For many years it was not well understood that the Central Nervous System (CNS), comprising the brain and the spinal cord, plays a crucial role in maintaining an organism's vital functions. To understand that role, one might begin by pondering how it is that the muscles of respiration “know” when to contract. Does this contraction happen in an automatic, periodic fashion or does it happen upon receiving some signal from the body's CNS? The answer is this: the contraction of the muscles of respiration is brought about by a signal sent from the respiratory center of the CNS. That center is located at the base of the brainstem,i in a structure known as the medulla oblongata (The anatomical references in this and the ensuing discussion are illustrated in Figure 4 on page 26.)

When sensors in the respiratory center detect a relatively high level of CO 2 in the blood, a signal is sent to the muscles of respiration, spurring them to contract. Each of the twelve to twenty inhalations per minute, then, is the body's response to the accumulation of the waste products of metabolism; for life to continue, the CO 2 must be expelled and new oxygen must be brought in.

Figure 4: The Brain and Brainstem, with Major Divisions

For the purposes of our inquiry, the crucial fact about the mechanics of breathing is this: When the brainstem's respiratory centers are incapacitated, the organism will not make or display any respiratory effort. The chest will remain absolutely still and the body's need for oxygen will go unanswered. If the death of the organism is to be prevented, some external “driver” of the breathing process—a mechanical ventilator—must be used.ⁱⁱ

The mechanical ventilator works by increasing and decreasing the pressure in the lung cavities so that oxygen-rich atmospheric air will travel down and CO 2 -rich air will travel back up the respiratory tree. Gas exchange in the lungs is then possible, although an external substitute for the patient's own respiratory effort cannot manage this exchange (and thus maintain ideal blood-gas levels) as effectively as the body free of injury can. The exchange of gases that the ventilator sustains will be of no benefit to the patient unless the blood is kept moving as well. Incoming oxygen must be transported to the tissues that need it, and accumulating carbon dioxide must be removed to the lungs for expulsion from the body. In other words, the ventilator will help the patient only if another vital organ system is operational, comprising the heart, working as a pump, and the conveying network of arteries, veins, and capillaries.

The action of the circulatory system is analogous to the action of the external respiratory system.ⁱⁱⁱ Each system acts to maintain the continuous motion of a fluid substance that fuels the metabolic work of the organism as a whole. The fluid substance is air in respiration and blood in circulation. Furthermore, in both respiration and circulation, the mechanism of action is the periodic contraction of muscle—the heart muscle in circulation, the muscles of respiration in breathing.^iv

There are important differences, however, between the circulatory work of moving blood and the respiratory work of moving air in the body. The movement of blood occurs only within the body, whereas the movement of air is an exchange between the body and the surrounding atmosphere. This point will be important to the discussion of “Position Two” in Chapter Four. Another difference, more relevant to the present explanation of external support of vital systems, is the fact that there is no part of the CNS that is absolutely indispensable for heart contractions in the way that the respiratory center in the brainstem is absolutely indispensable for the muscular contractions involved in breathing.

Again, in healthy circumstances, stimuli from the CNS will alter the rate and strength of contractions: the heart rate will change in response to danger, excitement, or other stimuli. But even when there is no stimulus whatsoever from the CNS, the heart can continue to beat. This property of the heart, known as its “inherent rhythmicity,” has been demonstrated dramatically by experiments in which an animal's heart is taken out of its body and stimulated to begin beating rhythmically again. It is also demonstrated by the heartbeat of an embryo, which begins before the CNS has developed.

D. Ventilator Support and Determination of Death

What, then, does it mean to say that the ventilator “externally supports the vital functions of breathing and circulation?” It means that, in the place of the organism's effort to breathe, stimulated by the respiratory centers of the CNS, an external device moves the lungs and facilitates the inflow and outflow of needed air. This allows the heart muscle to continue to function, because its cells, like all other cells in the body, need oxygen to stay alive. The defense of the neurological standard for determining death begins with these observations: respiratory motion supported in this way is not in itself a “sign of life.” It is, rather, an artifact of technological intervention. Nor is a beating heart, in these circumstances, a “sign of life.” It is, instead, merely the continuation of an automatic process that would quickly cease if the ventilator were withdrawn. The defense of the neurological standard begins with these points, but it does not rest its case there. The loss of the ability to breathe on one's own is not a sufficient condition for declaring that an individual has died. Two other conditions are necessary: (1) other functions indicative of life must be lost, and (2) these functional losses must be irreversible. Each of these conditions warrants further explanation.

Any doubt that the loss of the ability to breathe spontaneously is insufficient for declaring death can be easily dispelled by considering cases of neurological injury that deprive a patient of the ability to breathe and yet leave untouched the ability to engage in activities dependent on other parts of the CNS. Patients with high spinal cord injuries present such a condition: they remain awake and alert but dependent upon ventilators for respiratory support.

