Is the NDE Only N-Methyl-D-Aspartate Blocking.pdf

(882 KB) Pobierz

Is the Near-Death Experience Only

N-Methyl-D-Aspartate Blocking?

Peter Fenwick, M.D., F.R.C.Psych.

Institute of Psychiatry, London, England

ABSTRACT:

Karl Jansen's interesting hypothesis that near-death experi-

ences (NDEs) result from blockade of the N-methyl-D-aspartate receptor has

several weaknesses. Some NDEs occur to individuals who are neither near

death nor experiencing any event likely to upset cerebral physiology as Jan-

sen proposed; thus his hypothesis applies only to a subset of NDEs that

occur in catastrophic circumstances. For that subset, the clarity of NDEs

and the clear memory for the experience afterward are inconsistent with

compromised cerebral function. Jansen's analogy between NDEs and

ketamine-induced hallucinations is weakened by the fact that most ketamine

users do not believe the events they perceived really happened. Temporal

lobe seizures do not resemble NDEs as Jansen postulated; they are confu-

sional, rarely ecstatic, and never clear, as are NDEs, nor are they remem-

bered afterward. Jansen's hypothesis assumes the standard scientific view

that brain processes are entirely responsible for subjective experience; how-

ever, NDEs suggest that that concept of the mind may be too limited, and

that in fact personal experience may continue beyond death of the brain.

Karl L. R. Jansen has proposed a hypothesis describing a mecha-

nism that makes a major contribution to the understanding of the

near-death experience (NDE). He suggested that the NDE is the re-

sult of the blocking of the phencyclidine (PCP) site on the N-methyl-

D-aspartate (NMDA) receptor. This is an interesting hypothesis, and

it is likely that the suggestion that the NMDA receptor is involved

in a subset of NDEs is correct. However, Jansen's paper, like many

before it, suffers from a number of weaknesses, some outlined by the

Peter Fenwick, M.D., F.R.C.Psych., is Consultant Neuropsychiatrist at the Bethlem

Royal and Maudsley Hospitals and Senior Lecturer at the Institute of Psychiatry in

London, England. Reprint requests should be addressed to Dr. Fenwick at the Institute

of Psychiatry, deCrespigny Park Road, London S.E.5, United Kingdom.

Journal of Near-Death Studies, 1611), Fall 1997

JOURNAL OF NEAR-DEATH STUDIES

author. In reviewing this hypothesis, it is important to look at its

implications from several different levels. When arguing for an ex-

planation of the NDE, chemical, clinical, and philosophical aspects

should all be included. I shall discuss these areas independently.

Jansen started his paper with a philosophical statement concerning

death and the nature of mind. This point requires answering, but

for the first part of this article I would like to take the position,

suggested by Jansen, that mind

arises

from neuronal activity, and

that consciousness is

local

to brain processes.

The first point is: how do we define an NDE? Are we to consider

only those NDEs that occur with catastrophic brain failure, or should

we include those NOEs that occur in different circumstances? Jansen

did not suggest that his theory is applicable to all cases of NDEs,

but argued that it can explain most experiences, put generally, be-

cause the PCP receptor is involved in perception.

The full breadth of near-death phenomena came to my attention

after a television program and publication of several articles in the

United Kingdom. The British branch of the International Association

for Near-Death Studies (IANDS-UK) and I have received more than

2,000 letters containing experiences. From these letters we selected

a subset of experiences that we felt were most typical of the core

NDE. We mailed 500 questionnaires to this group of people and re-

ceived over 370 replies (Fenwick and Fenwick, 1995). The selection

of this data set was biased by several important factors. First, the

group was self-selected. Second, the people who wrote were those

who were sufficiently interested in their experiences to want to com-

municate something that was important to them. This adds a sig-

nificant selection bias, in that people who have had negative or

neutral experiences are much less likely to want to communicate

them than those who have had positive experiences. However, ac-

cepting these deficiencies, these NDEs were reported as having oc-

curred under many different situations, some of which were not near

death, nor accompanied by any threatening event likely to have upset

cerebral physiology in the way proposed by Jansen's hypothesis.

Experiences were reported to have occurred when experiencers

were awake and relaxed, when they were depressed, and in minor

infections and in routine anesthesia. We rejected those that were re-

ported to have occurred in sleep. The largest number certainly oc-

curred in catastrophic circumstances. Our sample makes the point

that NDEs judged entirely by their phenomenology occur in many

different circumstances; thus any theory that links the NDE only to

PETER FENWICK

brain catastrophe or to a special brain physiological mechanism must

provide only a partial and limited explanation. Elizabeth Fenwick

and I (Fenwick and Fenwick, 1995) have suggested that a detailed

look at the phenomenology of the NDE allocates it to a group of

experiences that is already well studied and understood, that of the

mystical experience. This explanation has the advantage that mys-

tical experiences too have multiple causes. The hypothesis put for-

ward by Jansen should thus be limited to a subset of NDEs that

occur in catastrophic circumstances.

Jansen argued, correctly in my view, that a clear sensorium and

a feeling of absolute reality do not negate the suggestion that these

experiences are hallucinations. From a scientific point of view it is

clear that the majority of the NDEs must be hallucination, if one

excludes those out-of-body experiences for which a veridical nature

is claimed, as the world described is private to the individual and

not held in common between subjects. The fact that we define the

NDE mainly as an hallucination is of little help in terms either of

the experience's likely genesis or of its philosophical explanation. It

simply raises questions about the subjective nature of mind. It does,

however, help to direct attention, as Jansen has done, to other situ-

ations in which hallucinations that have a similar form occur.

