body; 3. entering a
transitional world of darkness (rapid movements through tunnels: 'the
tunnel experience'); 4. emerging into bright light; and 5. 'entering the
light'. 60% experienced stage 1, but only 10% attained stage 5 (Ring,
1980). As might be expected in a mental state with a neurobiological
origin, more mundane accounts also occur, e.g. children who may 'see' their
schoolfellows rather than God and angels (Morse, 1985). It is clear that
NDE's are not as homogeneous as some have claimed.
Ketamine and Phencyclidine
Ketamine is a short-acting, hallucinogenic, dissociative anaesthetic
related to phencyclidine (PCP). Both drugs are arylcyclohexylamines - they
are not opioids and are not related to LSD. In contrast to PCP, ketamine is
relatively safe, an uncontrolled drug in most countries, and remains in
use as an anaesthetic for children (White et al., 1982). Anaesthetists
attempt to prevent patients from having NDE's (emergence phenomena) by the
co-administration of benzodiazepines and other sedative substances which
produce 'true' unconsciousness rather than dissociation (Reich and Silvay,
Ketamine produces an altered state of consciousness which is very
different from that of the 'psychedelic' drugs such as LSD (Grinspoon and
Bakalar, 1981). It can reproduce all features of the NDE, including travel
through a dark tunnel into light, the conviction that one is dead,
'telepathic communion with God', hallucinations, out-of-body experiences
and mystical states (see ketamine references above). If given
intravenously, it has a short action with an abrupt end. Grinspoon and
Bakalar (1981, p34) wrote of: '...becoming a disembodied mind or soul,
dying and going to another world. Childhood events may also be re-lived.
The loss of contact with ordinary reality and the sense of participation in
another reality are more pronounced and less easily resisted than is
usually the case with LSD. The dissociative experiences often seem so
genuine that users are not sure that they have not actually left their
A psychologist with experience of LSD described ketamine as 'experiments in
voluntary death' (Leary, 1983, p375). Sputz (1989, p65) noted:'one
infrequent ketamine user reported a classic near-death experience..."I was
convinced I was dead. I was floating above my body. I reviewed all of the
events of my life and saw a lot of areas where I could have done better".
The psychiatrist Stanislav Grof stated: "If you have a full-blown
experience of ketamine, you can never believe there is death or that death
can possibly influence who you are" (Stevens, 1989, p481-482).
'Ketamine allows some patients to reason that ...the strange, unexpected
intensity and unfamiliar dimension of their experience means they must have
died..' (Collier, 1981, p552).
Attempts to explain NDE's as hallucinations are sometimes rejected by
spiritualists because many persons insist upon the reality of their
experiences (Osis and Haraldsson, 1977; Ring, 1980). However, 30% of normal
subjects given ketamine were certain that they had not been dreaming or
hallucinating, but that the events had really happened (Rumpf et al., 1969;
see also Siegel, 1978). What is a hallucination ?
