The effects of ketamine on the brain have been studied by Karl Jansen, who proposed a ketamine model of the near-death experience (1989; 2001). He suggests that both ketamine and the NDE involve events at glutamate receptors called N-methyl-D-aspartate (NMDA) receptors, which are fundamental for vital functions such as memory and learning.
It has been discovered that a sudden deprivation of oxygen in the brain, as occurs in a heart attack or brain damage, triggers an abnormal release of a neurotransmitter called glutamate,6 which kills neurons by over-stimulating them. The phenomenon is known as 'excito-toxicity' (Jansen 1989; Fenwick 1997). These nerve cells quickly die, and there is a loss of further neurons from related chemical reactions. Glutamate works by attachment to NMDA receptors, proteins on the cell surface. Ketamine is one of the drugs that block these proteins, and it can therefore prevent glutamate from harming neurons. When the brain suffers an injury such as a stroke, neurons release glutamate onto nearby neurons, which become excited, overloaded with calcium, and die. Normal neurotransmission is altered during injury, causing excess calcium to activate enzymes, which eventually leads to destruction of the cell. Since this occurs through glutamate receptors, including NMDA receptors, scientists believe that damage can be stopped through the use of agents that block the receptors. One of these is ketamine.
Several objections can be made to Jansen's ketamine model of the NDE. As David Fontana has pointed out, ketamine does not 'reproduce NDEs or any other mental state' (2005: 398), but it may eventually facilitate the conditions under which these states can occur. However, this is not the same as 'reproducing them'. Thus even if glutamate inhibition (or any other abnormal, chemically induced brain process) is present during the NDE, it is too strong to say that it has caused or created it. It may merely be a facilitating condition. Another observation emerges from the fact that out-of-body experiences, which sometimes occur as part of an NDE, do not involve an excessive release of glutamate, and they can occur when the individual is perfectly well both physically and mentally (ibid.: 399). The same is true of some mystical experiences that are phenomenologically very similar to NDEs, but which again can occur when there is no sign of any physical or psychological trauma (Marshall 2005: 95-6).
However, rather than entirely reducing this phenomenon to a neuro-biological event, Jansen has been prepared to consider a wide range of hypotheses in his book Ketamine: Dreams and Realities (2001). For example, he does not dismiss suggestions that 'the brain can act as a transceiver, converting fields beyond the brain into features of the mind, in a manner similar to the way a television converts waves in the air into sounds and vision' (ibid.: 92). From this particular perspective, only one of several that he explores, the effect of 'ketamine on the brain can be seen as a metaphorical "mental modem", which can potentially "connect" the mind to "everything else", allowing a peek behind the curtain at the inner workings of this and other realities' (ibid.: 44). But he also warns that ideas such as these 'must be approached with care, as there can be a risk of collusion with maladaptive beliefs of persons suffering from a serious mental illness requiring medical treatment' (ibid.: 44), and unlike Stanislav Grof, a psychiatrist who clearly favors such hypotheses (Grof and Grof 1986), Jansen does not commit himself to any particular view. His warning was aimed at ideas expressed in works such as Stanislav and Christina Grof's article 'Spiritual emergency: understanding and treatment of transpersonal crises' (1986), which he considered to be a potentially hazardous path for psychiatry to pursue.7
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