I was interested in the comment that only 30 percent of normal

subjects given ketamine were certain that the events had really oc-

curred. In NDEs this percentage is much higher, and this point weak-

ens a ketamine-like effect as the only explanation. However, in

defense of the ketamine hypothesis, it could be that those people

given ketamine would naturally tend to attribute whatever experi-

ence they had to the drug, and so would be less likely to regard it

as "real."

The phenomenon of a clear sensorium in catastrophic brain states

is more difficult to explain. Any physician dealing with head injury,

epilepsy, or altered cerebral physiology knows that as cerebral func-

tion becomes compromised it becomes disorganized. Even in such

simple circumstances as ordinary fainting, recovery from the faint is

recovery from a confusional process. Acute cerebral catastrophes re-

sult in confusion and not clarity. This important fact is overlooked

by those attributing simple chemical explanations to the NDE. Al-

though ketamine may produce experiences that are similar to the

NDE, and Jansen has argued cogently that it does, he does not ex-

plain how these same experiences can arise in a dysfunctional brain.

His argument is that when brain processes have been so disorganized

JOURNAL OF NEAR-DEATH STUDIES

that there is loss of consciousness, consciousness can then be resyn-

thesized in its clarity by a brain mechanism such as flooding the

brain with NMDA inhibition. Surely the very fact that consciousness

has been lost would argue that cortical activity is insufficient to sus-

tain high quality and clear consciousness as would be required for

NDE.

The only way round this dilemma is to argue that the experience

arises as consciousness is being recovered or lost, when cerebral func-

tion is still sufficiently intact to maintain coherent and clear cerebral

experience. There are arguments, mainly related to memory, that I

will discuss further below, which make it unlikely that many NDEs

could occur as consciousness is being lost. The alternative conclusion

would therefore have to be that NDEs occur with the return of the

cerebral processing involved in ordinary conscious experience. How-

ever, the difficulty here is that recovery from a cerebral catastrophe

is via a confusional state and it thus seems unlikely that an arousal

through confusion could produce both the clarity of the experience

and the confusion of arousal.

In our series there were some specific accounts that made this

point even more starkly. We had patients who were head-injured and

whose arousal was confusional and showed all the characteristics and

mental states that would be expected after a severe head injury. Yet

within this dense confusional state, but attributed by the individual

to the time of unconsciousness, was full memory of a wonderfully

clear NDE. It is worth noting that in severe head injury memory for

the accident and for the confusional awakening in hospital is absent,

and this was so in our cases of head injury. Except by special plead-

ing, it is not possible with our current understanding of cerebral

functioning to explain, on a simple chemical theory, how, within dense

unconsciousness and with absence of memory, the brain can structure

and remember a clear comprehensive experience. This is an inter-

esting point and is a challenge to our current understanding of brain

function (Cartlidge, 1991; Teasdale, 1991).

One of the most puzzling features of NDEs, besides their clarity

in the presence of cerebral catastrophe, is the clear memory for the

experience. As mentioned above, memory is very sensitive to brain

injury, and length of amnesia before and after unconsciousness is a

way of determining the severity of the injury. It is thus unlikely that

cerebral events occurring during this period of total amnesia would

ordinarily be remembered (Cartlidge, 1991; Teasdale 1991).

PETER FENWICK

Jansen described the excitatory and inhibitory properties of

ketamine and decided on balance against it being excitatory, though

it is probably neuroprotective. He concluded that it is likely to be

inhibitory. This leads to a discussion of the role of epilepsy in NDEs.

There is much about the possible role of epilepsy, abnormal temporal

lobe functioning, and abnormal hippocampal functioning in the NDE

literature (Saavedra-Aguilar and Gomez-Jeria, 1989), which Jansen,

quite rightly, wanted to include in his theory. In my view much of

the discussion of temporal lobe epileptic (TLE) activity as a compo-

nent of the NDE argues without the data to support it.

Let's start with temporal lobe seizures. We can divide these into

those starting in the lateral temporal cortex and those arising from

the hippocampus or the amygdala, the medial temporal structures.

Let's consider those arising from the hippocampus or the amygdala.

The international definition of these seizures is partial complex sei-

zures; they are termed "complex" because they lead to an alteration

of consciousness. This alteration in consciousness is confusional.

When patients have seizures originating in the medial temporal

structures they usually have a disorder of consciousness, and the

mental phenomena are usually those of fear or extreme fear.

Positive auras and feelings, so common in the NDE, are reported

in only a very small minority of medial temporal, seizures. In William

Gowers' (1881) study of 505 epileptic auras only 3 percent were said

to be emotional and none positive. In William Lennox's (1960) study

of 1,017 auras, only 9 were said to be pleasant (0.9 percent), and of

these "only a few showed positive pleasure." Wilder Penfield and

Kristian Kristiansen (1951) cited only one case with an aura of a

pleasant sensation and it was followed by an epigastric feeling of

discomfort. Until 1980, no cases of temporal lobe epilepsy and an

ecstatic aura had been reported (Cirignotta, Todesco, and Lugaresi,

1980). Despite this, ecstatic states were frequently attributed in the

literature to TLE. As Henri Gastaut (1978) explained, this was be-

cause people expected ecstatic states to be present (Fenwick, 1983).

Thus the phenomenology of discharges in this brain area bears no

resemblance to that of the NDE. More importantly, when the seizures

spread out from the medial temporal structures into the temporal

cortex more complex phenomena may arise, but these are always

confusional and never complex and clear like the NDE. It is thus

unlikely that any alterations in electrical activity of a seizure type

arising in the medial temporal structures could contribute to the

NDE.

Plik z chomika:

hailee

Is the NDE Only N-Methyl-D-Aspartate Blocking.pdf

Plik z chomika:

Inne pliki z tego folderu:

Inne foldery tego chomika: