Consciousness Beyond Life: The Science of the Near-Death Experience (24 page)

Since 2001 the Dutch study has been frequently cited in scientific articles and books (121 times), in science programs on radio and television, and in other publications. Our NDE study was the reason why Professor Janice Holden awarded me the Bruce Greyson Research Award on behalf of the International Association of Near-Death Studies in the United States in September 2005. And in September 2006 the president of India, Dr. A. P. J. Abdul Kalam, awarded me the Lifetime Achievement Award in New Delhi following a lecture I presented on our study at the World Congress on Clinical and Preventive Cardiology 2006.

To the best of my knowledge, no negative commentaries were ever published in any peer-reviewed scientific journals, with the exception of the mildly critical commentary in
The Lancet
itself. I did, however, receive some extremely critical comments in the Netherlands from Dr. C. Renckens, gynecologist and chair of the Dutch Association Against Quackery. As well as linking our study with “multiple personality disorder, chronic fatigue syndrome, fibromyalgia and alien abduction syndrome,” he described me as “a failed prophet with the personality of a pre-morbid quack.”

In Belgium I received some blunt comments from W. Betz, professor of family medicine in Brussels and a member of Skepp (the Belgian study group for the critical evaluation of pseudoscience and the paranormal). Betz’s initial response to our study appeared in an article in Belgian newsmagazine
De Tijd
on 29 December 2001: “When scientists start spouting nonsense, the public must be warned.” According to the magazine, he was “livid,” criticized the study and me as “post-modern deception,” “pseudoscience,” “nonsense,” and “a veritable cult.” “Van Lommel belongs to a sect,” he wrote, and he associated the research with “astral bodies, the paranormal, and graphology.” Describing NDE as “a hallucination,” he tried to refute the published out-of-body experience that includes the story of the dentures by hinting at a lack of integrity on the part of both the nurse who wrote the report and the authors of the article: “enthusiastic researchers, convinced of being in the right, are only too keen to ‘help’ the victim of an NDE retrieve his memories.” Betz suggested that patients “can be talked into believing they had an NDE” even years after a cardiac arrest. In an interview in another publication, Belgian magazine
Humo,
he described our study as “complete nonsense” and claimed that “the publication lacks any kind of cohesion.” He concluded by saying, “Imagine there were any truth to Van Lommel’s claims…admit it, wouldn’t that be most peculiar?”

Comparison with Prospective NDE Studies in the United States and the United Kingdom

One American and two British studies among cardiac arrest patients, with the same prospective design as our Dutch study, found near-identical percentages of NDE after a successful resuscitation.
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None of these four studies, comprising a total of 562 patients, could produce a definitive scientific explanation for the phenomenon (see table “Four Prospective NDE Studies Among Cardiac Patients”).

Four Prospective NDE Studies Among Cardiac Patients

The American Study

As part of Bruce Greyson’s prospective study in the United States, a total of 1,595 patients were interviewed at the cardiac units of the University of Virginia Hospital. It emerged that 5 percent of these patients had experienced a previous NDE. Excluding cardiac arrest diagnoses, only 1 percent of the heart patients reported an NDE. The comparative study, however, looked at 116 cardiac arrest patients, of whom 9.5 percent reported an NDE with a score of 6 or higher, and 6 percent reported an NDE with a low score. A total of 15.5 percent of the cardiac arrest survivors reported an NDE that satisfies our more liberal criteria. This study also identified a younger mean age of people with an NDE. The medical files were not systematically analyzed for physiological, psychological, and pharmacological factors. Diagnoses such as “clinically dead,” “close to death” or “no mortal danger” were not based on objective criteria but were made by the patients themselves. This was why so few people in the study were described as having been clinically dead—because most patients were unable to recollect their resuscitation. Similarly, the diagnoses “loss of consciousness,” “diminished consciousness,” and “normal consciousness” were made by the patients themselves. So unfortunately this study recorded mostly subjective and few objective medical data. In his conclusion, Greyson writes,

The First British Study

The British prospective study by Sam Parnia, an intensive care physician, and Peter Fenwick, a neuropsychiatrist, looked at 63 cardiac arrest survivors at Southampton General Hospital over a one-year period. Of these, 4 patients (6.3 percent) reported an NDE, and 3 patients (4.8 percent) had an experience with a low score, bringing the total to 11 percent according to our more liberal criteria. The only objective data to be recorded were arterial blood gases (oxygen and carbon dioxide) and the drugs administered. The number of patients in this study was too small for statistical analysis. Significantly, hidden signs were affixed near the ceilings of the patient rooms at the coronary care unit. But unfortunately, as in our study, none of the patients had an out-of-body experience with perception of one of these signs. According to the authors, the data suggest that the NDE arises during unconsciousness. “This is a surprising conclusion,” in their view,

Another frequently cited explanation might be that the experiences occur either during the early stages of unconsciousness or during the recovery of consciousness. However, Parnia and Fenwick claim that the verifiable elements of an out-of-body experience during unconsciousness, such as patients’ reports of their resuscitation, render this extremely unlikely.