" a hallucination has the immediate sense of reality of a true perception
.....transient hallucinatory experiences are common in individuals without
mental disorder" (APA, 1980). The apparently clear sensorium of some
persons who have had NDE's has also been used to argue that the NDE is
'real' and not a hallucination (Osis and Haraldsson, 1977; Ring, 1980). It
is thus important to note that hallucinations in schizophrenia typically
occur in clear consciousness and are believed to be real (APA, 1980). A
personal conviction of the 'reality' of an NDE does not invalidate
scientific explanations. Some users of LSD have claimed that their minds
are clearer than usual, and that the LSD world is real while the 'normal'
world is a veil of illusion (Grinspoon and Bakalar, 1981). Cardiac arrest
survivors have been reported as describing their resuscitation in detail
(Sabom, 1982). Ketamine can permit sufficient sensory input to allow
accounts of procedures during which the patient appeared wholly unconscious
Glutamate, NMDA and Sigma Receptors, and the Hippocampus
Most large neurones in the cerebral cortex use glutamate as their
neurotransmitter. Glutamate, an excitatory amino acid, is central to the
function of the hippocampus, temporal and frontal lobes (Cotman et al.,
1987; Fagg and Foster, 1983; Greenamyre et al., 1984; Monaghan, Bridges and
Cotman, 1989; Jansen et al., 1989c, 1990a) and plays a vital role in all
cognitive processes involving the cerebral cortex, including thinking,
memory and perception (Monaghan, Bridges and Cotman, 1989; Oye et al.,
The major neuronal binding site for ketamine is called the PCP receptor,
which is itself attached to the NMDA receptor (Monaghan, Bridges and
Cotman, 1989). As they are part of the same macromolecular complex, the two
terms are sometimes used interchangeably. It was formerly believed that the
sigma and PCP sites were the same entity, but it is now clear that sigma
receptors are very different, have a unique distribution in the CNS, and
are not a form of opioid receptor (Walker et al., 1990; Jansen et al.,
There was initially some debate as to whether the hallucinogenic
properties of ketamine were due to NMDA or sigma receptors (Jansen, 1990b).
These effects are now largely attributed to NMDA receptor blockade
(Krystal et al., 1994). Sigma ligands with a high degree of specificity
(e.g. (+)pentazocine) do not produce NDE's at doses where most of the
binding is to sigma rather than NMDA and/or kappa opioid receptors
(sigma receptor ligands frequently have affinity for NMDA and/or kappa
opioid receptors at higher doses) (Musacchio et al., 1990; Walker et al.,
When glutamate is present in excess, neurones die via a process called
excitotoxicity. Conditions which have been proven to lead to excessive
release of glutamate include hypoxia/ischaemia, epilepsy and hypoglycaemia
(e.g. Rothman, 1984; Rothman and Olney, 1986, 1987). Blockade of PCP
receptors prevents cell death from excitotoxicity (e.g. Rothman et al.,
1987). The brain may thus have a protective mechanism against a glutamate
flood: release of a counter-flood of substances which block PCP receptors,
preventing neuronal death. Considering the sophistication of the brain's
many known defences, and the vulnerability of neurones to hypoxia, a
protective mechanism against excitotoxicity seems very likely. This is the
only speculation in the process outlined above: the other statements are
strongly supported by experimental evidence (Benveniste et al.,1984; Simon
et al., 1984; Ben-Ari, 1985; King and Dingledine, 1986; Rothman et al.,
1987; Westerberg et al., 1987; Hoyer and Nitsch, 1989). A peptide called
a-endopsychosin, which binds to the PCP receptor, has been found in the
brain (Quirion et al., 1984). Certain ions such as magnesium and zinc also
act as endogenous PCP channel blockers (Thomson, 1986; Westbrook and
Mayer, 1987; Cotman, Monaghan and Ganong, 1988), and it is possible that
these ions are centrally involved in producing NDE's.
Scientific Hypotheses and NDE's
Claims that NDE's must have a single explanation (e.g. Ring, 1980), or
that a scientific theory must explain all of the experiences ever given
the name of NDE (e.g. Gabbard and Twemlow, 1989) are difficult to justify.
It is well established that mental phenomena have multiple causes and
variable expressions. The NDE is more likely to be the final common
expression of several different causes. Even then, the final 'common'
expression contains sufficient variability to suggest different types of
NDE, for example in Ring's study (1980), only 10% 'enter the light'. A
multi-levelled interpretation is thus the most useful. The glutamate
hypothesis of the NDE is not intended to apply to every NDE, and is not
necessarily incompatible with the theories described below.
Temporal Lobe Epilepsy
It has been claimed that there is some similarity between the phenomena
experienced in temporal lobe epilepsy (TLE) and NDE's (Persinger and
Makarec ,1987; Saavedra-Aguilar and Gomez-Jeria,1989). Glutamate is the key
neurotransmitter in the temporal lobe, particularly in the hippocampus, and
is implicated in epilepsy. The neuropathology of epilepsy is believed to
result from excito-toxic cell death (Ben-Ari, 1985; King and Dingledine,
1986; Olney, Collins and Sloviter, 1986; Mody and Heinemann, 1987; Cotman,
Monaghan and Ganong, 1988).
A neuroprotective system might become active in any excitotoxic situation
including epilepsy. The degree of damage, and the mental state, resulting
from a glutamate flood may depend on the final balance in each neuronal
pathway between excito-toxic forces and neuroprotective mechanisms. Persons
who were oxygen deprived for prolonged periods and had a profound NDE,
sometimes survived the episode unimpaired (Sabom, 1982). The lack of
apparent brain damage may result from a very effective mechanism for
glutamatergic blockade in those individuals.
It is also possible that ketamine has its effects by mimicing some of the
pathological processes seen in temporal lobe epilepsy. Even though ketamine
blocks glutamatergic transmission, and prevents excitotoxic cell death, the
effect of ketamine upon the human electroencephalograph (the EEG) suggests
that it can be epileptogenic - the final result of ketamine acting in the
brain is the result of a complex interplay of forces. There is a reduction
in a wave activity, but b, d and q wave activity are increased (Schwartz
et al. 1974; Pichlmayr et al., 1984). Ketamine acts both as an
anticonvulsant (e.g. McCarthy et al., 1965; Celesia and Chen, 1974;
Taberner, 1976; Leccese et al., 1986; Mares et al., 1992) and as a
pro-convulsant (Bennet et al., 1973; Gourie et al., 1983; Myslobodsky,
1981). Myslobodsky (1981) reported that ketamine could produce epileptiform
EEG patterns in human limbic and thalamic regions, but that there was no
evidence that this affected other cortical regions or that fits were likely
to occur. This is consistent with the NDE model presented by
Saavedra-Aguilar and Gomez-Jeria (1989) involving limited electrical
abnormalites in the limbic system. Thus production of NDE's by ketamine is
not at odds with proposals that NDE's may result from abnormal electrical
activity. Reich and Silvay (1989): " it is hard to draw objective
conclusions regarding the anti-convulsant properties of ketamine...animal
data are particularly difficult to interpret because of interspecies
variations". Ketamine is probably anticonvulsant at NDE producing doses
(Myslobodsky, 1981) suggesting that a PCP receptor blocker is released to
produce the NDE.
A Flood of Endorphins
Carr (1981, 1989) proposed that NDE's resulted from a flood release of
endogenous opioids (endorphins). It had been reported that survival time
was increased by giving opiate antagonists (e.g. naloxone) in fatal
circumstances (Holoday and Faden, 1978). More recently, a sudden increment
of b-endorphin has been reported in the brain and body fluids of dogs who
are 'conscious' at the moment of death (Sotelo et al., 1995). It is now
known that a glutamate flood results in excitotoxic cell death in
hypoxia/ischaemia and epilepsy (see above). However, glutamate is an amino
acid. Endorphins are unlikely to produce NDE's as they are not potent
dissociative hallucinogens (Oyama et al., 1980). Injection of b-endorphin
into the CSF has analgesic effects lasting well over 22 hours (Oyama et
al.,1980). This does not match the time course of a typical NDE which is
relatively brief. Ketamine produces brief, deep analgesia (White et al.,
1982) due to NMDA (PCP) receptor blockade ( e.g. Schouenberg and Sjolund,
1986; Parsons et al., 1988). The limited psychotomimetic properties of some
opioids (e.g. (-) pentazocine) result from binding to k opioid receptors,
and to PCP receptors at higher doses (Pfieffer et al., 1986; Mussachio et
al., 1990). However, the effects of (-)pentazocine binding to k receptors,
at doses which are relatively selective, are described as 'feelings of
cheerfulness and strength' (Belville and Forrest, 1968), a description
bearing no resemblance to the dramatic effects of ketamine or NDE's. With
higher doses, more marked effects may appear as a result of binding to PCP
receptors - but pentazocine is not an endorphin. Claims that sigma-
selective (+)isomers of benzomorphan opiates have psychotomimetic effects
are not generally supported by human trials, carried out in the 1960's,
which demonstrated that it is the (-)isomers which have psychotomimetic
properties - and these may prefer PCP receptors rather than sigma sites
(review: Mussachio,1990). The naloxone-reversible component is due to k
opioid receptor binding, while the naloxone insensitive component is due to
PCP (i.e. NMDA) receptor binding, not sigma binding (Walker et al., 1990).