Furthermore, even the loss of all functions of the CNS is not a sufficient criterion for declaring death if this loss of function is not irreversible. Again, there are critical care cases that demonstrate the importance of this qualification — for instance, when a patient is in a deep, non-breathing (“apneic”) coma during a critical emergency and the support of the ventilator allows time for CNS functions to return. In some cases like this, a full recovery of CNS functions occurs. More often, though, the functions that return will only be enough to leave the patient in a “vegetative state” that, if it persists, will be labeled a PVS (a persistent vegetative state). PVS will be discussed more fully in Part V, but the point here is that the deep, non-breathing coma that the patient was in prior to “waking” into the vegetative state could not have been death since the loss of functions proved to be reversible.

This discussion should make it clear why the condition typically called “brain death” and referred to in this report as “total brain failure” is called “irreversible apneic coma”^v by some commentators. “Apneic” and “coma” describe the critical functional losses and “irreversible” adds the necessary qualification to rule out transient losses of these functions.

In view of these complications, how can a clinician determine whether a patient has suffered total brain failure? This question concerns the tests that must be conducted to distinguish patients with this condition from other brain-injured individuals for whom recovery of (at least some) brain functions remains possible. The next part takes up this issue directly.

II. The Diagnosis of Total Brain Failure

The diagnostic criteria that a physician uses to determine whether a patient has suffered total brain failure begin with the obvious but important requirement that the patient be in a completely unresponsive coma.^vi This means that the eyes are closed and no response whatsoever is made to any verbal or painful stimuli.

Another requirement for the diagnosis of total brain failure concerns the patient's history. The cause of the patient's brain injury cannot be hypothermia, poisoning, drug intoxication, or any such cause that brings about metabolic changes that can mimic the effects of total brain failure. The reason that a total brain failure diagnosis is ruled out in these cases is plain: A condition like this is often transient—it may clear up when the cause of the metabolic change passes out of the patient's system or is otherwise removed.^vii

If the patient being diagnosed is determined to be in a deep, unresponsive coma and none of the excluding causes just mentioned is present, then a battery of further tests must be conducted. These tests can be divided into two complementary groups: clinical or bedside tests and laboratory or imaging tests. The bedside tests are performed by trained clinicians, usually neurologists, and do not involve any high-tech instruments. The laboratory tests do involve such equipment and are intended to provide a more complete picture of what the clinician observes during the clinical examination.

With the clinical bedside tests for total brain failure, the clinician examines the comatose patient for any signs of brainstem function (See Figure 4). The functional status of this part of the brain is important for several reasons. First, the functions that depend on the brainstem are central to the basic work of the organism as a whole. This has already been noted with respect to the brainstem's (particularly, the medulla's) involvement in breathing. Brainstem function is also critical to an organism's conscious life. One part of the brainstem, known as the “reticular activating system,” is essential for maintaining a state of wakefulness, which is a prerequisite for any of the activities associated with consciousness.

In addition to its significance for the patient's functional capacities, the condition of the brainstem also has a general diagnostic significance in most cases, for the brainstem is the most resilient part of the brain as a whole. As will be elaborated in Part III, if a brain injury has progressed to the point at which the brainstem retains no function, it has probably ravaged the more fragile parts of the brain as well. Thus, the bedside tests for brainstem function are tests for the extent of destruction both to the brainstem and to the parts of the brain “above the brainstem”—the so-called “higher centers.”^viii

How, then, do the clinical tests determine the status of the brainstem? One marker of brainstem function has already been explored in depth: the signal that is sent from the respiratory centers to the muscles of respiration. Thus, the patient's drive to breathe must be tested with an apnea test. “Apnea” is the technical term for an inability to breathe. Although all patients who receive ventilator support need the machine's help to breathe, most are not so injured that they have no drive to breathe whatsoever. The purpose of the apnea test for total brain failure is to establish that the patient has no drive to bring air into the body even when the sensors in the brainstem are receiving an unambiguous signal that breathing is required.

Recall from the previous discussion that these sensors serve to trigger movement of the muscles of respiration when high levels of carbon dioxide in the blood are detected. In the apnea test, then, the ventilator is removed and the level of carbon dioxide in the patient's bloodstream is permitted to increase beyond the point that would normally trigger inhalation.^ix If the examining clinicians see any signs that the chest is moving, the brainstem clearly has some vitality left and thus the patient cannot be diagnosed with total brain failure.

Another set of indicators of brainstem function are the automatic responses or “brainstem reflexes.” Elicited by appropriate stimuli, these include the gag reflex, the cough reflex, and the reflex to move the eyes in certain ways under certain conditions (e.g., when the head is moved, which normally causes the oculocephalic reflex or doll's eyes phenomenon, or when cold water is injected into the ear canal). The examining clinicians will provide the appropriate stimuli to detect the presence or absence of these reflexes. If any are present, a diagnosis of total brain failure is ruled out.

