How We Die_ Reflections On Life's Final Chapter Part 4

In 1907, Alzheimer published a paper ent.i.tled "On a Distinctive Disease of the Cerebral Cortex," reporting the case of a woman who had been admitted to the psychiatric hospital in November 1901. This is the first study of a patient in whom the eponymous sickness was recognized as a singular ent.i.ty to be differentiated from all others. Except that the language is far more stark, we might just as well be reading Esquirol; except that Alzheimer does not specifically outline the boundaries of each of the "four degrees of incoherence," we might just as well be reading Prichard. Alzheimer presented a fifty-one-year-old woman who had gone through the successive symptoms of jealousy, failure of memory, paranoia, loss of reasoning powers, incomprehension, stupor, and, finally, "After 4 years of the disease, death occurred. At the end, the patient was completely stuporous; she lay in her bed with her legs drawn up under her, and in spite of all precautions she acquired bedsores."

The description of the patient's clinical course was not the reason Alzheimer reported her case. Such patients had been familiar to physicians even before Pinel and Esquirol, although the two French clinicians were the first to separate them into the new category of dementia. In fact, the term presenile dementia presenile dementia had been introduced long before Alzheimer, even as early as 1868, in order to differentiate those patients who were still in their middle years when afflicted. Nor did Alzheimer wish to content himself merely with describing yet another demented cortex that was obviously atrophic on simple inspection with the naked eye. His purpose in the 1907 paper was to tell of what he had found when he sectioned this woman's brain, applied special stains to the thinly sliced segments, and examined them under the microscope. had been introduced long before Alzheimer, even as early as 1868, in order to differentiate those patients who were still in their middle years when afflicted. Nor did Alzheimer wish to content himself merely with describing yet another demented cortex that was obviously atrophic on simple inspection with the naked eye. His purpose in the 1907 paper was to tell of what he had found when he sectioned this woman's brain, applied special stains to the thinly sliced segments, and examined them under the microscope.

Alzheimer had discovered that many of the cells of the cortex contained one or several hairlike fibrils, which in other cells merged into groups, of increasing density. At what appeared to be a somewhat later stage, the nucleus and indeed the entire cell disintegrated, leaving only a dense bundle of the fibrils in its place. Alzheimer considered the fact that the fibrils absorbed a different dye than did the normal cell to be evidence that the deposition of some pathological product of metabolism was the cause of the lethal outcome. Between one-quarter and one-third of his patient's cortical cells either contained fibrils or had disappeared entirely.

In addition to the destructive processes in the cells, Alzheimer found numerous microscopic clumps or plaques scattered throughout the cortex, which resisted taking up the dye. In later years, these were shown to be composed of degenerated portions of the intercommunicating nerve extensions called axons, cl.u.s.tered around a core of the protein substance beta-amyloid. To this day, the invariable presence of so-called senile plaques and fibrillary tangles are the primary criteria upon which a microscopic diagnosis of Alzheimer's disease is made.

It has been recognized, however, that neither the amyloid plaques nor the neurofibrillary tangles are found exclusively in Alzheimer's. There is a variety of other chronic conditions of the human brain in which one or the other or both can be identified. Even in normal aging, at least a few of both types of structures appear, though hardly in the large quant.i.ties characteristic of Alzheimer's. We will know a great deal more about the process of brain aging once the origins of the plaques and tangles of this disease have been discovered.

Alzheimer was wise enough to recognize that "we are apparently confronted with a distinctive disease process." His mentor, Kraepelin, went one step further: Referring to the new ent.i.ty in the eighth edition of his textbook in 1910, he christened it "Alzheimer's disease." Kraepelin seemed uncertain about the significance of the comparatively young age of Alzheimer's patient, in view of the fact that her history was so similar to those of people who had previously been put into the category of senile dementia. He wrote, "The clinical significance of Alzheimer's disease is still unclear. Although the anatomical findings suggest that this condition deals with an especially severe form of senile dementia, some circ.u.mstances speak against this; namely the fact that the disease may arise even at the end of the fifth decade. One would describe such cases at least in terms of senium praec.o.x [precocious senility], if not preferably that this disease is more or less independent of age." This uncertainty by a man whom many considered the high priest of organic psychiatry may have influenced later authors to attach more significance to Kraepelin's use of the term senium praec.o.x senium praec.o.x and to have overlooked his suggestion that "this disease is more or less independent of age." Probably as a consequence of this misinterpretation, the notion that Alzheimer's is a and to have overlooked his suggestion that "this disease is more or less independent of age." Probably as a consequence of this misinterpretation, the notion that Alzheimer's is a presenile presenile dementia became fixed in medical nomenclature for more than half a century. dementia became fixed in medical nomenclature for more than half a century.

Within a few years of Alzheimer's paper, other workers reported on similar patients. In each case, the clinical course was not unlike that of Alzheimer's original woman, and the autopsies revealed a diffuse atrophy which, while it involved the entire brain, was particularly evident in the cortex. On microscopic examination, great numbers of the senile plaques and fibrillary tangles could be demonstrated. By 1911, there had been twelve such additional reports.

The relative youth of some of the patients seemed to set the findings off from later descriptions of autopsies in which senile plaques and fibrillary tangles were being found in people of all ages and apparently with a variety of clinical histories. By 1929, there were four reports of the disease in patients below the age of forty, and even one whose symptoms began when he was seven. The problem may have been compounded by a certain selectivity in reporting-physicians are more likely to write up cases that seem unusual than those that are run-of-the-mill. Also, in those countries (and they are in the majority) where autopsies are not mandatory, by far the greater number are done on patients who are "interesting." What is more interesting than a young man with an old man's disease? Thus, by the late 1920s, the great majority of the many cases of Alzheimer's disease in the world medical literature were patients in the relatively young fifty-to-sixty age group.

Although perceptive clinicians obviously appreciated that the age criteria continued to have fuzzy margins, the syndrome continued to be designated as Alzheimer's presenile dementia for decades. That was the name by which I first encountered it in textbooks during my medical school years in the 1950s.

The process by which "Alzheimer's presenile dementia" was transformed into the much more accurate "senile dementia of the Alzheimer type" is a tale paradigmatic of the way biomedical culture has evolved in the last third of the twentieth century. By this, I mean a combination of science, government involvement, and a factor that may best be understood by the term consumer advocacy consumer advocacy. For sixty years following Alzheimer's initial work, evidence slowly acc.u.mulated that there is little or no validity in differentiating between the senile and presenile forms of a disease when both are characterized by the same microscopic pathology. After the point was finally hammered home at a 1970 conference on Alzheimer's and related conditions, there began to arise a scientific consensus that the persistence of such an arbitrary distinction was not only erroneous but misleading.

