“Within the brain a central transactional core has been identified between the strictly sensory or motor systems of classical neurology … capable of grading the activity of most other parts of the brain.”
—H. W. MAGOUN, The Waking Brain, 1958
“There are several ways for a body to be a body, several ways for consciousness to be consciousness.”
—M. MERLEAU-PONTY, Phenomenology of Perception, 1962
How did some physicians come to describe the features of irreversible coma? Critics of the Committee asked what evidence supported the criteria and upon what basis the Committee arrived at the apparent assumption in the Report that meaningful consciousness was necessary for life. The evidence the Committee relied on included decades of clinical observations on coma and published reports on outcomes at Massachusetts General Hospital for patients with coma. Research on the neurology of consciousness also had an impact on the evolution of the criteria, but a complex one. This chapter and the one that follows look at these sources, focusing first on a background of research as to how the neurology of consciousness was understood.
There was a vibrant and largely forgotten research interest in the neurology of consciousness in the decades preceding the Report that cannot be fully described here. The approach, then, in this chapter is to outline the particular work on EEG and consciousness that several members of the Committee, primarily Schwab and Adams, specifically referenced and drew upon. It is almost as important to capture how much this work did not answer the questions Schwab and his colleagues faced, as to consider how much it did. Eventually this work—with all its ambiguities and limitations—helped answer two key questions: How accurately can the brain’s activity, and especially signs of the irreversible loss of activity, be “seen”? What are the consequences of these visible signs for drawing conclusions about the functioning of consciousness and of the body?
By the summer of 1967, Schwab estimated that he had consulted on approximately 150 cases in which a simple set of criteria that he had developed were used to end treatment. The connection between the demise of the brain and death had interested Schwab since the beginning of his MGH career. In 1941, in cooperation with the Boston Medical Examiner William Brickley, he performed a continuous EEG and EKG tracing on a patient in the MGH emergency ward who had a fatal spinal cord injury and “would surely die in a few hours.” There was no respirator used to treat a patient with such an injury at the time. The two men were brought together out of a mutual interest in the question of which electrical activity persisted longer, heart or brain, and the subsequent question of what role EEG could have in determining time of death. Schwab’s description of the event continued:
Five minutes before death the right side showed no electrical activity at all but there was a single burst of rather normal appearing alpha activity on the left side. Respiration ceased at 6:44 as is shown by movement artifact produced by the doctor placing the stethoscope on the chest. The amplitude of the electrocardiogram became very low. Although there was no pulse discernible the amplifier recorded the electrocardiogram when the amplitude was raised … There was no electroencephalographic recording from this point on. All electrical activity ceased … eight minutes after death but the heart resumed spontaneous activity one minute later. Twenty-six minutes after death moving the chest produced three abnormal electrocardiographic beats. There was nothing in the electroencephalogram … It is obvious from this example that the electrocardiogram is a better indicator [of the exact time of death].1
Thirteen years later, Schwab was confronted with another case:
[I was] called to the hospital on an emergency Saturday evening where a patient about to be operated on for a large intracranial clot had stopped breathing, was immediately put on a respirator, and maintained with normal heart, blood pressure. There was no visible sign of response to stimuli. Reflexes were totally absent, and the question arose as to what to do with the operating room about to close for the night and Sunday. The electroencephalogram was recorded … and there was nothing whatever to see in the tracing. The question was, “Is this patient alive or dead?” Without reflexes, without breathing, and with a total absence of evidence of an electroencephalogram, we considered that this patient was dead in spite of the presence of an active heart maintaining peripheral circulation. The respiration was therefore turned off and the patient pronounced dead.2
The latter description is presumably the first known description of the use of a brain death construct to determine death in the history of medicine. It is dramatic to compare these two deaths. They describe two fundamentally different conclusions drawn by Schwab as to criteria for determination of death—absent heart activity in the first; absent EEG tracing, reflexes, and breathing in the second. But in the 1941 impromptu experiment, death was defined only in part by the heart stopping. The degree to which the action of the heart as a pump drew the line between life and death was undermined by finding that electricity outlived the pulse. The electricity of the body, specifically of the heart, persisted beyond any value of the heart as a mechanically effective pump.