In summary, a diagnosis of total brain failure can be made only when each of the following four conditions has been met:

1. The patient has a documented history of injury that does not suggest a potentially transient cause of symptoms, such as hypothermia or drug intoxication.
2. The patient is verified to be in a completely unresponsive coma.
3. The patient demonstrates no brainstem reflexes.
4. The patient shows no drive to breathe during the apnea test.

A result indicating that all of these conditions have been met must be confirmed with a second examination some hours after the initial positive results are obtained. The appropriate length of time between these examinations is a matter of some debate. According to a consensus statement developed by the American Academy of Neurology in 1995, “[A] repeat clinical evaluation [six] hours later is recommended, but this interval is arbitrary.” 1 The six-hour interval is far shorter than the interval recommended by the medical consultants to the President's Commission in 1981: they suggested twelve hours in cases of a non-anoxic etiology (e.g., head trauma of any kind, a stroke) and twenty-four hours in cases of an anoxic origin (e.g., a heart attack that leads to temporary cessation of circulation to the brain). 2 The standard interval between examinations also varies from one country to another, ranging from two hours to twenty-four hours.3

Questions about the appropriate interval between examinations are related to questions about what laboratory or imaging tests are needed to confirm the clinical diagnosis. These tests include the electroencephalogram (EEG), tests for evoked responses (brainstem auditory evoked potentials, somatic evoked potentials, and motor evoked responses), and tests for blood flow through the vessels that feed the brain (classic arteriography, radioisotope studies, and transcranial Doppler ultrasonography).4 Standard practice in the United States dictates that these tests should be optional, to be used by the clinician in difficult cases—for example, when some factor interferes with clinical testing or when there is a need to abbreviate the interval before a second round of testing. In some other countries, the laboratory tests are mandatory.5

Neurologist James Bernat, a noted expert on the brain and its injuries, has recommended that tests of intracranial blood flow be included among the routine tests for total brain failure (or “brain death”) in the United States.6 These imaging tests are particularly useful for determining whether the pathophysiological events that lead to total brain failure have in fact occurred. Those events will be described and clarified in Part III.

First, however, we should make note of some well-known obstacles to making the diagnosis of total brain failure in infants and children. These obstacles have led to recommendations for longer observation times between clinical examinations, more extensive use of imaging tests, and modifications to the tests themselves.7

For both children and adults, some studies have shown that testing for the condition known as “brain death” is not always carried out in a consistent way from one institution to another.8 In light of the very serious consequences of this diagnosis, it is especially important to ensure that variations in practice do not lead to errors or abuse.

III. Total Brain Failure: Pathophysiology

The question addressed in Part II was, How can the clinician distinguish the patient with total brain failure from other brain-injured patients? In this part we turn to the question, What events in the brain and body of the patient lead to total brain failure? As we have indicated, a diagnosis of total brain failure involves a judgment that the brainstem and the structures above it have been destroyed and therefore have lost the capacity to function ever again. In most cases, however, this destruction did not accompany the initial injury to the brain but instead came about through a self-perpetuating cascade of events—events that progressively damaged more and more tissue and finally destroyed the brainstem.

The source of this self-perpetuating cascade of damaging events is the rigidity of the skull, which, after injury, can cause elevated pressure in the cranial vault that holds and usually protects the brain. Consider the three most common injuries leading to total brain failure. These are (1) head trauma (sustained, for example, in an automobile accident or as a result of a gunshot wound), (2) cerebrovascular accident (i.e., “stroke”), and (3) cerebral anoxia (deprivation of oxygen) secondary to cardiac arrest. These three different causes have a common effect: severe damage to the cells comprising the tissues of the brain, that is, to the neurons and the cellular networks that they form. This damage leads, in turn, to edema, the abnormal accumulation of fluid. With little or no space in which to expand, the swelling brain suffers steady increases in intracranial pressure (ICP ). Elevated ICP prevents oxygen-laden blood from making its way up and into the cranial cavity and thus deprives brain tissues of essential nutrients. This, in turn, leads to additional damage, which leads to more edema and swelling. Neurologist Alan Shewmon describes the result:

A vicious cycle is established in which decreasing cerebral perfusion and increasing cerebral edema reinforce one another until blood no longer enters the cranial cavity and the brain herniates though the tentorium and foramen magnum.9

The herniation that Shewmon refers to here can crush the brainstem, leading to the functional losses that are revealed by the examination for total brain failure. That condition is the end point of a vicious cycle—the point at which the brain, including its lower centers in the brainstem, has been rendered permanently dysfunctional.

This description of the physiological events that lead to total brain failure shows the utility of yet another term for the clinical state under discussion: “total brain infarction.”^x An “infarction” is defined as a “sudden insufficiency of arterial or venous blood supply…that produces a macroscopic area of necrosis.”10 When death is declared based on the currently accepted neurological standard, the self-perpetuating cascade of events in the brain following the initial injury has run its full course. “Running its full course,” in this context, means that total destruction of the brain has occurred due to infarction or lack of blood supply—hence, “total brain infarction.”