One of the obvious effects of the changed att.i.tude was the inclusion under the diagnostic umbrella of a perfectly huge population of elderly patients and their families. As research interests were spurred, scientists quite correctly began to clamor for more funding and sought it from government sources. In the United States, this meant the involvement of the National Inst.i.tutes of Health (NIH) and the enlistment of every advocate of the elderly who might have some political influence. The creation of the National Inst.i.tute on Aging (NIA) was the natural outgrowth of this process. The coordinating of the efforts of the scientists, the NIA, and caregivers resulted in the founding of the ADRDA. A malady thought in my medical school days to be so unusual that it was used as a trivia question in late-night study sessions had emerged as one of the leading causes of death in World Health Organization statistics. As a result of all the coordinated effort, the Alzheimer's research budget in the United States in 1989 was some eight hundred times what it had been only ten years earlier.

In spite of the great progress that has been made during the last decade and a half in the care of patients and the support of those who must provide that care, the advancements in the more biomedical aspects of the disease, such as cause, treatment, and prevention, have not yet led to the discovery of any distinct cause of the disease, a method of curing it, or any way in which it might be prevented.

There is some evidence that there may be a genetic predisposition to Alzheimer's, but it is less than convincing with regard to older patients and not yet satisfactorily proven for the younger, even though certain chromosomal defects have been identified in small numbers of people with the disease. Explorations into the effect of external factors such as aluminum and other environmental agents, viruses, head trauma, and decreased sensory input sometimes yield suggestive findings and other times do not. As in other maladies of obscure etiology, changes in the immune system have been studied without definitive outcome, and even that ubiquitous villain the cigarette has been suspected by some. What seems very likely is that there will prove to be a range of different pathways each of which leads eventually to the degenerative process of Alzheimer's.

Certain physical and biochemical changes have been found to be accompaniments of the disease process, but their role is still unclarified. For example, biopsy of a patient's cerebral cortex demonstrates a 60 to 70 percent decrease in levels of acetylcholine, a key factor in the chemical transmission of nerve impulses. In fact, attempts to find some effective treatment have focused to a large extent on the search for drugs that might improve the defects in neurotransmission.

Evidence has recently appeared to indicate that acetylcholine may have a role in regulating the body's production of amyloid. It appears that amyloid increases when levels of acetylcholine are low. This finding provides a possible direct link between the chemical characteristics of the disease and its microscopic pathology, and it may lead to new methods of treatment. Especially provocative has been the suggestion that beta-amyloid is toxic to nerve cells; if this still-controversial idea can be substantiated, there will probably be some real reason for optimism in the search for effective therapy. To ill.u.s.trate the degree of scientific controversy, it must be appreciated that neurobiologists continue to disagree over the question of whether amyloid causes the degeneration of nerve cells or is merely the result of the breakdown of those cells.

Also, a third microscopic characteristic has been added to the duo of fibrillary tangles and senile plaques, which is the presence within certain cells in the hippocampus of empty s.p.a.ces called vacuoles, surrounding densely stained granules of uncertain significance. Hippocampus Hippocampus is the Greek word for seahorse, bestowed by the physicians of antiquity on this graceful curving structure within the temporal lobe of the brain because its elongated shape evoked the image of that peculiar animal. The hippocampus is involved with the storage of memories. Other of its functions have remained enigmatic, and no one is quite sure of the significance of the vacuoles and their contained granules. is the Greek word for seahorse, bestowed by the physicians of antiquity on this graceful curving structure within the temporal lobe of the brain because its elongated shape evoked the image of that peculiar animal. The hippocampus is involved with the storage of memories. Other of its functions have remained enigmatic, and no one is quite sure of the significance of the vacuoles and their contained granules.

And so the laboratory scientists remain puzzled and hard at work. It is difficult to believe, considering the vast amount of research being done and the many findings already being scrutinized, that the present state of knowledge is not the prelude to a period when the small discoveries will begin to coalesce into some very large ones. That is, after all, the way science usually works in this last third of the twentieth century, rather than by huge leaps forward.

Physicians are now at the point where they can make the diagnosis accurately in about 85 percent of cases without resorting to such extreme measures as biopsies of the brain. Among the several important reasons for early diagnostic efforts is the very direct one that there are certain treatable ent.i.ties which exhibit enough of the characteristics of dementia that they may be confused with it, thereby compounding the tragedy. Among them are depression, medications, anemia, benign brain tumor, low thyroid function, and some of the reversible effects of trauma, such as blood clots pressing on the brain.

There are no consolations in the diagnosis of Alzheimer's disease. The anguish may be mitigated by good nursing care, support groups, and the closeness of friends and family, but in the end it will be necessary for patient and loved ones together to walk through that very tortuous valley of the shadow, in the course of which everything changes forever. There is no dignity in this kind of death. It is an arbitrary act of nature and an affront to the humanity of its victims. If there is wisdom to be found, it must be in the knowledge that human beings are capable of the kind of love and loyalty that transcends not only the physical debas.e.m.e.nt but even the spiritual weariness of the years of sorrow.

VI.

Murder and Serenity MAN IS AN obligate aerobe": There, stated with the simple directness of any of the most quoted aphorisms of ancient Hippocrates, stands the secret of human life. The dependence on air of all mankind, and indeed all known terrestrial animals, was recognized by primitive tribesmen long before any of them were distinguished from their fellows by being called healers. No matter the technological sophistication of ultramodern molecular research, and no matter the increasingly abstruse terminology of its current literature, the circle of knowledge always returns to its starting point: In order to live, man must have air. obligate aerobe": There, stated with the simple directness of any of the most quoted aphorisms of ancient Hippocrates, stands the secret of human life. The dependence on air of all mankind, and indeed all known terrestrial animals, was recognized by primitive tribesmen long before any of them were distinguished from their fellows by being called healers. No matter the technological sophistication of ultramodern molecular research, and no matter the increasingly abstruse terminology of its current literature, the circle of knowledge always returns to its starting point: In order to live, man must have air.

