To evaluate whether current clinical criteria and confirmatory tests for the diagnosis of ‘brain death’ satisfy the requirements for the irreversible cessation of all functions of the entire brain including the brainstem.
Medical, philosophical and legal literature on the subject of ‘brain death’.
We present four arguments to support the view that patients who meet the current operational criteria of ‘brain death’ do not necessarily have the irreversible loss of all brain (or brainstem) functions. First, many clinically ‘brain-dead’ patients maintain residual vegetative functions that are mediated or coordinated by the brain or the brainstem. Second, it is impossible to test for any cerebral function by clinical bedside exam, because the tracts of passage to and from the cerebrum through the brainstem are destroyed or nonfunctional. Furthermore, since there are limitations of clinical assessment of internal awareness in patients who otherwise lack the motor function to show their awareness, the diagnosis of ‘brain death’ is based on an unproved hypothesis. Third, many patients maintain several stereotyped movements (the so-called complex spinal cord responses and automatisms) which may originate in the brainstem. Fourth, not one of the current confirmatory tests has the necessary positive predictive value for the reliable pronouncement of human death.
According to the above arguments, the assumption that all functions of the entire brain (or those of the brainstem) in ‘brain-dead’ patients have ceased, is invalidated. Reconsideration of the current concept of ‘brain death’ is perhaps inevitable.
The concept of ‘brain death’ was introduced in the medical literature as a new criterion of death in 1968 by the ad hoc Committee of the Harvard Medical School.1 The Committee defined death in neurophysiological and philosophical terms, as irreversible loss of all brain functions (including those of brain stem) and proposed criteria to reflect that definition.2 The philosophical aspect of the determination of human death has also been stressed by many investigators in past and recent years.
The neuropathologic entity of total brain infarction was first described in 1902 by Cushing, but its clinical findings were first described in 1959 (Fishgold and Mathis, 1959; Jouvet, 1959; Mollaret and Goulon, 1959; Wertheimer et al., 1959);3 however, it is worthwhile mentioning that these investigators did not equate this condition with death itself.3
Machado et al.4 recently argued that the neuropathologic entity of total brain infarction/destruction did not evolve to benefit transplantation of vital organs; nevertheless, the term ‘brain death’ did not enter the medical terminology until the mid-1960s, in response to the rapidly developing field of transplantation medicine.3
The ad hoc Committee of the Harvard Medical School report did not base its neurological criterion of death on any concept of death, but rather ‘was primarily concerned with futility of care and finding ways to help physicians with withdrawal of support’.2 Others have posited, however, that the concept of ‘brain death’ was developed to permit vital organs transplantation.3, 5 Although ‘brain death’ has been accepted by most clinicians, health care workers, legislators and society at large, opinions to the contrary have been expressed both in the distant past and recently. It has been argued that ‘brain death’, either referring to the entire brain or to the brain stem alone, is a concept without precise clinical or pathological basis and, for this reason, the criteria employed in its diagnosis are arbitrary.6
In 1971 the neurosurgeons Mohandas and Chou7 suggested that in patients with known but irreparable intracranial lesions irreversible damage to the brain stem was the ‘point of no return’ and the diagnosis could be based on clinical judgment. Their suggestions became known as the Minnesota criteria and influenced the practice in the United Kingdom considerably.
Practice in the United Kingdom has been based on two memoranda; the first asserted that permanent death of the brainstem constitutes brain death while the second identified brain death with death itself. Additionally, a new document proposed by Christopher Pallis8 was that death can be defined as the ‘irreversible loss of the capacity for consciousness combined with the irreversible loss of the capacity to breathe’.
The stated definition of ‘brain death’ (the complete cessation of all functions of the entire brain) is now acknowledged even by supporters of the concept of ‘brain death’ to be only an approximation.9
Scientific knowledge alone is insufficient in determining the necessary criteria for the diagnosis of human death, since the definition of death, at the conceptual level, is a matter of philosophical, religious, legal and policy choice.
The definition-criteria and criteria-tests inconsistencies in many patients who meet the current clinical criteria for the diagnosis of ‘brain death’ invalidate this diagnosis. Especially, the new insight presented in this article involves the interpretation of the so-called spinal reflexes and automatisms; it is argued that these movements may originate in the brainstem, thus invalidating the clinical diagnosis of ‘brain death’ in a significant number of ‘brain-dead’ patients.
A compelling argument against even the notion of ‘absence of cerebral functions’ is that in the context of brain stem infarction/destruction, which is always part of brain death, it is impossible to test for any cerebral function by clinical bedside exam, because the tracts of passage to and from the cerebrum through the brain stem are destroyed or nonfunctional.
Not one of the various ‘confirmatory’ tests has the necessary positive predictive value (100%), for the pronouncement of human death. Nevertheless, brain SPECT with Tc99m-HMPAO might be proved the most accurate and specific test in the diagnosis of ‘brain death’. Confirmatory tests, for the time being, cannot confirm the destruction of every part of the brain or the irreversible absence of every brain function, but only prevent misdiagnosis when clinically unsuspected functions or structural integrity are revealed.
Considering all the above, we wonder whether it is time to abandon the concept of ‘brain death’ and return to the traditional lung – heart criteria for the diagnosis of human death (irreversible cessation of cardiac and lung function).
Although we propose that neither ‘brain death’ nor ‘irreversible apneic coma’ are per se death, we would agree with the suggestion that the concept of ‘brain death’ could be substituted by the more accurate old term ‘irreversible apneic coma’. The expected benefits from the change of terminology and current criteria of ‘brain death’, would be the avoidance of misinformation and confusion of the public regarding the concept of human death as well as avoidance of using utilitarian criteria for its definition.
The main question addressed in this article was whether the concept of ‘brain death’ is still valid. According to the presented arguments, the concept of ‘brain death’ as a synonymous term with human death (diagnosed according to the criterion of irreversible cessation of lung and cardiac function) is invalid.
We consider that the interest of the organ transplantation program would be better served by ‘openness and honesty’. The harvesting of vital organs for transplantation from patients suffering from ‘irreversible apneic coma’ (an identical clinical condition to ‘brain death’)—who had already given their informed consent for this purpose at an unsuspected time—would be socially and morally acceptable in societies which consider that the autonomy of the person justifies such a donation.
However, others consider—on philosophical grounds—that they are not justified in taking their own life for any reason; nevertheless, they would agree with the donation of one of the paired vital organs or part of a single organ from healthy volunteers or of whatever organ from donors who are already irreversibly dead (according to the cardiopulmonary criterion of death) and have given their informed consent at an earlier time.
I deeply thank Professors Robert Truog (Harvard Medical School, E-mail address: Robert.Truog@childrens.harvard.edu) and D Alan Shewmon (UCLA School of Medicine, e-mail address: firstname.lastname@example.org) for their encouragement and their kind help in the preparation of this manuscript.
No funds were used to support this work. No conflict of interest with the work.