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ketamine_and_near_death_experience [2007-06-12 13:34] – nikketamine_and_near_death_experience [2007-06-12 13:35] – nik
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-==== Psychological Explanations of the NDE==== 
  
 +==== Psychological Explanations of the NDE====
  
  
- 1. Depersonalisation+1. Depersonalisation
  
 The depersonalisation theory proposes that the NDE is an adaptive mechanism of the personality which alerts one to the threat of death while potentially overwhelming emotion is held at bay, allowing the reality to be integrated without panic (Greyson, 1983; Noyes and Kletti, 1976a,b). While protecting nerve cells from ischaemic damage is largely irrelevant when one is falling from a cliff, the NDE-producing situation which first resulted in this hypothesis, NMDA receptors would certainly be involved in producing the experience of depersonalisation as they play a central role in cognition and perception. The depersonalisation theory proposes that the NDE is an adaptive mechanism of the personality which alerts one to the threat of death while potentially overwhelming emotion is held at bay, allowing the reality to be integrated without panic (Greyson, 1983; Noyes and Kletti, 1976a,b). While protecting nerve cells from ischaemic damage is largely irrelevant when one is falling from a cliff, the NDE-producing situation which first resulted in this hypothesis, NMDA receptors would certainly be involved in producing the experience of depersonalisation as they play a central role in cognition and perception.
  
  
- +1. Regression in the service of the ego
- 1. Regression in the service of the ego+
  
 This theory maintains that confronting death leads to a cutting off the external world. The result is regression to a pre-verbal level which can be experienced as mystical ineffability (Greyson, 1983). Certainly a loss of contact with the external world is one of the most characteristic effects of ketamine.This is probably the result of blockade of NMDA receptors involved in sensory transmission. NMDA receptors play a key role in the transmission of incoming signals from all sensory modalities (Davies and Watkins, 1983; Greenamyre et al., 1984; Headley et al., This theory maintains that confronting death leads to a cutting off the external world. The result is regression to a pre-verbal level which can be experienced as mystical ineffability (Greyson, 1983). Certainly a loss of contact with the external world is one of the most characteristic effects of ketamine.This is probably the result of blockade of NMDA receptors involved in sensory transmission. NMDA receptors play a key role in the transmission of incoming signals from all sensory modalities (Davies and Watkins, 1983; Greenamyre et al., 1984; Headley et al.,
  
- 1. ; Cotman et al., 1987; Cline et al.,1987; Monaghan, Bridges and Cotman, 1988; Kisvardy et al., 1989; Oye et al.,+1. ; Cotman et al., 1987; Cline et al.,1987; Monaghan, Bridges and Cotman, 1988; Kisvardy et al., 1989; Oye et al.,
  
- 2. ).+2. ).
  
  
  
- 1. A state dependent reactivation of birth memories+1. A state dependent reactivation of birth memories
  
 This theory explains the movement through tunnels towards 'the light' as a memory of being born (Grof and Halifax, This theory explains the movement through tunnels towards 'the light' as a memory of being born (Grof and Halifax,
  
- 1. ). The NDE is thus actually a 'near-birth experience' rather than a 'near-death experience'.+1. ). The NDE is thus actually a 'near-birth experience' rather than a 'near-death experience'.
  
 NMDA receptor blockade could certainly be the underlying mechanism for the release of extremely primitive memories not normally available to consciousness. NMDA receptor blockade could certainly be the underlying mechanism for the release of extremely primitive memories not normally available to consciousness.
  
  
- +1. The NDE as a sensory deprivation phenomenon
- 1. The NDE as a sensory deprivation phenomenon+
  
 This hypothesis maintains that memories may normally be suppressed by a mechanism which acts as a gate, admitting primarily external signals when we are fully conscious and concentrating upon an external task (Siegel,1980, 1981). If this input is dramatically reduced , for example when we are dreaming, have been given drugs such as ketamine, or have just had a heart attack, in combination with a high level of central stimulation (e.g. as would result from excessive glutamate release during hypoxia, ischaemia, epilepsy, or arising without external provocation), stored perceptions are released and become 'organised' by the mind into an experience with some symbolic meaning. According to Ron Siegel (1980), the 'white light' may result from CNS stimulation mimicing light on the retina, and a lowering of the phosphene perceptual threshold. Sensory deprivation itself produces a profound alteration in consciousness which is certainly mediated via NMDA receptors (see 'regression in the service of the ego' above (Lilly, 1961,1978). This hypothesis maintains that memories may normally be suppressed by a mechanism which acts as a gate, admitting primarily external signals when we are fully conscious and concentrating upon an external task (Siegel,1980, 1981). If this input is dramatically reduced , for example when we are dreaming, have been given drugs such as ketamine, or have just had a heart attack, in combination with a high level of central stimulation (e.g. as would result from excessive glutamate release during hypoxia, ischaemia, epilepsy, or arising without external provocation), stored perceptions are released and become 'organised' by the mind into an experience with some symbolic meaning. According to Ron Siegel (1980), the 'white light' may result from CNS stimulation mimicing light on the retina, and a lowering of the phosphene perceptual threshold. Sensory deprivation itself produces a profound alteration in consciousness which is certainly mediated via NMDA receptors (see 'regression in the service of the ego' above (Lilly, 1961,1978).
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 Ketamine blocks this channel at the molecular level and, at a higher level, closes the 'gate' to incoming information (Monaghan, Bridges and Cotman, 1989; Morris et al., 1986; Collingridge, 1987; McNaughton? and Morris, Ketamine blocks this channel at the molecular level and, at a higher level, closes the 'gate' to incoming information (Monaghan, Bridges and Cotman, 1989; Morris et al., 1986; Collingridge, 1987; McNaughton? and Morris,
  
- 1. ; Cotman, Monaghan and Ganong, 1988).+1. ; Cotman, Monaghan and Ganong, 1988).
  