In the late eighteenth century, it was found that not air in general but one particular component of it, oxygen, is the crucial factor on which life depends. The conception of man as an obligate aerobe then took on a more specific meaning: We have no choice-without oxygen, our cells die and we die with them. Oxygen absorption was soon thereafter shown to be the reason that the color of blood turns instantly from a dark tiredness to the bright red of vibrant life as it pa.s.ses through the lungs; its departure into the cells of the body's distant tissues was recognized as the cause of blood's exhaustion when it returns depleted and blue from the long journey, figuratively gasping for air. Since then, the role of this most vital of nature's elements has been explored generation after generation by thousands upon thousands of researchers, who have recorded their findings in virtually every one of the world's written languages. Oxygen is at the focal point of the lens through which the sustaining processes of living things must be studied.

After all the years and all the research, the scholars of human biology come ever back to the few words that have always been inherent in an individual's understanding of what he must do to stay alive: Man is an obligate aerobe. I could have plucked one of the many variations of that maxim from almost any of the past two centuries' profusion of writings on the subject, but its actual source is instructive. I found it in a recent issue of the Bulletin of the American College of Surgeons Bulletin of the American College of Surgeons, ent.i.tled "What's New in Surgery-1992." It appeared not as the time-honored nutsh.e.l.l of wisdom it is but as an experimentally proven, molecular-level certainty. What may be even more revealing are the statement's surroundings; it is situated smack in the middle of the Bulletin Bulletin's highly technical article on the latest developments in critical care, that brand-new (the trendy term is cutting edge cutting edge) superspecialty created to defend the very border of a desperately ill person's flickering existence, the ultimate battleground contested between the strained forces of life and the powerful a.s.saults that disease is launching in order to overwhelm them.

The new specialty's venue is the intensive care unit; its primary defensive strategy is to maintain a dependable supply of oxygen to the beleaguered cells of the body. Certainly our cave-dwelling forebears would have agreed that this is the right thing to do. The late Milton Helpern, to whose autopsy rooms patients were sent for study if the battle was lost, spent his career seeking out the "ten thousand several doors" to death, and he always came up with the same underlying answer: not enough oxygen.

Oxygen takes a remarkably direct route in making its way from the inhaled air to its ultimate destination, which is the aerobically obligated cell. After pa.s.sing readily through the thin walls of the lung's alveoli and their attached network of capillaries, the oxygen molecules link themselves to the protein pigment of the red cells which we call hemoglobin. Thereafter known as oxyhemoglobin, the combined molecules are carried from the lung to the left heart and then out through the aorta to the broad highways and narrow footpaths of the arterial circulation, until they reach the distant capillaries in the tissues whose sustenance is the object of their journey.

Once arrived, the oxygen separates itself from its traveling companion, hemoglobin. It leaves the red cell like a pa.s.senger getting off a railroad car, and enters the individual tissue cell along with biochemical substances required for that cell's normal function. In what may be thought of as an exchange, carbon dioxide diffuses into the circulating blood, which also carries away the waste products of cellular life, to be destroyed or released through those magnificently mult.i.talented organs of purification, the liver, the kidneys, and the lungs.

Like any good system of delivery and pickup, this one depends on a predictably consistent flow of traffic, in this case the traffic being blood. Shock Shock is the term used to describe the course of events that ensues when the blood flow is inadequate to meet the needs of the tissues. Although shock may be caused by a variety of mechanisms, the majority of cases are due to failure of the heart's pumping action (as in myocardial infarction) or to a major decrease in circulating blood volume (as in hemorrhage). The two mechanisms are called, respectively, cardiogenic and hypovolemic shock. Another common instigator of shock is septicemia, the entrance into the bloodstream of the products of infection. So-called septic shock has profound effects on cellular function, as will be discussed later, but one of its major actions is to induce a redistribution of blood so that it pools in certain extensive networks of veins, like those of the intestine, thereby becoming lost to the general circulation. Regardless of cause, all forms of shock have a similar outcome: Cells are deprived of their source of biochemical exchange and oxygen, the ultimate factor in their death. is the term used to describe the course of events that ensues when the blood flow is inadequate to meet the needs of the tissues. Although shock may be caused by a variety of mechanisms, the majority of cases are due to failure of the heart's pumping action (as in myocardial infarction) or to a major decrease in circulating blood volume (as in hemorrhage). The two mechanisms are called, respectively, cardiogenic and hypovolemic shock. Another common instigator of shock is septicemia, the entrance into the bloodstream of the products of infection. So-called septic shock has profound effects on cellular function, as will be discussed later, but one of its major actions is to induce a redistribution of blood so that it pools in certain extensive networks of veins, like those of the intestine, thereby becoming lost to the general circulation. Regardless of cause, all forms of shock have a similar outcome: Cells are deprived of their source of biochemical exchange and oxygen, the ultimate factor in their death.

Whether or not they do die, and whether enough of them die so that the patient is also killed, is determined by the duration of the shock. If it lasts long enough, it is always lethal. The long enough long enough is, of course, a relative term. Just how long is long enough? It depends upon the degree of the circulation's inadequacy. If flow is stopped completely, as in cardiac arrest, death occurs within minutes; if it is merely decreased to levels somewhat less than those needed for survival, dying takes more time and occurs at different rates in different tissues, depending upon how much oxygen their cells require. The brain being particularly sensitive to deficiencies of oxygen and glucose, it fails quickly; because its viability is the legal criterion of being alive, there is obviously a very narrow margin between mortality and continued existence in those people whose cerebral circulation is at all compromised. Interference with oxygen delivery to the brain is a factor in a wide variety of violent deaths. is, of course, a relative term. Just how long is long enough? It depends upon the degree of the circulation's inadequacy. If flow is stopped completely, as in cardiac arrest, death occurs within minutes; if it is merely decreased to levels somewhat less than those needed for survival, dying takes more time and occurs at different rates in different tissues, depending upon how much oxygen their cells require. The brain being particularly sensitive to deficiencies of oxygen and glucose, it fails quickly; because its viability is the legal criterion of being alive, there is obviously a very narrow margin between mortality and continued existence in those people whose cerebral circulation is at all compromised. Interference with oxygen delivery to the brain is a factor in a wide variety of violent deaths.