Bedside tests that establish loss of all brainstem reflexes can show that the destructive storm has indeed run its course, because the brainstem is often the last structure to be compromised in this process. Confirmatory tests and, in particular, various sorts of angiography (measurements of cranial blood flow) can be very useful in confirming that the gross infarction that is required for a diagnosis of total brain failure has actually occurred.11

At this point, it is important to take note of some qualifications regarding the word “total” in the context of total brain failure. One medically based objection to the neurological standard for determining death is based on a particular understanding of this word. Critics point out that the destructive storm that leads to “total” brain failure can leave certain areas of the brain intact. Again, from the description provided by Shewmon:

It should be mentioned that the self-destruction of the brain is not complete. Islands of sick but not totally necrosed brain tissue sometimes remain, presumably due to inhomogeneities of intracranial pressure and/or blood supply from extracranial collateral vessels.12

When the preserved areas of the brain do not support any recognizable function, this lack of total anatomical annihilation is less troubling. As the President's Commission noted in its report, the neurological standard for death requires an irreversible loss of all brain functions, not complete anatomical destruction of the tissue.13 Isolated metabolic or electrical activity in dispersed cells cannot be a sign that a patient is still alive; after all, such activity, supporting no function of the whole organism, can continue even in some cells of a corpse after the heart has stopped beating.

As critics have pointed out, however, the physiological facts are not so simple.14 In some cases, the preserved tissue in a body with total brain failure actually does support certain isolated functions of the brain. Most notably, some patients with total brain failure do not exhibit the condition known as “diabetes insipidus.” This condition develops when a hormone known as ADH (anti-diuretic hormone) is not released by a part of the brain known as “the posterior pituitary.” The absence of diabetes insipidus suggests that the “dead” brain is continuing to secrete the hormone; thus, at least with regard to this one function, the brain remains functional. It is therefore a fair criticism of the neurological standard, as enshrined in the UDDA, that “all functions of the entire brain, including the brainstem” are not, in fact, always irreversibly lost when the diagnosis is made. ^xi

It may be helpful to emphasize that the word “total” in the phrase,“total brain failure,” refers to the fact that the brain injury has reached the endpoint of a process of self-perpetuating destruction of neural tissue. In any event, whether or not the word “total” is justified, the patient diagnosed with total brain failure is in a condition of profound incapacity, diagnostically distinct from all other cases of severe injury. Whether this state of profound incapacity warrants a determination of death remains a matter of debate, with advocates of the neurological standard arguing that it does, while critics maintain that it does not. The release of ADH and other signs of isolated brain function do not settle the fundamental issue: Is the organism as a whole still present?

IV. Total Brain Failure: “Health” and “Prognosis”

Contemporary controversies about total brain failure as a suitable standard for human death focus attention on certain medical findings and on conclusions drawn from these findings by critics of today's practice. In this part, we will examine two important types of such findings which are often cited as highly relevant to the debate.

The first type of medical finding concerns the “somatic health” of the body of a patient diagnosed with total brain failure (or “whole brain death”). The appropriateness of the word “health” in this context is, itself, a point of contention. If the body is a cadaver then, of course, it is no longer fitting to speak about its “health.” Nonetheless, something like health is still present in the body of a patient with this diagnosis. This can be seen clearly in the “donor management” procedures that are a regular part of organ retrieval from heart-beating (“brain dead”) cadavers. These procedures aim to maintain the body in a relatively stable state of homeostasis so that the patient's heart does not stop beating prior to surgery and the organs procured remain as healthy as possible.15 Thus, there is some degree of somatically integrated activity that persists in the bodies of patients who have been declared dead according to the neurological standard. The bodies of these patients do not “come apart” immediately upon succumbing to total brain failure.

This point deserves emphasis because of the history of the debate about the neurological standard for death in the United States. In that debate, certain exaggerated claims have been made about the “loss of somatic integration” that occurs in a body with a destroyed brain. A good example of this can be found in a very influential paper published in 1981 by James Bernat, Charles Culver, and Bernard Gert. In that paper, they assert the following:

This criterion [whole brain death] is perfectly correlated with the permanent cessation of functioning of the organism as a whole because the brain is necessary for the functioning of the organism as a whole. It integrates, generates, interrelates, and controls complex bodily activities. A patient on a ventilator with a totally destroyed brain is merely a group of artificially maintained subsystems since the organism as a whole has ceased to function. 16

The claim that the body of a patient diagnosed with “whole brain death” is a mere “group of artificially maintained subsystems” was repeated often enough to become established in the United States as the standard rationale for equating total brain failure with human death: patients with this condition are dead because the systems of the body do not work together in an integrated way.