Through this electrical window, the body looked different. Schwab gives no indication in his account that he thought of using EEG to define death when he followed the tracing with Brickley. However, a quarter of a century later he listed this event at the start of a chronology of events leading to his criteria for brain death, which he prepared for an anticipated manuscript with Curran on “cerebral death” soon after the Report appeared.3 Schwab ranked this vigil with Brickley second in importance only to 1930s physiological research that demonstrated permanent loss of EEG in experimental animals after the interruption of circulation to the brain. Yet his publications before the late 1950s—including a review, which also appeared in 1941, of the varying uses of EEG—made no mention of the possible role of EEG in determining death or even prognosticating cerebral function after anoxic injury.4 Schwab’s description of the Brickley episode was not presented to a larger clinical audience until a decade later in his textbook on EEG. It was described there in order to simply demonstrate the relative persistence of different electrical currents in the body, not as an observation in support of reconsidering the physiological markers used for determining death.5 As Schwab later wrote, “Dr. Brickley was seeking information as to how long the brain survived after the heart ceased to beat.”6 In fact, his account first appeared in a forum unlikely to reach the attention of any physician: the pages of Electrical Engineering, in 1941. Here, observations of this dying patient appeared as a footnote to a published excerpt of the EEG tracing itself, presented again to illustrate the variable persistence of electrical currents in different tissues. Basic physiologic properties of tissues, not new methods of prognostication and definition, were the focus.
But we can glimpse with Schwab the newly layered confusions of past and present tenses in the definition of life that this new way of seeing the body, this new structuring of knowledge, brought:
Brain waves disappear ten minutes before death. Legal death [occurred]. … when intern placed stethoscope on chest to prove inaudible heartbeat … Electrocardiogram continues one minute after death, stops and then begins again.7
Forward to 1954, when everything seems to have changed compared with the 1941 case, despite persistent heartbeat, death was found because of loss of brain electricity and physical signs of brain functioning. In 1954, that persistence lost the significance it previously had. There are three ideas, though, that unite these two accounts even in their differences. First is an “electricocentric” account of biology: that electrical cellular activity either could replace or more precisely reveal functional attributes of an organ and/or the organism—attributes critical to the reliable determination of it as living. Second is the suspicion that loss of brain electrical activity was the final event of human life. Third, and more implicit, is the emerging understanding that death was a slippery construct without clear lines or technical or clinical signs. Death did not close a door on an array of other continuing biological events that were a part of dying.
Other key changes between 1941 and 1954 included the use of respirators as well as the growth of EEG-based research in describing consciousness and brain function. This chapter describes a largely forgotten burst of EEG studies in the mid-twentieth century, focusing specifically on how they framed Schwab’s purposes on the wards of MGH where respirator-dependent patients elevated the visibility and relevance of electricocentric life.
This research changed how physicians talked about patients, such as a man, age nineteen, who suffered the end-stage results of a growing brain tumor. Hospitalized in Britain, the patient was cared for by British neurologist Kinnier Wilson, early in his career. Wilson later wrote:
June 23, 1905, at 11.10 pm, I was called to see the patient. He was lying on his back, with head turned slightly to the right, and was quite unconscious … When the lids were lifted the eyes were seen to be fixed and staring straight front … 11.45 p.m. About this time both arms became rigid, the left elbow rather more than the right … This striking position of the arms was henceforth maintained; at intervals the whole arm would stiffen still further, as it were, and the attitude become more accentuated, as if by waves of contraction passing down the musculature … 12.20 a.m. Another fit started. Patient suddenly became absolutely stiff in the decerebrate position, and his face reddened, while respiration became occasionally labored, down to four per minute … The eyes were open, staring straight in front; pupils were dilated to their widest and did not react to light … The phenomena exhibited by the patient during these hours resemble in minute particulars those of mesencephalic transection in experimental animals. Until hemorrhage and increasing pressure killed him he was little more than a decerebrate preparation.8
The author considered this man’s condition and those of similar patients to be analogous to a “decerebrate preparation” used in experiments with animals. These kinds of experiments were developed by Charles Sherrington, who was awarded the 1932 Nobel Prize in Medicine for his work on the basic architecture of nerve cells as fundamental units of brain function.9 In the experiments, the area between the cerebral hemispheres and upper spinal cord was severed. Higher cuts, up closer towards the brain hemispheres and cortex, such as in the midbrain, produced the typical rigid, deformed, or “decerebrate” responses that Wilson described. Lower cuts, moving in the opposite direction toward the spinal cord and into the brainstem, caused flaccid unresponsiveness instead.