The Second British Study

Over a period of four years, Dr. Penny Sartori, a senior intensive care nurse, carried out an even smaller study of NDE. Only 1 percent of the 243 patients who survived their stay in intensive care in a Welsh hospital reported an NDE. However, her study focused on 39 cardiac arrest patients, of whom 18 percent reported an NDE and 5 percent only an out-of-body experience without any of the other NDE elements, bringing the total to 23 percent according to our more liberal criteria. Sartori notes that only two patients with a deep NDE reported their experience “spontaneously” the other NDEs were reported during the purposive interviews. This may be a result of reluctance to discuss this extremely profound experience. Three patients with an NDE died soon after their cardiac arrest, which is another parallel with our study. Similarly, Sartori’s study featured hidden signs, which were not noticed during an NDE. One patient, however, recounted an extremely detailed out-of-body experience, many aspects of which proved to be accurate upon inquiry. A control group of people who had been successfully resuscitated but who had not had an NDE made a great many fundamental mistakes when asked to describe their own resuscitation. The cardiologist Sabom reached a similar conclusion in his study.
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The medication administered or the arterial blood gases (oxygen and carbon dioxide) measured in a few patients failed to explain why patients in Sartori’s study did or did not experience an NDE. But this study was also too small in scope for statistical analysis. Sartori concludes,

Only the large-scale Dutch study allowed statistical analysis of the potential contributing factors to an NDE. The results failed to confirm the aforementioned physiological, psychological, and pharmacological explanations. Our study was also the first to include a longitudinal component with follow-up interviews after two and eight years, which allowed us to compare the processes of change in people with and without an NDE. We identified a distinct pattern of change in people with an NDE and found that integrating these changes into everyday life is a long and arduous process. Cardiac arrest patients without an NDE also underwent a gradual but in many ways different process of change.

On the strength of the four prospective studies among cardiac arrest survivors, we concluded that they experienced all the previously mentioned NDE elements during their cardiac arrest, during impaired blood flow to the brain. Nonetheless, the question how this is possible remains unanswered.

Although the content of consciousness depends in large measure on neuronal activity, awareness itself does not…. To me, it seems more and more reasonable to suggest that the mind may be a distinct and different essence.

—W
ILDER
P
ENFIELD

Scientific research into the phenomenon of NDE highlights the limitations of our current medical and neurophysiological ideas about the various aspects of human consciousness and the link between consciousness, memories, and the brain. According to the prevailing paradigm, memories and consciousness are produced by large groups of neurons or neuronal networks. For lack of evidence for the usual explanations for the origins and content of an NDE, the commonly accepted but never proven concept that consciousness is localized in the brain should be questioned.

How can an extremely lucid consciousness be experienced outside the body when the brain has momentarily stopped functioning during a period of clinical death? What happens when blood supply to the brain ceases? And what do we really know about normal brain function? The next chapters will look at these important questions in more detail.

The four prospective NDE studies discussed in the previous chapter all reached one and the same conclusion: consciousness, with memories and occasional perception, can be experienced
during
a period of unconsciousness—that is, during a period when the brain shows no measurable activity and all brain functions, such as body reflexes, brain-stem reflexes, and respiration, have ceased. It appears that at such a moment a lucid consciousness can be experienced independently of the brain and body. This conclusion was reached on the basis of compelling evidence that the NDE occurs
during
the period of clinical death and not shortly before or after the cardiac arrest. It was the studies’ prospective design that enabled this conclusion. If the cardiac arrest involved an NDE with clear perception of the patient’s surroundings, its contents could be verified immediately after the report. The story of the lost dentures in chapter 2 is a good example of this.

The precise onset of an NDE is important because it rules out any conclusion other than that the NDE is experienced at a point in time when the brain shows no activity and all brain function has ceased. If the prevailing hypothesis, that consciousness is produced by the brain, were correct, there could be no sign of consciousness at the moment when the brain shows no activity. Indeed, this is reported in most cases of clinical death, coma, or brain death. But as the NDE studies have shown, there are exceptions to this rule. This finding all but forces us to reconsider the relationship between the brain and consciousness. After all, how can people experience an exceptionally lucid consciousness during a period of temporary loss of all measurable brain function?