But this standard rationale was soundly criticized in another influential paper, published by UCLA neurologist Alan Shewmon in 2001. In “The Brain and Somatic Integration: Insights Into the Standard Rationale for Equating ‘Brain Death' With Death,” Shewmon argues forcefully that patients who are positively and reliably diagnosed with “brain death” (total brain failure) continue to exhibit many functions that one can hardly avoid calling “somatically integrative.” Examples include the maintenance of some degree of hemodynamic stability and body temperature, the elimination of wastes, the immune response to infection, the exhibiting of a stress response to the incision made for organ retrieval, and others. 17

The reason that these somatically integrative activities continue, Shewmon rightly notes, is that the brain is not the integrator of the body's many and varied functions. In normal circumstances, the brainstem does play an important and complex role in supporting bodily integration. But no single structure in the body plays the role of an indispensable integrator. Integration, rather, is an emergent property of the whole organism—a property that does not depend upon directions from any one part, but is the product of the orchestration of multiple parts.

Based on his critique of the “somatic integration rationale,” Shewmon draws the conclusion that there is no defensible biological account to justify the equation of total brain failure with human death. As he puts it, “If [brain death] is to be equated with death, therefore, it must be on the basis of an essentially non-somatic, non-biological concept of death.”18 In Chapter Four, we will re-examine the medical facts noted here to determine whether Shewmon's conclusion, repeated often by others, is warranted.

B. Prognosis

Just as it is paradoxical to talk about the “health” of the body of a patient who has been declared dead based on the neurological standard, it is also paradoxical to talk about the “prognosis” of that individual. Only a living creature can have a “prognosis,” strictly speaking. Because our concern here is with the question of whether the patient with total brain failure is dead or alive, we should avoid language that implies that the matter is settled.

Hence, “prognosis,” here, should be taken to have a very particular meaning—it refers to the likely timing of events that will result in the total collapse of the body's systems despite aggressive treatment to prevent that collapse. The President's Commission addressed “prognosis” in this sense when it claimed:

In adults who have experienced irreversible cessation of the functions of the entire brain, this mechanically generated functioning can continue only a limited time because the heart usually stops beating within two to ten days. (An infant or small child who has lost all brain functions will typically suffer cardiac arrest within several weeks, although respiration and heartbeat can sometimes be maintained even longer).19

Most neurologists agree with this assessment of how long the body of a patient with total brain failure can persist even with aggressive treatment. Many have even based their confidence in the suitability of the neurological standard on the “fact” that bodies found to have no brainstem function will quickly become asystolic (i.e., have no heartbeat) no matter what help is given to them. The loss of all functions of the brain is typically referred to as a “point of no return,” meaning no amount of medical effort can prevent the body from losing its integrity as an entropy-resistant system.20

As skeptics of today's neurological standard point out, there are two problems with this assessment. First, improvements in intensive care techniques over the years—prompted in part by the need for better “donor management” to procure usable organs—have made predictions of maximum survival time for bodies with total brain failure uncertain. Second, in practice, there turn out to be very few situations in which the truth of this matter can be tested. A diagnosis of total brain failure, when leading to a pronouncement of death, is a self-fulfilling prophesy: The patient with that diagnosis will become an organ donor (and the heart will stop in the process), or the ventilator will be withdrawn because it is understood to be “ventilating a corpse.” As the late neurologist Ronald Cranford put it:

It is impossible to know with certainty the extent of prolonged survival in brain death because a systematic clinical study in which the cardiac and circulatory functions are sustained for prolonged periods (weeks, months, or years) in a large number of patients is morally indefensible, extraordinarily expensive in terms of money and resources or manpower and intensive care unit beds, and legally prohibitive.21

For this reason, there is no effective way to determine how many patients could be stabilized in the condition of total brain failure and for how long. Uncontrolled observations must suffice. Such observations have been made in cases of patients who were pregnant at the time of their diagnosis with total brain failure. In some of these cases, efforts have been made to keep the body going until the fetus reaches viability. Eleven such cases are reported in a 2003 survey by Powner and Bernstein. According to these authors, no descriptions of unsuccessful attempts at fetal support after maternal brain death were found. The length of time that support continued after “brain death” ranged from thirty-six hours to 107 days.22 These cases justify caution and skepticism toward sweeping claims about the total instability of the “brain dead” body and the imminent collapse of the body's systems.

V. Total Brain Failure and the Vegetative State

We conclude this chapter with an attempt to bring some clarity to a common misunderstanding of the difference between “whole brain death” and the condition known as the “vegetative state.” Such confusion is exacerbated by the common and imprecise use of the term “brain dead” to describe patients who have clearly not been diagnosed with total brain failure and who do not exhibit the same level of incapacitation. Individuals such as Karen Ann Quinlan, Nancy Cruzan, and Terri Schiavo have been the subject of legal disputes and media attention because of family requests to withdraw various forms of life-sustaining treatment. With some frequency, these women have been inaccurately referred to as being “brain dead,” when in fact they were all in a persistent vegetative state (PVS).