Tumors or bleeding in this same region, or pressure exerted on this region by similar lesions in other parts of the brain that expanded in the closed space of the skull, created unfortunate human equivalents of these laboratory models, with varying abnormalities in breathing and in reflexes of the cranial nerves (i.e., reflexes of central nervous system nerves within the skull such as pupil, cornea, and other eye movements and reflexes). The anatomy of the nuclei, or centers, of cranial nerves was well understood in this part of the nervous system, and it had been known since the turn of the nineteenth century that destruction of a certain part of the lower brainstem ended respiration. Tracking cranial nerve and limb movements became the basis of a neurological examination that used external signs to locate injury in the cortex and lower brain regions such as the brainstem. What changed over time was the explanation of what these signs meant, and especially what they meant for the machinery of consciousness and the overall prognosis for survival.
The association between irreversible brain injury and loss of circulation or adequate oxygenation was also quite old. Humane societies in the eighteenth century were well aware of the need to rapidly resume halted breathing lest it reach a point beyond which resuscitation was impossible.10 Study of the effects of anoxia on nerve cells and nervous system function is almost two hundred years old. Twentieth-century research often cited Astley Cooper’s 1836 publication on arterial occlusion in rabbits.11 At the turn of the twentieth century, a fairly hefty scientific literature existed exploring the histological changes that occurred in nerve cells when deprived of oxygen. These studies were meant to answer the still vexing question of what aspects of anoxic injury to cells indicated “which of them might recover under proper conditions, and which of them were injured beyond the possibility of recovery.”12
In 1934, with EEG technology (and agreement that it in fact reflected activity in the brain) less than a decade old, Simpson and Derbyshire reported in the American Journal of Physiology that disappearance of detectable electrical activity occurred within approximately twenty seconds of experimentally produced anoxia in the cat motor cortex.13 Experiments by Sugar and Gerard, frequently cited by Schwab, demonstrated how areas of the brain lost discernible EEG when deprived of oxygen at different rates.14 So, while neatly linked together, the leap from positing a physiological relationship between cell death and loss of EEG to (eventually) a complete map of irreversible loss of specific brain functions, was a work in progress.
During the mid-1930s, experiments by Belgian researcher Frederic Bremer found that cats with severed, or transected, midbrains had EEG patterns similar to those seen during sleep. This level of brain isolation, called cerveau isole, was contrasted with transection lower down in the brainstem, which resulted in isolation of the whole brain, or encephale isole. The encephale cats showed wakefulness and nonsleep EEG patterns. These cat brains were still able to receive afferent—or incoming—sensory signals from the rest of the nervous system. The higher transection, cerveau isole, cut off more of these afferent connections. The prevailing deafferentation hypothesis—that alertness and consciousness were fueled by activation from afferent sensory information received from the body—thus seemed confirmed by these experiments.