The Paradox of a Lucid Consciousness During the Loss of Brain Function

As mentioned, the four prospective NDE studies reached remarkably similar conclusions. In our article in
The Lancet
we argued, “NDE pushes at the limits of medical ideas about the range of human consciousness, and the mind-brain relation.”
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Bruce Greyson concluded,

Sam Parnia and Peter Fenwick wrote in their conclusion:

Finally, Penny Sartori concluded,

These NDE researchers start from the assumption that when a cardiac arrest disrupts the supply of blood to the brain, the brain becomes devoid of activity. Indeed, all brain function appears to be lost. To prove this hypothesis, we need conclusive evidence of this loss of function. This makes it imperative to ascertain what happens in the brain in the absence of a blood supply when the heart has stopped beating. The loss of blood pressure and breathing results in immediate unconsciousness and the loss of all body and brain-stem reflexes. Does it really mean that all brain function has ceased? Can this be measured? And has all electrical brain activity ceased as well, resulting in a flat EEG? Has there been any research in this area?

Measuring the Loss of Brain Activity During a Cardiac Arrest

Research in both humans and animals has shown that during an induced cardiac arrest the loss of function of both the cerebral cortex and the brain stem results in unconsciousness within seconds. All brainstem reflexes are gone too: there is no cornea reflex (the blinking of the eye upon touch) and no gag reflex, and the dilated pupils do not react to light. The respiratory center near the brain stem has also stopped functioning, as evidenced by the suspension of breathing (apnea).
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Patients’ blood flow to the brain stops altogether when a cardiac arrest is induced for threshold measurements during the implanting of internal cardiac defibrillators (ICDs). These ICDs are implanted in patients with recurring life-threatening arrhythmias that are not or not sufficiently responsive to medication. Blood flow in the brain can be measured very accurately in the middle cerebral artery with the use of ultrasound (Doppler ultrasonography). This test shows that blood flow stops completely at the onset of the cardiac arrest and is restored within seconds of an electric shock (defibrillation) reestablishing the heartbeat.
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Some studies in humans have also used electroencephalograms (EEG) to register the electrical activity of the cortex, and in animals also the electrical activity of the deeper structures of the brain have been measured. Results have shown that after a very short time the electrical activity in the cerebral cortex and in the deeper structures disappears completely.
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The first symptoms of oxygen deficiency are recorded, on average, 6.5 seconds after the onset of the cardiac arrest. If the heartbeat is not immediately restored, the complete loss of all electrical activity in the cerebral cortex
always
results in a
flat EEG
after ten to twenty (a mean of fifteen) seconds.
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In tests on animals, auditory evoked potentials, or measures of brain-stem viability, can no longer be induced, which means that the reaction caused in a normal functioning brain stem by sound stimulation is no longer produced.
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If the cardiac arrest lasts longer than thirty-seven seconds, the EEG does not normalize immediately. After a complicated resuscitation with persistent coma, it can take hours or days for the EEG to return to normal. Despite maintaining normal blood pressure in the period following resuscitation, this ultimately depends on the duration of the cardiac arrest.
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The longer the cardiac arrest, the greater the brain damage, the longer the coma, and the longer the EEG remains flat or highly irregular.

Normalization of the EEG may actually create an overly positive impression of the recovery of the brain’s metabolism. After the heart begins beating again and blood flow resumes, oxygen supply to the brain may be reduced for a long time. Following a cardiac arrest lasting longer than thirty-seven seconds, measurements of blood flow to the brain after the heartbeat is restored initially show an increase of blood flow (an overshoot) followed by a significant decrease of up to 50 percent less than normal blood flow as a result of the swelling of the brain (edema). The result is undersaturation of oxygen in the brain during this period of time.
¹¹

Many argue that the loss of blood flow and a flat EEG do not exclude some activity somewhere in the brain because an EEG primarily registers the electrical activity of the cerebral cortex. In my view this argument misses the point. The issue is not whether there is some immeasurable activity somewhere but whether there is any sign of those specific forms of brain activity that, according to current neuroscience, are considered essential to experiencing consciousness.
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And there is no sign whatsoever of those specific forms of brain activity in the EEGs of cardiac arrest patients. A flatline EEG is also one of the major tools for diagnosing brain death, and in those cases the objection about not ruling out any brain activity is never mentioned. Besides, there are circumstances in which the EEG registers brain activity, yet no waking consciousness is experienced. This phenomenon occurs under general anesthesia, during which, depending on the medication used, the EEG shows clear changes but certainly not complete loss of brain activity. The same happens during deep dreamless sleep (non-REM sleep), when no consciousness is experienced despite demonstrable activity in the EEG. Later I will look in more detail at the brain structures that must actively cooperate to allow the experience of waking consciousness.

It is also highly unlikely that the out-of-body experience takes place immediately after regaining consciousness, as is sometimes claimed. The reason is that the time between the restoration of blood circulation after a successful resuscitation and the recovery of consciousness varies from five minutes to seventy-two hours, with a mean of six hours, which is much later than when the reported and verifiable perceptions during resuscitation must have taken place.
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Patients with a myocardial infarction who suffer a cardiac arrest at the coronary care unit are usually successfully resuscitated within one to two minutes; at a nursing ward, however, this takes at least two to five minutes. In the event of a cardiac arrest in the street (an out-of-hospital arrest) it takes, at best, five to ten minutes for a patient to be successfully resuscitated and usually longer, resulting in the death of nearly 90 percent of these patients. Only patients with an induced cardiac arrest, as part of electrophysiological studies or for threshold measurements during the implantation of ICDs, are successfully treated within fifteen to thirty seconds.

Needless to say, no EEG is carried out at the moment patients with a myocardial infarction suffer a cardiac arrest. Medical staff want to resuscitate the patient as quickly and effectively as possible. However, we know from the already-mentioned blood flow and EEG registrations that all cardiac arrest patients included in the prospective NDE studies have suffered a loss of blood flow and electrical brain activity. Their clinical picture also reflects the loss of all cerebral cortex and brainstem activity. In this state the brain can be compared to a computer that has been disconnected from its power supply, unplugged, and all its circuits disabled. Such a computer cannot function; in such a brain even so-called hallucinations are impossible. Nonetheless, during such temporary loss of all measurable brain function, a number of these patients experienced a period of exceptionally lucid consciousness.

What Happens in the Brain When the Heart Stops?

What exactly happens in the brain when the heart stops? The brain accounts for only 2 percent of overall body weight, but it uses 15 to 20 percent of the body’s total energy supply, primarily for maintaining the membrane potential (the electric charge across a cell membrane) of the nerve cells, or neurons. Oxygen deficiency causes a functional loss of all cell systems and organs in the body. But some cells respond better to oxygen deficiency than others. Neurons respond badly because their sole source of energy is glucose. Unlike the muscle cells in our body, our brains do not store glucose in the form of glycogen as a ready supply of cell energy. The parts of the brain that are most susceptible to oxygen deficiency are the neurons in the cerebral cortex, the hippocampus, and the thalamus.
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Oxygen deficiency reduces these structures, which form an important link between the brain stem and cerebral cortex, to utter chaos and wipes out their connections. Synapses are the junctions that enable communication between neurons, and when these synapses stop functioning cooperation is no longer possible. But research drawing on magnetic resonance imaging (MRI), for example, has shown that the joint and simultaneous activity of the cerebral cortex and brain stem, with their shared pathways (hippocampus and thalamus), is a prerequisite for conscious experience.

If the absence of blood flow to the brain prevents the supply of glucose and oxygen, a neuron’s first symptom is the inability to maintain its membrane potential, resulting in the loss of neuronal function.
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The acute loss of electrical and synaptic activity in neurons can be seen as the cell’s inbuilt defense and energy-saving response (a pilot-light state). When these functions cease, the remaining energy sources can be deployed very briefly for the cell’s survival. In the case of short-term oxygen deficiency, dysfunction can be temporary and recovery possible because the neurons will remain viable for a few more minutes.

The Difference Between Temporary and Permanent Dysfunction

Cardiologists draw on a comparable temporary loss of function of the cardiac muscle to check if somebody with chest pain after exertion (angina pectoris) shows signs of oxygen deficiency in a certain part of the heart muscle. I cite this example not only because I am a cardiologist, but also because this process is much easier to explain in the heart than in the brain. During an exercise test, which induces oxygen deficiency in the heart, ultrasound (echo) or nuclear imaging (SPECT scan) registers contraction of the heart muscle. As soon as oxygen deficiency sets in, the ECG changes and part of the heart muscle no longer contracts. This part of the heart muscle has stopped functioning normally because obstruction of the coronary artery has caused oxygen deficiency. As soon as the test is discontinued and the oxygen flow is restored, the heart muscle resumes normal function. The loss of function was temporary and reversible, and is known as “stunning” of the heart. A similar kind of stunning (pilot-light state) takes place in the neurons, but if the oxygen deficiency is too prolonged, the death of cells causes irreparable damage and the loss of function will be permanent and irreversible. In the heart this is known as a myocardial infarction. Permanent loss of all brain function as a result of a cardiac arrest is known as brain death because after five to ten minutes the neurons are irreversibly damaged by the disintegration of the cell membrane, which leads to an influx of calcium and the formation of so-called free radicals. The proteins in the neurons break down, and the cell dies.
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