The initial clinical state of a patient who is eventually diagnosed with PVS may be similar to that of a patient diagnosed with total brain failure. But the previously described tests for total brain failure will provide the evidence to discriminate between the two groups: only the patient with total brain failure will show evidence of a completely destroyed brainstem. In the patient with a lesser brain injury, the brainstem, and possibly parts of the brain above the brainstem, will be found to be functionally preserved.

Although he or she might initially be in the same eyes-closed, unresponsive coma as the patient with total brain failure, the less injured patient will eventually emerge from this coma and display the typical signs of the vegetative state. These include opening the eyes, going through sleep/wake cycles, moving the limbs, breathing spontaneously, and, in some cases, displaying a minimal responsiveness to pain stimuli. Because spontaneous breathing, under the regulation of the medulla oblongata in the brainstem, resumes, the PVS patient will not need the continual support of the ventilator. In most cases, however, he or she will need to receive nourishment through a feeding tube. If such sustaining treatment and diligent nursing care are provided, a patient can survive for many years in a vegetative state.

Because it will be important to the discussion in Chapter Four, the question of “consciousness” in the PVS patient should be briefly addressed here. The degree of consciousness present in a patient in a vegetative state is a matter of some dispute. It is often said that PVS patients retain the capacity for wakefulness but have lost the capacity to be aware. This latter assertion, however, is increasingly controversial in light of recent findings indicating that at least some patients in a vegetative state retain a residual capacity for willful and consciously aware interaction with their surrounding environment. 23 The cautionary advice of Steven Laureys, an expert on PVS and other brain-injured states, should be kept in mind:

There is an irreducible philosophical limitation in knowing for certain whether any other being possesses a conscious life. Consciousness is a multifaceted subjective first-person experience and clinical evaluation is limited to evaluating patients' responsiveness to the environment. As previously discussed, patients in a vegetative state, unlike patients with brain death, can move extensively, and clinical studies have shown how difficult it is to differentiate ‘automatic' from ‘willed' movements. This results in an underestimation of behavioural signs of consciousness and, therefore, a misdiagnosis, which is estimated to occur in about one third of patients in a chronic vegetative state… Clinical testing for absence of consciousness is much more problematic than testing for absence of wakefulness, brainstem reflexes and apnoea in whole brain or brainstem death. 24

Deciding whether ambiguous signs of wakeful life indicate consciousness is beyond the power of medicine, at least at this time, and possibly in principle. Thus, in cases where wakefulness is evident (as it is for PVS patients), there is good reason to be very cautious about assuming that conscious life is extinguished.

VI. Total Brain Failure: From Clinical Presentation and Pathophysiology to the Philosophical Debate

In this chapter, we have sought to explicate and clarify the condition usually called “brain death” or “whole brain death,” emphasizing developments in medical understanding since the President's Commission published its seminal work in 1981. In certain respects, the medical facts have introduced complications for those who would defend the equation of this condition with the death of the human being: Patients diagnosed with total brain failure may retain certain limited brain functions (such as the secretion of ADH to regulate urine output), and they certainly retain enough somatic integrity to challenge claims that the body immediately becomes “a disorganized collection of organs” once the brainstem is disabled. In addition, advances in intensive care techniques, displayed in cases of prolonged somatic “survival” after “whole brain death,” challenge claims that the body cannot continue in its artificially supported state beyond a short window of time.

Alongside these challenging findings, however, are facts that confirm the diagnostic and pathophysiological distinctiveness of total brain failure. Patients with this degree of injury are, indeed, singled out by the battery of tests (bedside and laboratory) first outlined and recommended by the Harvard committee in 1968. Moreover, no patient diagnosed with “total brain failure” has ever recovered the capacity to breathe spontaneously or shown any sign of consciousness—including the minimal and ambiguous signs routinely displayed by patients who emerge into the vegetative state.

Having drawn this detailed picture of the medical facts, we can now address the fundamental philosophical question of this report, Are patients diagnosed with total brain failure (or “whole brain death”), by virtue of this fact, truly dead?

_______________________

EndNOTES

1. American Academy of Neurology, Quality Standards Subcommittee, “Practice Parameters for Determining Brain Death in Adults (Summary Statement),” Neurology 45, no. 5 (1995): 1014.

2. President's Commission for the Study of Ethical Problems in Medicine and Biomedical and Behavioral Research, Report of the Medical Consultants on the Diagnosis of Death, “Guidelines for the Determination of Death,” JAMA 246, no. 19 (1981): 2184-6.

3. E. F. Wijdicks, “Brain Death Worldwide: Accepted Fact but No Global Consensus in Diagnostic Criteria,” Neurology 58, no. 1 (2002): 20-5.

4. See F. Plum, “Clinical Standards and Technological Confirmatory Tests in Diagnosing Brain Death,” in The Definition of Death: Contemporary Controversies, ed. S. J. Youngner, R. M. Arnold, and R. Schapiro (Baltimore: The Johns Hopkins University Press, 1999) 34-65; and E. F Wijdicks, “The Diagnosis of Brain Death,” N Engl J Med 344, no. 16 (2001): 1215-21.

5. Wijdicks, “Brain Death Worldwide, ” 20-5.

6. J. L. Bernat, “On Irreversibility as a Prerequisite for Brain Death Determination,” Adv Exp Med Biol 550 (2004): 161-7; and J. L. Bernat, “The Whole-Brain Concept of Death Remains Optimum Public Policy,” J Law Med Ethics 34, no. 1 (2006): 40.

7. See Report of the Medical Consultants on the Diagnosis of Death, “Guidelines for the Determination of Death,” 2184-6; Task Force for the Determination of Brain Death in Children, “Guidelines for the Determination of Brain Death in Children,” Neurology 37, no. 6 (1987): 1077-8; R. Vardis and M. M. Pollack, “Increased Apnea Threshold in a Pediatric Patient with Suspected Brain Death, ” Crit Care Med 26, no. 11 (1998): 1917-9; R. J. Brilli and D. Bigos, “Apnea Threshold and Pediatric Brain Death,” Crit Care Med 28, no. 4 (2000): 1257; S. Ashwal, “Clinical Diagnosis and Confirmatory Testing of Brain Death in Children,” in Brain Death, ed. E. F. Wijdicks (Philadelphia: Lippincott Williams & Wilkins, 2001); and K. J. Banasiak and G. Lister, “Brain Death in Children,” Curr Opin Pediatr 15, no. 3 (2003): 288-93.

8. See R. E. Mejia and M. M. Pollack, “Variability in Brain Death Determination Practices in Children,” JAMA 274, no. 7 (1995) : 550-3; M. Y. Wang, P. Wallace, and J. P. Gruen, “Brain Death Documentation: Analysis and Issues,” Neurosurgery 51, no. 3 (2002) : 731-6; M. Y. Chang, L. A. McBride, and M. A. Ferguson, “Variability in Brain Death Declaration Practices in Pediatric Head Trauma Patients,” Pediatr Neurosurg 39, no. 1 (2003) : 7-9; and D. J. Powner, M. Hernandez, and T. E. Rives, “Variability Among Hospital Policies for Determining Brain Death in Adults,” Crit Care Med 32, no. 6 (2004): 1284-8.

9. D. A. Shewmon, “Recovery from ‘Brain Death': A Neurologist's Apologia,” Linacre Q 64, no. 1 (1997): 30-96.

10. T. L. Stedman, Stedman's Medical Dictionary, 26th ed. (Baltimore: Lippincott Williams & Wilkins, 1995): 868.

11. Bernat, “Irreversibility as a Prerequisite, ” 161-7.

12. Shewmon, “Neurologist's Apologia,” 40.

13. Defining Death, 75-76.

14. See, for instance, A. Halevy and B. Brody, “Brain Death: Reconciling Definitions, Criteria, and Tests, ” Ann Intern Med 119, no. 6 (1993): 519-25.

15. A discussion of the physiological consequences of total brain failure from the perspective of donor management is provided in R. Arbour, “Clinical Management of the Organ Donor,” AACN Clin Issues 16, no. 4 (2005): 551-80. Also see J. M. Darby et al., “Approach to Management of the Heartbeating ‘Brain Dead' Organ Donor,” JAMA 261, no. 15 (1989) : 2222-8; and D. Wikler and A. J. Weisbard, “Appropriate Confusion over ‘Brain Death',” JAMA 261, no. 15 (1989): 2246.

16. J. L. Bernat, C. M. Culver, and B. Gert, “On the Definition and Criterion of Death,” Ann Intern Med 94, no. 3 (1981): 391.

17. A. D. Shewmon, “The Brain and Somatic Integration: Insights into the Standard Biological Rationale for Equating ‘Brain Death' With Death,” J Med Philos 26, no. 5 (2001): 457-78. For a more complete list of integrated functions that persist after “brain death,” see Chapter Four, Table 2.

18. Ibid., 473.

19. Defining Death, 17.

20. J. Korein, “The Problem of Brain Death: Development and History,” Ann NY Acad Sci 315 (1978): 19-38.

21. R. Cranford, “Even the Dead Are Not Terminally Ill Anymore,” Neurology 51, no. 6 (1998): 1531.

22. D. J. Powner and I. M. Bernstein, “Extended Somatic Support for Pregnant Women after Brain Death,” Crit Care Med 31, no. 4 (2003): 1241-9. This survey includes sources for both pregnancy cases and non-pregnancy cases of prolonged survival after a diagnosis of “brain death.”