Although viability of the brain is currently the legal criterion by which mortality is determined, there is still usefulness in the time-honored way in which clinical physicians have always diagnosed death. Clinical death Clinical death is the term used to encompa.s.s that short interval after the heart has finally stopped, during which there is no circulation, no breathing, and no evidence of brain function, but when rescue is still possible. If this stoppage occurs suddenly, as in cardiac arrest or ma.s.sive hemorrhage, a brief time remains before vital cells lose their viability, during which measures such as cardiopulmonary resuscitation (CPR) or rapid transfusion may succeed in resuscitating a person whose life has seemingly ended-the time is probably no more than four minutes. These are the dramatic moments we read about and see portrayed on our television screens. Although the attempts are usually futile, they succeed just often enough that, under the appropriate circ.u.mstances, they should be encouraged. Because individuals most likely to survive clinical death are those whose organs are healthiest and who do not have terminal cancer, for example, or debilitating arteriosclerosis or dementia, their continuing existence is still possible and potentially most valuable to society, at least in terms of ability to contribute. It is for this reason that the principles of CPR should be taught to every motivated person. is the term used to encompa.s.s that short interval after the heart has finally stopped, during which there is no circulation, no breathing, and no evidence of brain function, but when rescue is still possible. If this stoppage occurs suddenly, as in cardiac arrest or ma.s.sive hemorrhage, a brief time remains before vital cells lose their viability, during which measures such as cardiopulmonary resuscitation (CPR) or rapid transfusion may succeed in resuscitating a person whose life has seemingly ended-the time is probably no more than four minutes. These are the dramatic moments we read about and see portrayed on our television screens. Although the attempts are usually futile, they succeed just often enough that, under the appropriate circ.u.mstances, they should be encouraged. Because individuals most likely to survive clinical death are those whose organs are healthiest and who do not have terminal cancer, for example, or debilitating arteriosclerosis or dementia, their continuing existence is still possible and potentially most valuable to society, at least in terms of ability to contribute. It is for this reason that the principles of CPR should be taught to every motivated person.

Clinical death is often preceded (or its first evidences are accompanied) by a barely more than momentary period termed the agonal phase agonal phase. The adjective agonal agonal is used by clinicians to describe the visible events that take place when life is in the act of extricating itself from protoplasm too compromised to sustain it any longer. Like its etymological twin, is used by clinicians to describe the visible events that take place when life is in the act of extricating itself from protoplasm too compromised to sustain it any longer. Like its etymological twin, agony agony, the word derives from the Greek agon agon, denoting a struggle. We speak of "death agonies," even though the dying person is too far gone to be aware of them, and even though much of what occurs is due simply to muscle spasm induced by the blood's terminal acidity. Agonal moments and the entire sequence of events of which they are a part can occur in all the forms of death, whether sudden or following upon a long period of decline into terminal illness, as in cancer.

The apparent struggles of the agonal moments are like some violent outburst of protest arising deep in the primitive unconscious, raging against the too-hasty departure of the spirit; no matter its preparation by even months of antecedent illness, the body often seems reluctant to agree to the divorce. In the ultimate agonal moments, the rapid onset of final oblivion is accompanied either by the cessation of breathing or by a short series of great heaving gasps; on rare occasions, there may be other movements as well, such as the violent tightening of James McCarty's laryngeal muscles into a terrifying bark. Simultaneously, the chest or shoulders will sometimes heave once or twice and there may be a brief agonal convulsion. The agonal phase merges into clinical death, and thence into the permanence of mortality.

The appearance of a newly lifeless face cannot be mistaken for unconsciousness. Within a minute after the heart stops beating, the face begins to take on the unmistakable gray-white pallor of death; in an uncanny way, the features very soon appear corpse-like, even to those who have never before seen a dead body. A man's corpse looks as though his essence has left him, and it has. He is flat and toneless, no longer inflated by the vital spirit the Greeks called pneuma pneuma. The vibrant fullness is gone; he is "stripped for the last voyage." The body of the dead man has already begun the process of shrinking-in hours, he will seem "to be almost half himself." Irv Lipsiner reenacted the deflation by blowing his breath out through pursed lips. No wonder we say of the recently deceased that they have expired.

Clinical death has a distinctive look about it. A few seconds' observation of the victim of cardiac arrest or uncontrolled hemorrhage will decide the appropriateness of attempts at resuscitation. Should any doubt remain, there are the eyes to consider. If open, they are at first gla.s.sy and unseeing, but if resuscitation does not commence they will in four or five minutes yield up their sheen and become dulled, as the pupils dilate and forever lose their watchful light. It is soon as though a thin cloud-gray film has been laid down over each eye, so that no one can look within to see that the soul has fled. Its rounded plumpness having depended on something no longer there, the eyeball soon flattens out, just enough to be noticeable. It is a flatness from which there is no rising.

The absence of circulation is confirmed by the absence of pulse-an observer's seeking finger on the neck or groin detects no sign of a throbbing artery beneath, and the surrounding muscles, if they are not still in an element of spasm, have begun to a.s.sume the flaccid consistency of meat slabbed in a butcher's display case. The skin has lost its elasticity, and that slight s.h.i.+ne is gone which once gleamed in reflected recognition of nature's light. At that point, life is over-no amount of CPR can retrieve it.

To be declared legally dead, there must be incontrovertible evidence that the brain has permanently ceased to function. The criteria of brain death currently being used in intensive care and trauma units are very specific. They include such signs as loss of all reflexes, lack of response to vigorous external stimuli, and absence of electrical activity as shown by a flat electroencephalogram for a sufficient number of hours. When these standards have been met (as when brain death is due to head injury or ma.s.sive stroke), all artificial supports can be withdrawn and the heart, if not already stilled, will soon stop, ending all circulation.

When circulation ceases, cellular death can complete itself. The central nervous system goes first and the connective tissue of muscle and fibrous structures goes last. With electrical stimulation, it is sometimes possible to induce muscular contraction even hours after death. Some few organic processes, called anaerobic because they require no oxygen, will also continue for hours, such as the liver cell's ability to break down alcohol into its component parts. The supposedly well-known fact that hair and nails will keep growing for varying periods of time after death is not a fact at all-no such thing happens.

In most deaths, the heartbeat ends before the brain ceases to function. Particularly in sudden deaths due to trauma other than head injury, the cessation of heartbeat is almost always the result of the rapid loss of more blood than can be tolerated-the trauma surgeon refers to such a hemorrhage as exsanguination exsanguination, which is a more elegant term than the more commonly used bleeding out bleeding out. Exsanguination may be due to direct laceration of a major vessel or to injuries of blood-filled organs like the spleen, liver, or lung; sometimes the heart itself is torn.

The rapid loss of approximately one-half to two-thirds of the body's blood volume is usually sufficient to arrest the heart. Since total blood volume is equal to some 78 percent of body weight, a bleed of eight pints in a 170-pound man or six pints in a 130-pound woman can be enough to cause clinical death. With laceration of a vessel the size of the aorta, the process takes less than a minute; a tear in the spleen or liver might take hours, or even days, on those very rare occasions when constant ooze remains unchecked.

With the loss of the first few pints, blood pressure begins to drop and the heart speeds up in an attempt to compensate for the decreased volume of each stroke. Finally, no amount of internal readjustment can keep up with the losses-the pressure and volume of blood reaching the brain become too low to sustain consciousness, and the patient lapses into coma. The cerebral cortex fails first, but the brain's "lower" parts, such as the brain stem and medulla, hold on a bit longer, so that respiration continues, though in an increasingly disorganized fas.h.i.+on. Finally, the near-empty heart stops, sometimes fibrillating before it does so. The agonal period then begins, and life flickers out.

This entire grim sequence of events-hemorrhage, exsanguination, cardiac arrest, the agonal moments, clinical death, and finally irretrievable mortality-was played out during a particularly vicious murder committed a few years ago in a small Connecticut city not far from the hospital where I work. The attack took place at a crowded street fair, in full view of scores of people who fled the scene in fear of the killer's maniacal rage. He had never laid eyes on his victim before the instant of the savage onslaught. She was a buoyant, beautiful child of nine.

Katie Mason was visiting the fair from a nearby town, along with her mother, Joan, and her six-year-old sister, Christine. Accompanying them was Joan's friend Susan Ricci, who had brought along her own two children, Laura and Timmy, about the same ages as the Mason kids-Katie and Laura, in fact, were fast friends and had been studying ballet together since they were both three. As they milled around with the crowd at a sidewalk sale in front of the local Woolworth's, little Christine began tugging at her mother's hand to attract her attention to the pony rides on the other side of the street, begging to be taken over there. Leaving Katie with the others, Joan and her younger daughter crossed the road toward the concession. Just as they reached the opposite sidewalk, Joan heard a hubbub from somewhere behind her and then a child's shrill scream. She turned, dropped Christine's hand, and advanced a few feet toward the sound. People were scattering in all directions, trying to get away from a large, disheveled man who stood over a fallen little girl, his outstretched right arm pummeling furiously away at her. Even through the haze of her frozen incomprehension, Joan knew instantly that the child lying on her side at the crazed man's feet was Katie. At first, she saw only the arm, then realized all at once that in its hand was clutched a long b.l.o.o.d.y object. It was a hunting knife, about seven inches long.

Using all his strength, up and down, up and down, in rapid pistonlike motions, the a.s.sailant was hacking away at Katie's face and neck. In an instant, everyone had fled-murderer and victim were suddenly alone. Unhindered at his frenzied work, the man first crouched and then sat alongside the child, chopping with those ceaseless plungings of his ferocious arm. As the pavement reddened with her child's blood, Joan, by then also alone, stood about twenty feet away, rooted there by disbelief and horror. She would later remember that the air seemed too thick to let her move through it-her body felt warm and benumbed, and she was enveloped in a dreamy mist of insulation.

Except for the ferocious chopping of that unremitting arm coming down again and again on the silent child, there was almost no movement in the entire unearthly scene. Anyone watching from inside the Woolworth's or the refuge of some other concealment might have seen a grotesque tableau of madness and slaughter being enacted on that soundless street.

Though Joan was certain the macabre scene would have no end, her fixed immobility could not have lasted more than a few seconds, but during that seeming protraction of time she saw the knife repeatedly enter her child's face and upper body. Two men suddenly appeared from somewhere beyond the margins of the tableau and grabbed at the killer, shouting as they tried to wrestle him down. But he could not be deterred-with psychotic determination, he kept stabbing at Katie. Even when one of the men began aiming powerful heavy-booted kicks at his face, he seemed not to notice, though his head was being knocked from side to side by the force of the blows. A policeman ran up and seized the knife-wielding arm; only then did the three men manage to subdue the struggling maniac and pin him to the ground.

As the crazed attacker was pulled off Katie, Joan rushed forward and took her daughter into her arms. Turning her gently over from her side onto her back, and looking into that lacerated little face, she said softly, "Katie, Katie" as if she were cooing to a cradled babe. The child's head and her neck were covered with blood and her dress was soaked in it, but her eyes were clear.

She was gazing at me and beyond me, and there was a warm feeling in me. Her head had fallen back. Then I raised her a bit, and I thought she was still breathing. I spoke her name a few times and told her I loved her. And then I knew that I had to take her to a safe place-I had to get her away from this man, but it was already too late. I lifted her up in my arms. I carried her that way a short distance, and then I thought, What am I doing? Where am I taking her? I got on my knees and very gently put her down. Her chest began heaving and she started to vomit blood. It came out in such huge amounts, constantly-I didn't think she would have so much blood in her; I knew she was emptying out the blood in her body. I screamed for help, but there was nothing I could do to stop the vomiting.

When I had first gone to her, I saw some glimmer in her eyes, almost like some sort of recognition. But by the time I laid her on the ground, her eyes had a different look. Even when she was vomiting blood, they had changed to a more gla.s.sy look. When I first went to her side, she still looked alive-but not anymore.

There was no look of pain in her eyes, but instead it was a look of surprise. And then when things changed, she still had that expression on her face, but her eyes had glazed over a little bit. A woman came over-I guess she was a nurse. She started CPR. I didn't say anything, but I thought to myself, Why is she doing that? Katie is not in her body anymore. She's behind me, up there above me, and floating. Her life isn't inside her anymore, and she's not coming back. Her body is just a sh.e.l.l now. At that point, everything was different than it had been when I first went to her side-I had an awareness that my daughter had died. I felt she was no longer in her body, that she was somewhere else.

The ambulance came, and they lifted her out of the pool of blood and tried to force air into her lungs with an Ambu bag. Her eyes were still wide open and she still had that gla.s.sy look. The look on her face was a look of utter surprise, like "What's happening?" It was a combination of being helpless, confused, and surprised, but definitely not a look of horror, and I remember being relieved that it wasn't, because I was looking for any sense of relief at that time....

Later, I went through months and months of asking myself, How much pain did she feel? I needed to know that. I saw her bleed all the blood out of her body when she vomited. Her chest and face were covered with cuts and gashes. She must have been moving her head from side to side, struggling to get free of this man. Later, I found out that he had appeared from nowhere and pushed Laura aside. He had grabbed Katie's hair and thrown her to the ground. It was Laura who screamed, not Katie. I had to know what she went through, what she felt....

Do you know what it looked like? It looked like a release. After seeing him attacking her that way, it gave me a sense of peace to see that look of release. She must have released herself from this pain, because her face didn't show it. I thought, Maybe she went into a state of shock. She looked surprised but not terrified-as terrifying as it was for me, it wasn't that way for her. My friend Susan saw the look, too, and said that maybe Katie had given up, but when I told her I thought it was a look of release, she said, "That's it, you're right!"

We once had a portrait of her made, and it's that same look that she has in her eyes. They were wide but not in a state of terror-it looks almost like an innocence-an innocent release. As her mother, amidst all of that blood and everything else, it was actually soothing to look into her eyes. There came a point when I was with her that I felt like she was out of her body, floating up there looking down on herself. Even though she was unconscious, I felt that somehow she knew I was there, that her mother was there when she was dying. I brought her into the world and I was there when she was leaving-in spite of the terror and horror of it, I was there.

The ambulance sped Katie to the nearest hospital, which was only a few minutes away. Although she was clearly pulseless and brain-dead on arrival, and beyond clinical death, the appalled emergency room team did every possible thing to bring her back, even with the certain foreknowledge that their attempts would be futile. When they finally gave up, their frustration and rage turned to grief. Tearfully, one of the doctors told Joan what she already knew.

The man who murdered Katie Mason was a thirty-nine-year-old paranoid schizophrenic named Peter Carlquist. Two years earlier, he had been acquitted by reason of insanity in the attempted knife murder of his roommate, whom he accused of putting poison gas into their radiator. He had a long history of such attacks on people, including his sister and several high school cla.s.smates. As early as age six, he had told a psychiatrist that the devil had come up out of the ground and entered his body. Perhaps he was right.

Following the a.s.sault on his roommate, Carlquist had been inst.i.tutionalized in a unit for the criminally insane on the sprawling grounds of the state mental hospital situated at the outskirts of the city visited by Katie Mason on that fateful July day. Only a short time before, an advisory board had judged him sufficiently recovered to be transferred to a unit housing an a.s.sortment of the mentally ill, where patients were permitted to sign themselves out for several hours at a time. On the morning of the a.s.sault, Carlquist strolled off the grounds, took a munic.i.p.al bus into town, and walked into a local hardware store. After buying a hunting knife, he came upon the street fair. And there in the crowd outside Woolworth's he saw the two pretty little girls wearing identical dresses. Somewhere in his deranged mind lies the secret of why he chose the dark-haired Katie to be his victim instead of blond Laura. Rus.h.i.+ng forward, he grabbed her by the arm, threw her to the ground, and began his demonic work.

Katie Mason died of acute hemorrhage leading to hypovolemic shock. Although she had been cut in many places on the upper part of her body, the main source of bleeding was a completely severed carotid artery emptying itself into a laceration of her esophagus. The blood pa.s.sed down the esophagus into her stomach; it was the source of the huge regurgitation.

A specific sequence of events takes place in people who bleed to death. At first, they will usually hyperventilate, which is the body's compensatory attempt to saturate the decreasing volume of circulating blood with as much oxygen as possible; the heart rate will speed up for the same reason. As more blood volume is lost, the pressure in the vessels begins to fall rapidly and the coronary arteries receive less and less of it. Were an electrocardiogram to be running, it would show evidence of myocardial ischemia; the ischemia causes slowing of the poorly oxygenated heart. When the blood pressure and pulse rate become low enough, the brain ceases to receive enough oxygen and glucose, and unconsciousness ensues, preceding brain death. Finally, the ischemic heart slows to a stop, usually without any fibrillation. With the stilling of the heartbeat, circulation is arrested, breathing ceases, there are a few agonal events, and clinical death has occurred. When a vessel the size of the carotid artery has been cut wide open, the entire sequence can take less than a minute.

All of this explains how Katie Mason died. But it does not explain a phenomenon witnessed by her mother, one that matches the descriptions of many other witnesses to such horrendous events. Why should a child who has suddenly been set upon by a knife-wielding psychopath obviously intent on her murder die not only without a look of terror on her face, but actually in a state of apparent tranquillity and release, an appearance of surprise rather than horror? Especially considering the savageries being perpetrated on her face and upper body during the brief time when she must have been fully conscious and seen what was being done to her-why was there no evidence of panic, or even fear?

What was described by Joan Mason has been a source of wonderment, in fact, for hundreds of years. For some soldiers, the absence of pain and fear has been the determining factor in their ability to fight on in spite of crippling wounds, feeling nothing except perhaps the euphoria of battle until the immediate danger is over, whereupon physical and mental agonies finally make their appearance, or death. There is far more at work here than the well-known "fight or flight" of a rush of adrenaline.

In his essay "Use Makes Perfect," Michel de Montaigne suggests that a lifelong acquaintance with the ways of death will soften one's final hours: I fancy there is a certain way of making it familiar to us, and in some sort of making trial what it is. We may gain experience, if not entire and perfect, yet such, at least, as shall not be totally useless to us, and that may render us more confident and more a.s.sured. If we cannot overtake it, we may approach it and view it, and if we do not advance so far as the fort, we may at least discover and make ourselves acquainted with the avenues.

Montaigne recounts an experience of being thrown from his mount by a horseman "thundering full speed in the very track where I was rus.h.i.+ng." Battered and bleeding, he thought at first that he had been shot in the head with a harquebus. But to his surprise, he remained quite calm: "Not only did I make some little answer to questions which they asked me, but they moreover tell me that I was sufficiently collected to order them to bring a horse to my wife, whom I saw struggling and tiring herself on the road."

He describes a sense of tranquillity, even though he refused the soporifics offered to him, "certainly believing that I was mortally wounded in the head. My condition was, in truth, very easy and quiet, I had no affliction on me, either for others or myself; it was an extreme languor and weakness, without any manner of pain." He pa.s.sed a serene two or three hours awaiting the death that never came, quite content to "glide away so sweetly and after so soft and easy a manner." At the end of that time, "I felt myself on a sudden involved in terrible pain, having my limbs battered and ground with my fall, and was so ill for two or three nights after, that I thought I was once more dying again, but a more painful death."

Whatever was the influence that had so tranquilized the mind of the grievously wounded Montaigne, it had worn off. After that initial period of a few hours, he suffered intense pain. Gone was the serenity, the languor, and the acceptance of an antic.i.p.ated easy death. The reality of his suffering and fear became inescapable.

Stories like Montaigne's are not rare-they are sometimes given a mystical quality by those who tell them, as though some unexplainable and perhaps supernatural event has taken place. But to a doctor who has spent his career in the company of trauma inflicted in the name of surgical cure, and those other traumas inflicted by the violence of modern life, there is a prototype for these tales of serenity and languorous comfort in the face of what would seem to be frightful and agonizing wounds. The prototype is the aftermath of the injection of an opiate or some other form of powerful narcotic painkiller. When the medication is well chosen and the dose is high enough, fear pa.s.ses and the distress of even the most unbearable incision or injury recedes into a soft cloud of indifference. Many patients report a sense of well-being, and I have even seen mild euphoria following a proper dose of a morphinelike narcotic.

It is not farfetched to believe that the human body itself knows how to make those morphinelike substances and knows how to time their release to correspond with the instant of need. The "instant of need," in fact, may be the very stimulus that sets off the process.

Such self-generated opiates do, in fact, exist, and they are called endorphins. They were given that name shortly after their discovery about twenty years ago-by contracting the two words that describe them: They are endogenous morphine endogenous morphine-like compounds. Endogenous Endogenous appeared in the lexicon of medicine at least a century earlier, adapted from the Greek appeared in the lexicon of medicine at least a century earlier, adapted from the Greek endon endon, meaning "within" or "inner," and gennao gennao, meaning "I produce." Accordingly, it refers to substances or conditions we create within our own bodies. Morphine Morphine, of course, recalls Morpheus, the Roman G.o.d of sleep and dreams.

Several structures in the brain are capable of secreting endorphins in response to stress, including the hypothalamus and an area called the periaqueductal gray matter, as well as the pituitary gland. Together with ACTH, a hormone that activates the adrenal glands, endorphin molecules are known to bind themselves, as do the other narcotics, onto foci, called receptors, on the surfaces of certain nerve cells. The effect is to alter normal sensory awareness. Endorphins seem to play a significant role not only in raising pain threshold but also in altering emotional responses. In addition, there is evidence that they interact with the adrenaline-like hormones, as well.

In the normal nonstressed, noninjured person, there is no evidence of the pain-relieving and mood-altering action of endorphins. It requires some definitive degree of trauma, whether physical or emotional, for them to swing into action. The level, or even the quality, of the necessary trauma has not yet been ascertained.

For example, it may be that the mere stimulation of acupuncture needles results in an outpouring of endorphins. During the course of a series of professional travels to Chinese medical schools over a period of years, I became interested in acupuncture after seeing several demonstrations of its effectiveness as an alternative to anesthesia in major surgery. In 1990, I visited Professor Cao Xiaoding, a neurobiologist who heads Shanghai Medical University's Acupuncture Anesthesia and a.n.a.lgesia Research Coordinating Group, an establishment of thirty faculty members and six laboratories of neuropharmacology, neurophysiology, neuromorphology, neurobiochemistry, clinical psychology, and computer science. Professor Cao's team has produced a vast body of rather impressive experimental and clinical evidence indicating that the basis of acupunture's undoubted success in certain applications is the stimulation of endorphin secretion by manipulation of the vibrating or rotating needles. Although a significant rise in endorphin levels during acupuncture has been repeatedly doc.u.mented not only in Shanghai but also in several Western laboratories, the neurological pathway by which the turn-on signal reaches the brain has not yet been elucidated. It may be similar to the mechanism that activates the familiar stress-induced response.

Since the late 1970s, endorphins have been shown to make their appearance in the presence of shock due to major blood loss or septicemia; their elevation in physical trauma of all sorts is well doc.u.mented in the surgical literature. Until fairly recently, this phenomenon had not been studied in children, but a recent report from the University of Pittsburgh demonstrates the same pattern as in adults-namely, a significantly higher increase in endorphins among patients whose injuries were most severe, as compared with those sustaining minor trauma. Some children whose only injuries consisted of abrasions were also shown to have somewhat elevated their levels.

We will never know the level of Katie Mason's endorphins (and some of my proof-demanding clinical colleagues will no doubt find fault with my a.s.sumption that it was high), but I am convinced that nature stepped in, as it so often does, and provided exactly the right spoonful of medicine to give a measure of tranquillity to a dying child. Endorphin elevation appears to be an innate physiological mechanism to protect mammals and perhaps other animals against the emotional and physical dangers of terror and pain. It is a survival device, and because it has evolutionary value it probably appeared during the savage period of our prehistory when sudden life-threatening events occurred with frequency. Many a life has no doubt been saved by the absence of panicky response to sudden danger.

Joan Mason, too, seems to have been protected by her endorphins. She told me that had it not been for her own feeling of almost supernal warmth and the sense of being surrounded by a thick insulating aura, she believes that she might have had a heart attack and died there on the street alongside her daughter. The primitive prehuman whose heart and circulatory system did not succ.u.mb to sheer terror at the moment of an animal attack was the one who survived to have offspring whose responsiveness was much like his own.

Although there are many narratives of this kind of thing, there has been very little attempt to study it in any systematic way. We read the philosophical lesson of a Montaigne, or a soldier's story, or perhaps the account of a mountain climber who experienced an unaccustomed inner peace while free-falling to an expected sudden death. Some of us have our own tales to tell. And then, of course, there are the times when endorphins fail and death comes in its full unrelieved anguish.

Because to some, endorphins would seem to involve matters of the body, and to others matters of the spirit, it is instructive to examine the experience of an articulate man whose goal was to heal both. Many tend to forget that the great explorer David Livingstone was a medical missionary. He survived a number of close calls during his African forays, but there is one that exemplifies the way in which protoplasm and ectoplasm sometimes work most closely with each other just at the moment when they seem about to part ways forever.

In February 1844, when Livingstone was thirty years old, he was one day set upon by a wounded lion from which he was trying to protect several native tribesmen in his party. The jaws of the enraged animal seized him by the left upper extremity, and he felt himself lifted off the ground and shaken violently as the lion's teeth sank deeply into his flesh, splintering the underlying humerus and ripping eleven jagged lacerations into the bleeding skin and muscle. One of Livingstone's party, an elderly convert named Mebalwe, had the presence of mind to pick up a rifle and discharge both barrels, which sufficiently frightened the animal that he dropped his prey and dashed off, only to die a short distance away of the bullet wound Livingstone had inflicted just before being pounced upon.

