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JOURNAL OF NEAR-DEATH STUDIES
Although these were accounts from people who did die, they were
similar to the few accounts of NDEs in India. Satwant Pasricha and
Ian Stevenson (1986) reported 16 cases of NDEs in India, and a com-
mon theme was the story of mistaken identity. Religious figures came
to take the person away, but then discovered that it was the wrong
person. Their cases seemed dramatically different from the type of
NDE first described by Raymond Moody (1975). There were no tunnels,
no bright lights, and no out-of-body experiences (OBEs), in which the
experiencers see their own bodies from a distance. This discrepancy
might be used to argue against the universality of NDEs, and is
particularly important for physiological theories.
Some researchers argue that all the features of the NDE can be
accounted for in terms of the processes going on in the dying brain, or
in the brains of those subjected to severe stress or fear of death. For
example, Juan Saavedra-Aguilar and Juan Gomez-Jeria (1989) have
presented a neurobiological model of the NDE in which they account
for all the features of the NDE in terms of the effects of hypoxia,
temporal lobe and limbic system dysfunction, and an imbalance in
neurotransmitters. The temporal lobe and limbic system are closely
related and have often been implicated in the NDE. For example,
direct electrical stimulation of the temporal lobe can give rise to
memory flashbacks (Penfield, 1955), and people with many signs of
limbic lobe lability are also more prone to religious, psychic, and
mystical experiences (Persinger, 1983).
Various neurotransmitters and neuromodulators have been impli-
cated in NDEs. For example, Daniel Carr (1982) was the first to
suggest that endogenous opiates, or endorphins, would be released
during the stress of a near-death event and could account for the
peaceful and joyful feelings. Moreover, endorphins lower the threshold
for seizure activity in the limbic system and temporal lobe, and so can
trigger the kind of limbic lobe syndrome often compared to NDEs. On
the other hand, Melvin Morse, David Venecia, and Jerrold Milstein
(1989) have argued that serotonin mechanisms are more likely to
provide an explanation than endorphins.
None of these theories directly addresses the origin of the tunnel. In
his early study of 102 people who had come close to death, Kenneth
Ring (1980) found that 23 percent had "entered the darkness" and 16
percent saw the light. These experiences are often equated with the
more obvious tunnels in which people describe flying through dark
spaces, or even through pipes or tubes. Tom Troscianko and I have
argued that the tunnel can be produced by any mechanism that causes
disinhibition and consequent random firing in the cortex (Blackmore
and Troscianko, 1989).
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