23. A. M. Owen et al., “Detecting Awareness in the Vegetative State,” Science 313, no. 5792 (2006) : 1402; and A. M. Owen et al., “Using Functional Magnetic Resonance Imaging to Detect Covert Awareness in the Vegetative State,” Arch Neurol 64, no. 8 (2007): 1098-1102.

24. S. Laureys, “Death, Unconsciousness and the Brain,” Nat Rev Neurosci 6, no. 11 (2005): 904-05. Citations omitted.

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Footnotes

i. On the functions of the brainstem, see Part II below.

ii. There is another sort of situation in which a ventilator is required to support vital functions: The respiratory center in the brain can be functional while the muscles of respiration themselves are paralyzed. This was the case for polio patients in the mid-20 th century who were the first wide-scale recipients of ventilatory treatment in the form of cumbersome iron lung machines (i.e., negative pressure ventilators). Here, one could say, the CNS signal to take action is being sent, but it is falling on “deaf ears.” Alternatively, one may say that the drive to breathe is present but the ability to turn that drive into action is absent. For many polio patients, the paralysis subsided when the virus was defeated and, as a result, normal breathing resumed.

iii. The external respiratory system is the part of the respiratory system that engages the organism with the outside world. By contrast, the internal respiratory system functions at the cellular level to assimilate oxygen from the bloodstream and deposit CO 2 back into the bloodstream.

iv. This description is incomplete insofar as it suggests that the heart is the only active part of the circulatory system. In fact, the vessels of circulation, far from being rigid “plumbing lines” that passively convey blood pumped by the heart, are living tissues that undergo changes (some driven by the CNS) to maintain an appropriate blood pressure. Patients who are receiving ventilatory support often must also be given drugs (e.g., pressors) to help keep the blood pressure in a healthy range.

v. See Chapter Two, Table 1.

vi. The discussion of testing for total brain failure in this section is meant only as a “layman's summary.” For a more complete description the reader should consult the clinical literature, in particular, American Academy of Neurology, Quality Standards Subcommittee, “Practice Parameters for Determining Brain Death in Adults (Summary Statement),” Neurology 45, no. 5 (1995): 1012-4; and E. F. Wijdicks, “The Diagnosis of Brain Death,” N Engl J Med 344, no. 16 (2001): 1215-21.

vii. For a clinical case study of a patient who showed all the signs of total brain failure after a snake bite but then recovered after rec eiving an antidote, see R. Agarwal, N. Singh, and D. Gupta, “Is the Patient Brain-Dead?” Emerg Med J 23, no. 1 (2006): e5.

viii. The exception to the rule discussed in the text is a case where a primary lesion of the brainstem leads to the diagnostic signs that usually indicate total brain failure. In such a case, the condition of the brainstem is not itself a reliable indicator of the condition of the higher centers of the brain. Among those w h o accept the neurological standard for determining death, there is controversy about the vital status of the patient about whom all that is known is the condition of the brainstem. See S. Laureys, “Science and Society: Death, Unconsciousness and the Brain,” Nat Rev Neurosci 6, no. 11 (2005): 901-02 ; J. L. Bernat, “On Irreversibility as a Prerequisite for Brain Death Determination,” Adv Exp Med Biol 550 (2004): 166 ; and C. Pallis and D. H. Harley, ABC of Brainstem Death, Second ed. (London: BMJ Publishing Group, 1996): 11-12. For the purposes of this report, such patients are excluded from the group considered to have “total brain failure.”

ix. The patient is prepared for this test by receiving, in advance, an elevated level of circulating oxygen that will prevent any further damage to tissues while the test is being carried out. Some inconsistencies in the way the apnea test is carried out in different places—including whether it is required at all in some countries—have been documented. For more information, see E. F. Wijdicks, “Brain Death Worldwide: Accepted Fact but No Global Consensus in Diagnostic Criteria,” Neurology 58, no. 1 (2002) : 20-5; R. Vardis and M. M. Pollack, “Increased Apnea Threshold in a Pediatric Patient with Suspected Brain Death,” Crit Care Med 26, no. 11 (1998) : 1917-9; and R. J. Brilli and D. Bigos, “Apnea Threshold and Pediatric Brain Death,” Crit Care Med 28, no. 4 (2000): 1257.

x. See Chapter Two, Table 1.

xi. Researchers suspect that function in the posterior pituitary is preserved partly because its (extradural) arterial source is distinct from that which feeds other tissue of the brain. The damage that is due to the rise in intracranial pressure, which leads to total brain failure, can spare these extradural arteries so that a portion of pituitary is preserved. For discussion of this point, see E. F. Wijdicks and J. L. Atkinson, “Pathophysiologic Responses to Brain Death,” in Brain Death, ed. E. F. Wijdicks (Philadelphia: Lippincott Williams & Wilkins, 2001).

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