  
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 The hypothesis presented in this paper is that much can be learnt about the mechanisms of the NDE by studying drug-induced hallucinations, specifically the state produced by ketamine. However, it is certainly not my argument that the NDE's reported by persons who have had heart attacks etc. are in any way due to drugs which they have been given. Administered drugs may explain a few cases of NDE's, but in most no drugs were given with effects which resemble the NDE (Sabom, 1982). The hypothesis presented in this paper is that much can be learnt about the mechanisms of the NDE by studying drug-induced hallucinations, specifically the state produced by ketamine. However, it is certainly not my argument that the NDE's reported by persons who have had heart attacks etc. are in any way due to drugs which they have been given. Administered drugs may explain a few cases of NDE's, but in most no drugs were given with effects which resemble the NDE (Sabom, 1982).
 +
  
  
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 It is also possible that there is no protective mechanism against excitotoxicity. Rather than mimicing a natural protective process, ketamine may have some of its psychological effects by mimicing some of the processes seen in temporal lobe epilepsy. Ketamine does block glutamatergic neuro-transmission and prevents excitotoxic cell death. However, the effect of ketamine upon human electrical brain waves (the electroencephalograph, EEG) suggests a complex interplay of forces. There is a reduction in alpha wave activity, while beta, delta and theta wave activity are increased (Schwartz et al. 1974; Pichlmayr et al., 1984). Ketamine has been reported to act both as an anticonvulsant (i.e. substance which prevents epilepsy) (e.g. McCarthy? et al., 1965; Celesia and Chen, 1974; Taberner, It is also possible that there is no protective mechanism against excitotoxicity. Rather than mimicing a natural protective process, ketamine may have some of its psychological effects by mimicing some of the processes seen in temporal lobe epilepsy. Ketamine does block glutamatergic neuro-transmission and prevents excitotoxic cell death. However, the effect of ketamine upon human electrical brain waves (the electroencephalograph, EEG) suggests a complex interplay of forces. There is a reduction in alpha wave activity, while beta, delta and theta wave activity are increased (Schwartz et al. 1974; Pichlmayr et al., 1984). Ketamine has been reported to act both as an anticonvulsant (i.e. substance which prevents epilepsy) (e.g. McCarthy? et al., 1965; Celesia and Chen, 1974; Taberner,
  
- 1. ; Leccese et al., 1986; Mares et al., 1992) and as a pro-convulsant (epilepsy inducing substance) (Bennet et al., 1973; Gourie et al., 1983; Myslobodsky, 1981). Myslobodsky (1981) reported that ketamine could produce EEG patterns in human limbic and thalamic regions resembling epileptic patterns, but that there was no evidence that this affected other cortical regions or that clinical seizures were likely to occur. This is quite consistent with the NDE model presented by Saavedra-Aguilar and Gomez-Jeria (1989) which involved limited electrical abnormalities in the limbic system.+1. ; Leccese et al., 1986; Mares et al., 1992) and as a pro-convulsant (epilepsy inducing substance) (Bennet et al., 1973; Gourie et al., 1983; Myslobodsky, 1981). Myslobodsky (1981) reported that ketamine could produce EEG patterns in human limbic and thalamic regions resembling epileptic patterns, but that there was no evidence that this affected other cortical regions or that clinical seizures were likely to occur. This is quite consistent with the NDE model presented by Saavedra-Aguilar and Gomez-Jeria (1989) which involved limited electrical abnormalities in the limbic system.
  
 The hippocampus is one of the core structures in the limbic system. Thus the production of NDE's by ketamine is not inconsistent with the hypothesis that NDE's may result from abnormal electrical activity in the brain. Reich and Silvay (1989) concluded: " 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". Nevertheless, most of the available evidence favors the conclusion that ketamine is anticonvulsant at doses required to produce NDE's (Myslobodsky, 1981), supporting the hypothesis that NMDA receptor blockade results in NDE's. The hippocampus is one of the core structures in the limbic system. Thus the production of NDE's by ketamine is not inconsistent with the hypothesis that NDE's may result from abnormal electrical activity in the brain. Reich and Silvay (1989) concluded: " 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". Nevertheless, most of the available evidence favors the conclusion that ketamine is anticonvulsant at doses required to produce NDE's (Myslobodsky, 1981), supporting the hypothesis that NMDA receptor blockade results in NDE's.
  • ketamine_and_near_death_experience.txt
  • Last modified: 2015-03-13 11:44
  • by nik