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ketamine_and_near_death_experience [2007-06-12 13:35] – nikketamine_and_near_death_experience [2007-06-12 13:35] – nik
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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