A Reply to Shermer
Medical Evidence for NDEs
Pim van Lommel
Only recently someone showed me the "Skeptic" article* by Michael Shermer. From a well respected and, in my opinion, scientific journal like the Scientific American I always expect a well documented and scientific article, and I don’t know how thoroughly peer-reviewed the article from Shermer was by the editorial staff before publication. My reaction to this article by Shermer is because I am the main author of the study published in The Lancet, December 2001, entitled: “Near-death experience in survivors of cardiac arrest; a prospective study in the Netherlands”. About what he writes about the conclusions from our study, as well as from the effect of magnetic and electrical “stimulation” of the brain, forces me to write this paper, because I disagree with his theories as well as with his conclusions.
We performed our prospective study in 344 survivors of cardiac arrest to study the frequency, the cause and the content of near-death experience (NDE). A near-death experience is the reported memory of all impressions during a special state of consciousness, including specific elements such as out-of-body experience, pleasant feelings, and seeing a tunnel, a light, deceased relatives, or a life review. In our study 282 patients (82%) did not have any memory of the period of unconsciousness, 62 patients (18%) however reported a NDE with all the “classical” elements. Between the two groups there was no difference in the duration of cardiac arrest or unconsciousness, intubation, medication, fear of death before cardiac arrest, gender, religion, education or foreknowledge about NDE. More frequent NDE was reported at age younger than 60 years, more than one cardiopulmonary resuscitation (CPR) during hospital stay, and previous NDE. Patients with memory defects after lengthy and complicated CPR reported less frequent NDE.
There are several theories that should explain the cause and content of NDE. The physiologic explanation: the NDE is experienced as a result of anoxia in the brain, possibly also caused by release of endomorphines, or NMDA receptor blockade.
In our study all patients had a cardiac arrest, they were clinically dead, unconscious, caused by insufficient blood supply to the brain because of inadequate blood circulation, breathing, or both. If in this situation CPR is not started within 5-10 minutes, irreparable damage is done to the brain and the patient will die. According to this theory, all patients in our study should have had an NDE, they all were clinical dead due to anoxia of the brain caused by inadequate blood circulation to the brain, but only 18% reported NDE.
The psychological explanation: NDE is caused by fear of death. But in our study only a very small percentage of patients said they had been afraid the seconds preceding the cardiac arrest, it happened too suddenly to realize what occurred to them. However, 18 % of the patients reported NDE. And also the given medication made no difference.
We know that patients with cardiac arrest are unconscious within seconds, but how do we know that the electro-encephalogram (EEG) is flat-lined in those patients, and how can we study this?
Complete cessation of cerebral circulation is found in cardiac arrest due to ventricular fibrillation (VF) during threshold testing at implantation of internal defibrillators. This complete cerebral ischaemic model can be used to study the result of anoxia of the brain.
In VF complete cardiac arrest occurs, with complete cessation of cerebral flow, and resulting in acute pancerebral anoxia. The Vmca, the middle cerebral artery blood flow, which is a reliable trend monitor of the cerebral blood flow, decreases to 0 cm/sec immediately after the induction of VF (2). Through many studies in human, as well as in animal models, cerebral function has been shown to be severely compromised during cardiac arrest and electric activity in both cerebral cortex and the deeper structures of the brain has been shown to be absent after a very short period of time. Monitoring of the electric activity of the cortex (EEG) has shown ischaemic changes consisting of a decrease of fast high amplitude waves and an increase of slow delta waves, and sometimes also an increase in amplitude of theta activity, progressively and ultimately declining to isoelectricity. More often initial slowing (attenuation) of the EEG waves is the first sign of cerebral ischaemia. The first ischaemic changes in the EEG are detected an average of 6.5 seconds after circulatory arrest. With prolongation of the cerebral ischaemia always a progress to an isoelectric (flat) line is monitored within 10 to 20 (mean 15) seconds from the onset of the cardiac arrest (3-6).


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