The role of opioid receptors in ketamine effects is contoversial (Reich and
Silvay, 1989). Naloxone could not reverse the effects of ketamine in humans
(Amiot et al., 1985) and dogs (Vaupel, 1983). However, ketamine is supplied
as a racemic mixture of (+)and (-) isomers. The controversy may be resolved
by studying the separate effects of the isomers, and the doses at which
these appear. As doses rise, drugs bind to a wider range of receptors.
Ketamine can induce NDE's at doses about four times less than those
required for anaesthesia (Stafford, 1977; Lilly, 1979; Grinspoon and
Bakalar, 1981; Sputz, 1989).
White et al. (1980) reported that it was (+)ketamine which has some opioid
binding properties and which produced the most anaesthesia, while
(-)ketamine produced more NDE's (described by anaesthetists as 'psychic
emergence reactions'). White et al. (1985) went on to show that (+)ketamine
is about four times more potent as a hypnotic and analgesic, and has
different effects upon the EEG.
Saavedra-Aguilar and Gomez-Jeria (1989) cited animal experiments showing
b-endorphin to be epileptogenic to support an argument that b-endorphins
produce NDE's (e.g. McGinty et al., 1986; Henriksen et al., 1978). While
b-endorphin may have had these effects within the rat paradigms used,
opioids usually produce calming, inhibitory effects in humans - not
excitation or states resembling epilepsy (Meltzer, 1987). Released peptides
probably have protective functions rather than contributing further to
excito-toxicity. The finding of Su, London and Jaffe (1988), that some
steroids bind to sigma receptors, was cited to suggest that steroids could
play a role in NDE's. However, the steroid was progesterone which is not a
hallucinogen. Schwartz et al. (1989) reported that the affinity of
progesterone for the sigma site is insufficient to result in significant
receptor occupancy, except in pregnancy.
Hypoxia and Hypercarbia
1. Hypoxia: Blacher (1980) suggested that hypoxia induced NDE's. This has
been criticised by some authors (Sabom, 1982) as studies involving a slow
fall in inspired oxygen produced mental clouding rather than NDE's
(Henderson et al., 1927). However, these studies are not an accurate model
of events in, for example, cardiac arrest. Sudden hypoxia causes an
excessive release of glutamate with resulting excitotoxicity, which can be
prevented by ketamine (see previous references).
2. Hypercarbia: a CO2-enriched breathing mixture can result in typical NDE
phenomena such as bodily detachment and the perception of being drawn
towards a bright light. Diverse personality types produced broadly similar
reports, suggesting a shared neurological substrate (Meduna, 1950).
Like endorphins, serotonergic effects may be contributory but are unlikely
to play a central role in the NDE. Psychedelic drugs such as LSD are
serotonergic in action and produce a mental state very different from
NDE's . There is frequently an overwhelming increase in sensory input
from the external environment (Grinspoon and Bakalar, 1981), in contrast
to the dissociation produced by ketamine. Psychedelic visual phenomena bear
little relationship to the dream-like images of ketamine and the NDE. 'Ego
dissolution' experienced on LSD has a different quality from the conviction
of having died which may arise with ketamine. Loss of contact with the
external environment leading rapidly to the 'tunnel experience' is not a
typical psychedelic drug effect, although it may occur.
1. Depersonalisation: The NDE may be an adaptive mechanism which alerts one
to the threat of death while potentially overwhelming emotion is held at
bay. The reality can then be integrated without panic (Greyson, 1983;
Noyes and Kletti, 1976a,b). This model is applicable when death is
psychologically near as when falling from a cliff. While protecting nerve
cells from excitotoxicity is then irrelevant, glutamate and NMDA receptors
would be involved in producing the experience as they play a key role in
cognition and perception.
2. Regression in the service of the ego: confronting death cuts off the
external world resulting in regression to a pre-verbal level. This is
experienced as mystical ineffability (Greyson, 1983). Losing contact with
the external world is one of the most typical effects of ketamine. This is
partially due to blockade of NMDA receptors involved in sensory
transmission. NMDA receptors play a central role in the transmission of
data from all sensory modalities (Davies and Watkins, 1983; Greenamyre et
al., 1984; Headley et al., 1985; Cotman et al., 1987; Cline et al.,1987;
Monaghan, Bridges and Cotman, 1988; Kisvardy et al., 1989; Oye et al.,
3. State dependant reactivation of birth memories (Grof and Halifax, 1977).
Movement through tunnels towards light may be a memory of being born : a
'near-birth experience'. NMDA receptor blockade could be the mechanism for
such a reactivation of primitive memories.
4. Sensory deprivation: memories may normally be suppressed by a 'gate'
which admits primarily external signals when we are fully conscious and
concentrating upon an external task (Siegel,1980, 1981). If this input is
dramatically reduced (e.g. by ketamine or a heart attack) in combination
with central stimulation (e.g. by excessive glutamate release during
hypoxia, epilepsy, or arising without external provocation), stored
perceptions are released and become 'organised' into a meaningful
experience by psychodynamic forces in the mind in question (Greyson, 1983).
The 'white light' may result from CNS stimulation , and also a possible
lowering of the phosphene perceptual threshold (Siegel,1980, 1981). Sensory
deprivation can produce profound alterations in consciousness (Lilly,
The hippocampus is the anatomical location of the 'memory gate' described
above. NMDA receptors form the molecular substrate of the gate. NMDA
receptors have their highest concentration in the hippocampus, a part of
the medial temporal lobe where data from the external world is integrated
with internal programs. The NMDA receptor plays an important role in
learning, and in the formation and retrieval of memories. The PCP receptor
is referred to as a 'gated channel'. Whether the gate is open or closed
depends on the degree of excitation - specifically, the position of a
magnesium ion in the channel. In simple terms, ketamine blocks this channel
and closes the gate to incoming data (Monaghan, Bridges and Cotman, 1989;
Morris et al., 1986; Collingridge, 1987; McNaughton and Morris, 1987;
Cotman, Monaghan and Ganong, 1988).
Drug-induced hallucinations ?
Administered drugs may explain some cases of NDE's, but in most no drugs
were given with effects of this nature (Sabom, 1982).
NDE's can be safely induced by ketamine, and the glutamate theory of the
NDE can thus be investigated by experiment. Discoveries in neuroscience
suggest a common origin for ketamine experiences and the NDE in events
occuring at glutamatergic synapses, mediated by NMDA receptors via their
PCP channel component. This hypothesis links most of the neurobiological
and psychological theories (hypoxia, a peptide flood, temporal lobe
electrical abnormalities, regression in the service of the ego,
reactivation of birth memories, sensory deprivation etc.) rather than being
an alternative to them. Most of the tenets of the hypothesis are strongly
supported by experimental evidence which implicates glutamate and NMDA
receptors in the processes which precipitate NDE's. The postulate that
anti-excitotoxic agents can flood the brain remains to be clearly
Spiritualists have sometimes seen scientific explanations of NDE's as dull
and reductionist. However, the exploration of the mind-brain interface is
one of the most exciting adventures which humans have ever undertaken. The
real reductionism lies in attempts to draw a mystical shroud over the NDE,
and to belittle the substantial evidence in favour of an scientific
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