The injured explorer had plenty of time to think about his narrow escape during the more than two months it took him to recover from the blood loss, the shattered compound fracture, and the serious infection that began draining pus within a short time. As much as he was amazed at his survival, so also was he by the equanimity he had felt while in the lion's grasp. He would later describe the event and his ineffable sense of peace in the autobiographical work he published in 1857, Missionary Travels and Researches in South Africa Missionary Travels and Researches in South Africa.

Growling horribly close to my ear, he shook me as a terrier dog does a rat. The shock produced a stupor similar to that which seems to be felt by a mouse after the first shake of the cat. It caused a sort of dreaminess, in which there was no sense of pain nor feeling of terror, though quite conscious of all that was happening. It was like what patients partially under the influence of chloroform describe who see all the operation but feel not the knife. This singular condition was not the result of any mental process. The shake annihilated fear, and allowed no sense of horror in looking round at the beast. This peculiar state is probably produced in all animals killed by the carnivora; and if so, is a merciful provision by our benevolent Creator for lessening the pain of death.

In that long-ago day when laboratory science was barely beginning its long partners.h.i.+p with bedside medicine, Livingstone's explanation for his remarkable calm was one with which most people probably agreed. It would have taken prescience, or perhaps a disavowal of faith, to have invoked physiology in those dawning moments when microscopy and chemical a.n.a.lysis were but swaddled newborns. For Livingstone to have somehow intuited the principles of stress-related biochemical alteration of states of consciousness was quite improbable. Absent a supreme leap of prophetic vision, beyond the capability of even an ordained Christian missionary, he could not have foreseen the discovery of such a phenomenon.

I have had the personal experience of one such episode. I am not by nature a fearful person, and yet there are two situations that scare me to the point of pathological irrationality: finding myself looking down from some great height, and being immersed in deep water. I need only to think about either of those two hazards to set off a spasm of tightness in each of my sphincters, from the top of the alimentary tube right down to its very end. It is not just that I am cautious about deep water, or even afraid of it-I am unmanned by it, reduced to craven, phobic cowardice. In a swimming pool surrounded by healthy young adults, any one of whom is capable of rescuing me without so much as straining a single fiber of Schwarzeneggeroid muscle, I have more than once felt the dread certainty of imminent drowning; it has been exploded into my brain by the simple realization that I have wandered a few inches beyond my depth.

With an American colleague and a half dozen faculty members of the Hunan Medical University near the south-central Chinese city of Changsha, I was leaving the site of an elaborate banquet (during which my entire alcoholic intake had consisted of one bottle of Tsingtao beer consumed during the early portion of a two-hour meal), chatting and strolling along a curving walkway that stretched a short distance through what appeared to be a shallow reflecting pool. I was fully dressed, and carried a partially filled carry-on bag slung over one shoulder. Having been at the guest-house two years earlier, I was not unfamiliar with the terrain, but I seem not to have taken into account the narrowness of the winding pavement or the virtual absence of outside lighting on that starless night. As I turned partly around in midstride to address a remark to one of my hosts walking behind me, I suddenly found myself with nothing under my right foot. In an instant, I was immersed well over my head in the impenetrably black water, and still sinking. Simultaneously with the flash of realization that I was fully vertical and continuing to go ever deeper, I felt a stunned surprise and a mild but very distant sense of ironic amus.e.m.e.nt, as though I were involved in some ill-advised and silly stunt that hadn't worked out quite as I had planned. At the same time, I was annoyed with myself for what I immediately recognized-even down there and seemingly headed through a narrow waterway leading through the earth's crust directly back to New Haven-as a bit of clumsiness that might interfere with the successful completion of my mission in Hunan. Most remarkably, there was no sensation of fear and certainly no thought that I might be drowning.

Although I was not aware of it, I must have finally hit bottom and instinctively kicked off from it like an experienced swimmer, because I soon found myself rising straight up, until my head broke the surface. Taking hold of the outstretched hands of my shouting, frightened companions, I clambered out of the pool, using as footholds the irregular projecting rocks that formed its sides. The bag was still on my shoulder; all I had lost were a pair of eyegla.s.ses and some of that necessary element of dignity the Chinese call mianzi mianzi, or "face." For a few moments, I stood there on the walkway, feeling stupid, embarra.s.sed, and suddenly very chilly.

My deep dip could not have lasted more than a few seconds, and the summoning of endorphins is only another presumption without possibility of proof. But I relate this episode as a personal testimony to a sudden unantic.i.p.ated circ.u.mstance that should have provoked chaotic loss of control, and yet resulted only in a detached imprint of calm and quite reasonable observations about the fix I had (literally) fallen into. The element of emotional shock seems to have triggered a stress response that deprived me of the awareness of danger, thereby preventing the panic-stricken disintegration that might otherwise have taken place. I was saved, it appears, from the ineffectual flailing of arms and the aspiration of a few quarts of stagnant water, not to mention the virtual certainty of slamming my thras.h.i.+ng head against the jagged rocks that were only inches away.

My brief moments of peril were hardly of the magnitude of sensory a.s.sault visited on a Montaigne or a Livingstone, and I am not so insensitive as to compare them with the tragic events that befell little Katie Mason. And yet, except for a vast difference in degree, they all seem to ill.u.s.trate the same phenomenon-apparent tranquillity instead of terror, and resignation in the place of self-defeating struggle. Many have pondered the reasons these things should be so, and the answers are spread out over a philosophical terrain as wide as the distance between spiritualism and science. Whatever the source, humankind and many animals often seem to be protected at the instant when sudden death approaches-protected not only from the horror of death itself but from certain kinds of counterproductive actions that might ensure it or extend its anguish.

Here I approach hazardous, but unavoidable, territory. The phenomenon called (and frequently capitalized for emphasis) the Near-Death Experience has been much discussed of late. No sensible observer can discount the many tales from the almost-beyond that have been collected by reliable investigators interviewing credible survivors. Those seeking to interpret their findings on a reasonably scientific basis have invoked a variety of possible causes, from the psychiatric to the biochemical. Others seek clarification in religious faith or parapsychology, while still others accept the experiences at face value, believing them to be not only real but, in fact, the first stages of entrance to a blissful afterlife, virtually always in heaven or its equ