These findings were soon linked to an earlier focus of EEG research—the so-called Berger Rhythm. EEG research initially studied single nerve potentials, the speed of nerve signal transmission, and paths of transmission in different parts of the nervous system. This kind of study portrayed an electrical brain characterized by momentary, local, and rapidly changing electrical bursts from one point to another. Berger, however, in the late 1920s and early 1930s, described a stable, persistent, generalized, and “slow” electrical rhythm that usually appeared on EEG at rest with closed eyes. When eyes opened or attention focused, the rhythm disappeared. The presence of a stable electrical rhythm in the human brain was not immediately accepted. However, Edgar Adrian and Bryan H. C. Matthews—established researchers in nervous system electrical potentials—confirmed and thus legitimated Berger’s findings in 1934. Adrian had just shared the Nobel Prize with Sherrington. He and Matthews offered evidence that the rhythm reflected the electrical characteristics of the brain, particularly the occipital area, when at rest.15 Some controversy persisted as to how much of the brain could produce this rhythm,16 but what emerged was an enormously influential model of electrical brain activity, which showed that there were stable, predictable patterns of electrical waveforms associated with different overall states of the brain such as attention, concentration, sleep, or rest. In general, research about consciousness and emotion shifted from studying people and their reported reactions and emotions to something known and observed through brain activity. EEG was an important part of that shift.17
Berger’s effort to measure brain electricity was part of a search for tangible signs of what he referred to as psychic energy, or “P. E.” P. E. was the physical, measurable aspect of thought and experience, the product of a series of energy transformations ultimately originating in God.18 These spiritual and holistic commitments were at odds with an emphasis by many contemporaries on unique, specialized functions of localized parts of the brain, as well as with later cybernetic, machine-mechanism metaphors for explaining consciousness, which proliferated in the 1950s and were strengthened through EEG-based research. These meanderings through localized, holistic, mechanical, and ephemeral metaphors for consciousness would continue over the following decades and produce a rich range of theories and experimental programs.19 It is worth revisiting that range in order to later contrast the degree to which similar metaphorical and conceptual descriptions were used in the critical bioethics literature in the decades following the Report, to argue over what type of loss of consciousness was—or should be—at stake in defining brain death and personhood. Used for that purpose, however, these descriptions of how the brain worked were generally stretched beyond their concrete referents of events in the brain such that they became consequentially detached from a process of medical knowledge-making.
Berger’s rhythm consisted of “synchronized,” regular, low-voltage waveforms that occurred during states such as sleep and relaxation and that could be disrupted and replaced by high-voltage, erratic, or “desynchronized” patterns with accompanying arousal, alertness, and focused attention. Producing desynchronization—that is, provoking and observing this shift away from an intrinsic, synchronized, electrical pattern—became a common experimental procedure. Desynchronization could be shown in cats with an encephale isole condition—transection at the first cervical vertebrae that spared cranial nerve connections and thus maintained significant sensory input to the brain. But in cerveau isole cats, in which these connections were severed, neither arousal (as evidenced in behavior or EEG pattern) nor desynchronization of the sleep EEG could be produced. Disruption from somnolence to alert behavior, and the accompanying desynchronization of EEG, occurred in encephale cats and not cerveau cats. This was interpreted by Bremer to show that arousal relied upon afferent stimulation through the usual pathways of sensory information from the body that converged in the brain. The loss of sensory afferents, or deafferentation, turned the brain “off.”
Others began to doubt that picture, considering instead that these transections were cutting into a lower brain center that wasn’t just a passage way for afferent traffic but a control center that manipulated these alternating electrical patterns of arousal and somnolence, synchronization and desynchronization—essentially acting as an electrical pacemaker of the functioning brain. According to this understanding, the lower brain areas were not merely passive cables that conveyed afferent stimulation that would, if severed, shut down the cortex. These lower areas instead actively managed this activity.
Research on the mechanism of sleep similarly suggested the possibility of active centers of consciousness. The American neuroanatomist Stephen Ranson, who directed the Institute of Neurology at Northwestern University for over forty years, attributed somnolence caused by certain hypothalamic lesions in monkeys to be due to the lesions’ impairment of the excitatory signals of that region. Withdrawal of those signals presumably caused sleep. Arousal, then, perhaps resulted from an intrinsic sophisticated electrical generator in midbrain or lower brain structures rather than from passive conveyance of sensations from the body. These structures actively caused waking, not sleeping. But this meant the lower centers did more than merely throw the switch for deafferentation. They selectively initiated and maintained arousal and consciousness directly. Electrophysiological study of these centers also expanded the ability to appreciate, distinguish, and argue about, the differences between these often non-distinguished terms (“arousal,” “alertness,” “consciousness,”).
In a seminal 1949 paper, Guiseppi Moruzzi and Horace W. Magoun provided evidence that bolstered this view of the active role of these centers, and accelerated new ways of thinking about consciousness.20 Stimulation of the “reticular activating system,” or RAS (a particular area of interconnecting fibers coursing through the brainstem) caused desynchronization even when other sensory nerves to the brain were cut.21 Transections of RAS blocked desynchronization. A complementary study was led by Donald Lindsley, a colleague at Northwestern University. Lindsley made important contributions to diverse fields such as learning, sleep, the behavior of animals in the wild, and challenges of long-term space flight. He joined Magoun in the latter 1950s to help create the Brain Research Institute at UCLA. When Lindsley and his research team destroyed RAS in “mesencephalic or diencephalic lesions … EEG activation was reduced or abolished and recurrent spindle bursts, like those of normal sleep or barbiturate anesthesia, dominated the cortical record.”22 From this he concluded:
The evidence given above points to the presence in the brain stem of a system of ascending reticular relays, whose direct stimulation activates or desynchronizes the EEG, replacing high-voltage slow waves with low-voltage fast activity. This effect is exerted generally upon the cortex and is mediated, in part, at least, by the diffuse thalamic projection system.23
EEG provided the opportunity to distinguish not only anatomical but functional relationships between areas of the brain. This line of experimentation involved a who’s who of twentieth-century neurophysiology, such as Nobel Laureate Walter Rudolph Hess, Ranson (who also taught Magoun in his doctoral thesis work), Robert Morison, Edward Dempsey, and Herbert Jasper. Jasper collaborated with the celebrated neurosurgeon Wilder Penfield, who did influential work in redescribing the nature of consciousness through brain stimulation of patients awake during surgery for epilepsy.24
The interaction between cortical and subcortical systems was a central focus of their work. Dancing and responding waveforms offered a new vision of the living brain. These waveforms not only made brain activity ostensibly visible; in this guise, they revealed brain function as orchestrated arousals emanating from small areas deep below the cortex. Speaking at a conference in Magoun’s presence, Jasper presented a paper that concluded:
The evidence to be brought forward by Magoun and his colleagues is in support of the relationship to spontaneous cerebral activity to the reticular portion of the brainstem independent of the main specific afferent pathways. The more diffusely interconnected, but topographically organized thalamic reticular system … provides a central coordinating mechanism for cerebral activities.25
The EEG vastly enlarged the available vocabulary with which to coherently claim that core functions of the brain and the phenomena of consciousness could be found below the cerebral hemispheres. This interest in the brainstem as the source of consciousness preceded the EEG. Within twentieth-century neurology literature, it was often traced to the kind of turn-of-the-century physiology captured in Martin Reichardt’s 1908 argument that the brainstem contained an almost mystical vegetative engine, the “Antrieb,” which provided the impetus, momentum, or source for life. The cortex permitted awareness of this impetus, and its capacity for reason balanced the Antrieb’s momentum to create a harmonious organism.26 Experience with patients further reinforced attention below the cortex in disturbances of consciousness in decorticate patients like Wilson’s and the 1920s experience with epidemics of encephalitis lethargica, a disease characterized by a prolonged “sleep.” Constantin von Economo, who characterized this frightening illness, associated its sleep or coma with damage just above the midbrain. This seemed consistent with previously known associations between other “vegetative” functions, such as body temperature and respiration, and similar areas of the brain.
In the 1930s, EEG tracings of slow, synchronized waveforms were obtained in patients with hypothalamic tumors, a human cerveau isole.27 Lindsley made the connection between the desynchronization role of RAS and “the clinical observation of somnolence following basal injury to the brain.”28 The interpretation of loss of consciousness as the result of a damaged lower brain center that maintained it increasingly challenged the prevailing understanding of a cortical/subcortical division of labor. The latter view, more common at the time, was well summarized in a popularized account of neuroscience in the 1920s and 1930s by University of Chicago scientist C. Judson Herrick:
The thalamus supplies the emotional coloring … the simple impulsive drives; the cortex supplies the intelligence guidance and rational control. The cerebral cortex at the top of the nervous axis is the center of highest dominance, and it exerts more or less control over all the lower centers and through these over everything the body does.29
Herrick’s popularized physiology was, however, itself a critical response to the so-called James-Lange theory of emotion, attributed to William James and C. G. Lange. They independently argued that emotion was, as James put it, “the feeling of the bodily changes as they occur.”30 Herrick reestablished the cortex as more the driver than the recipient of emotions, but also acknowledged the need to break down the division of labor between local brain regions, attributing machine-like mechanisms to the brain. Machines, Herrick argued, were not dry or dehumanized entities. Instead, like the body and brain, machines moved energy for specific purposes. Unlike Berger, Herrick was opposed to spiritualist and holistic agendas, but still found it hard to talk about the brain without a teleological bent. EEG was also used by Hess to argue for a larger vision—in this case, that the harmonization of vegetative and animal energies it portrayed could be a roadmap for peaceful societies.31 Appeals to holism in science have served many purposes over time,32 and EEG provided an empirical basis for both mechanistic and holistic visions to reject a mind–body dualism.
EEG-based research on arousal and consciousness, then, fueled vying agendas and paradigms for the life sciences—a profusion of metaphors and models that were often contradictory. Commitments to holism, localization, mechanism, dualism, or higher agency were all projected onto bits of evidence about how consciousness worked.
In many ways this terrain did not much differ from the back and forth over the proper way to conceptualize life, identity, mind, and consciousness, in the ethical debates that later swirled around brain death, and that will be revisited in Chapter Six. In sharp distinction from much of that later debate, this earlier round of conceptual and metaphysical categories was instructively different in terms of the degree to which such discourse related to medical and neuroscientific domains. These conceptual schema were sorted and arbitrated as they linked with and matched up against experiment and, especially in Schwab’s case, clinical experience. What was useful for care emerged from that process. The EEG was a crucial translator for that linkage and iterative learning.
The possibilities presented by this new description of a dynamic brain were evident in a 1953 UNESCO symposium that brought together the key investigators—Adrian, Bremer, Hess, Jasper, Magoun, Moruzzi, Morison, and Penfield among them. That group also included Mary Brazier of MGH, a member of both Beecher’s Department of Anesthesiology and a collaborator with Schwab’s research team. Magoun recalled the event as an anxious coming of age of his work—an opportunity for legitimacy as well as new criticism.33
Old vocabularies took on new meanings to describe consciousness. “Integration” in particular became a common—though complex—metaphor. In the nineteenth century, British neurologist Hughlings Jackson found integration in layered functions of the “lower” nervous system, but still posited the frontal lobes of the cortex as the high seat of consciousness. However, integration in the hands of many RAS researchers upended this schema. When Wilder Penfield selectively applied small electrical shocks to the exposed brains of his conscious patients in the 1930s, he was struck by how observed muscle movements or experiences reported by the patient could occur, but be understood by the subject as either not real or not of their own purposeful making. The persistence of an experienced “I” that was sustained through this electrical hijacking of the cortex led Penfield to conclude:
[I]t seems reasonable to assume that there is a discrete area of the brain the integrity of which is essential to the existence of conscious activity … a level of integration much higher than that to be found in the cerebral cortex, evidence of a regional localization of the neuronal mechanism involved in this integration … [lying] not in the new brain but the old.34
Penfield tweaked familiar words and a more familiar, Jacksonian heritage of progressive, ordered, sensorimotor “integrations” but turned these terms literally on their heads.
This view of consciousness faced many challenges, not only within neurology but elsewhere in the biological and social sciences. Listen, for example, to the five-year conversation between various leading figures in American science, sociology, anthropology, and psychiatry sponsored by the Macy Foundation.35 Annually from 1950 to 1954, the foundation gathered notable behavioral scientists such as NIMH Director Seymour S. Kety, Talcott Parsons, Margaret Mead, and prominent psychiatrists. Donald Lindsley was also included, as was Henry Beecher.36
This Macy-sponsored conversation contained a rich palette of themes, investigatory strategies, and metaphors used to describe consciousness. Psychoanalytic descriptions of personality formation shared the meeting agenda with reviews of how glucose was used by the brain. Some argued for limiting the study of consciousness to measurable behaviors; others felt consciousness essentially was not an isolatable object of study but an introspective, subjective experience. In a telling statement, one participant, reflecting on the five-year experience, summarized well my own impression of the transcripts in terms of where the group stood: “So, although I still do not know what anybody else means when he says ‘consciousness,’ I have a much better understanding as to what I mean by it, even though I cannot put it into words.”37
Lindlsey presented the desynchronization/RAS findings of Moruzzi and Magoun, and the use of EEG at times seemed to anchor the group’s conversation, proving versatile enough to serve very different approaches to consciousness. It could incorporate psychoanalytic and sociological paradigms whereby RAS served as an intermediary, rendering the “symbolization” of stimuli at the heart of consciousness as well as satisfying a shared objective to more concretely measure and objectify research in this area. Nonetheless, the Conference ended without a dominant, shared narrative. While the methodological rigor and flexible application of EEG were useful for incorporating a range of paradigms, EEG research on subcortical activity and consciousness did not make its case across this audience. As one program presenter wrote, “I think the arguments that Penfield, Jasper and some of the others make about subcortical centers are beside the point, because an isolated cortex is useless to an animal.”38 Whether or not that was so—in what ways lower functions were necessary as opposed to sufficient for consciousness, and for physiologic survival—became a central question for Schwab’s and others’ efforts to treat and examine coma.
The claims put forth by Moruzzi, Magoun, Jasper, Morison, Lindsley, and a growing roster of investigators did, however, resonate with many other audiences. For Stanley Cobb, the founding Chief of Psychiatry at MGH, EEG could advance understanding of his own point of view that consciousness was “a function of nervous tissue in action, just as much as contraction is a function of muscle … What is needed is a method that will quantitatively determine the amount of some physiochemical process that parallels what we know about consciousness.”39
At a “symposium on the brain and the mind” that took place at the annual meeting of the American Neurological Association in June of 1951, Magoun, Penfield, and Jasper made such claims explicit and further argued that their work could fill the need for such a method. Responded one participant at that event:
The suggestions of Dr. Magoun and Dr. Jasper and their co-workers that the lower brainstem levels exercise an important influence over the conditions of awareness and responsiveness are fascinating and open up great fields for further investigation by means of methods which have not hitherto been available.40
Cobb was among a network of medical investigators whom the Rockefeller Foundation, especially through the initiatives of Alan Gregg, turned to in an effort to unravel the connections between brain and mind. Cobb saw RAS and EEG research as an opportunity to break from the dominant hold of the cortex and consider new models more amenable to experimental study. Linking the complexity of a mass of neurons with the phenomenon of consciousness required breaking a code. Biological systems can often be reduced to recombinations of basic patterns of protein function or chemical reactions that can be manipulated and amplified to do many things, much the way that all of language relies on a few sounds or letters. What then, Cobb asked, were the basic elements, or letters, of consciousness?
The increasing focus on RAS-consciousness connections, along with a patterned-building-blocks approach to the biology of consciousness, led to other possibilities for understanding EEG signals. Instead of reflecting some general working state of the whole brain, perhaps the Berger rhythm and others were each one of a core set of possible brain states. Through desynchronization, RAS selectively manipulated these states in versatile sequences or combinations, like playing many melodies from a few keys or notes, so as to queue selected attention for the cortex. This possibility explained certain experimental phenomena that were otherwise difficult to account for. For example, beta rhythms over motor cortex desynchronized only immediately before the initiation of the act of clenching a fist, then quickly returned to baseline soon after the initiation despite the persistence of the observable clenching action.41 Rather than marking conscious activity itself, perhaps desynchronization was part of a mechanism that recruited cells to implement the work of types of conscious activity.
RAS experiments could suggest that the reticulum helped order and manage where the cortex should place its attention. The basal rhythm of the brain, in this scenario, was then misleading if understood directly as the unity of active conscious activity. Adrian, who helped established Berger’s rhythm as real, came to see it in this way—as the appearance of what the brain does when not participating in consciousness. The basal rhythm was a holding pattern. Desynchronization, then, would be the key event of full consciousness. It provided a mechanism for selectively directing the attention of certain neuronal networks and making them specifically accessible to the messages that reached them. The brain needed a centralized relay, parceling out cortical freedom from the alpha rhythm to be briefly and specifically engaged with (and of use to) the body.42
That orchestration of moment-to-moment changes in patterns of desynchronization, though, seemed at odds with the continuous and free-floating experience of consciousness. But perhaps that continuous experience was misleading and was different than the biological reality underlying it. French neuroscientist Alfred Fessard argued that “one can be conscious without being conscious of one’s self.” The continuous “I” sense of consciousness could be an artifact. In yet another twist on the metaphor of “integration,” Fessard suggested that experienced integration, or “EI,” was the core phenomenon of our experience and that “the essentiality of EI can be assumed to be present in the most primitive forms of sensibility as well as the highest levels of intellectual life.”43 “Integration” by the brain of the sequence of events comprising thought made consciousness seem unified when it was in fact built from fragmentation, from a constantly edited set of rapidly sequenced snapshots. As Cobb put it, “mind is the integration itself.”44 RAS was the integrator.
The idea of achieving unrestricted effects by varying the sequence and pattern of a restricted set of neuron patterns—Cobb’s “letters of the alphabet”—made it plausible, to some, for a limited menu of properties in a functional center like RAS to be able to mediate diverse behavioral outputs. This concept had a strong and mutually reinforcing connection to the explosive field of “cybernetics” exemplified in Norbert Weiner’s 1948 publication of Cybernetics: or Control and Communication in the Animal and the Machine.45 The connection was explicitly made in books, papers, and transcribed conference discussions. At the 1951 American Neurological Association meeting, Cobb cited MGH’s Mary Brazier’s observation that work by Weiner and the field of cybernetics resulted in a “change in concepts of the nervous system … so great that it is almost impossible to overestimate it. In brief, it is a change from the concept of a passive, static nervous system, to an active, dynamic one.”46 Weiner summarized much of that impact:
I was compelled to regard the nervous system in much the same light as a computing machine, and I communicated this idea to my friend Rosenbleuth and to other neurophysiologists. I managed to get a group … together at Princeton for an informal session, and I found on the part of each group a great willingness to learn what the other groups were doing to make use of their terminology. The result was that very shortly we found that people working in all these fields were beginning to talk the same language, with a vocabulary containing expressions from the communication engineer, the servomechanism man, the computing-machine man, and the neurophysiologist. For example, all of them were interested in the storage of information to be used later, and all of them found that the word memory … was a convenient term to cover the whole scope of these different fields. All of them found that the term feedback, which had come from the electronics engineer … was an appropriate way of describing phenomena in the living organism as well as in the machine. All of them found that it was convenient to measure information in terms of numbers of yeses or noes, and sooner or later they decided to term this unit of information the bit. This meeting I may consider the birthplace of the new science of cybernetics, or the theory of communication and control in the machine and the living organism.47
Warren S. McCullough emphasized this focus on the on-off property of neuro-information:
When an impulse reaches the end of a nerve fiber, it combines with various other impulses that have reached the same level to determine whether the next nerve fiber discharges. In other words … the nerve fiber is a logical machine in which a later decision is made on the basis of the outcome of a number of earlier decisions. This is essentially the mode of operation of an element in a computing machine.48
For these investigators, the objects of the study of mind shifted from cells, membranes, and anatomy to the characteristics of the movement of on-off information, the behavior of binary systems of communication and computation, and the reconfiguration of “representations of life and society as systems of decisions and signals.” Taken together, “it was a techno-epistemic transformation.”49
Cybernetics also proved quite an elastic umbrella. It supported the idea of a small, defined, neuronal switching station as key to consciousness. Weiner used Lindsley’s findings of a subcortical gating mechanism to justify his own views of the alpha EEG rhythm as a kind of clock that regulated neuroreactivity.50 At the same time this viewpoint was aligned with a different, more spatially and functionally diffuse description of brain activity. Lashley, for example, was critical of work on RAS and yet his experiments were also a resource to cybernetic investigators interested in the brain.51 Lashley’s research in the 1920s addressed the seemingly endless dispute over localization versus diffusion of cortical functions. Since at least the nineteenth century, experiments that removed chunks of animal cortex found, in many cases, few significant effects. Lashley quantified removal and its impact on standardized problem-solving tasks by rodents, such as navigating a maze path and then recalling it in later trials. He found that only the amount of tissue destroyed, not the particular region, interfered with learning and recall. This research was itself pursued in response to prevailing theories of the time in which the accumulation and reinforcement of local and specific neuronal reflex arcs mediated thinking. Instead, Lashley offered a vision of dispersed cortical neuronal capacity for those functions:
Such facts can only be interpreted as indicating the existence of some dynamic function of the cortex which is not differentiated with respect to single capacities. … In this there is close harmony with theories of a general factor determining efficiency in a variety of activities.52
Lashley argued that neural cortical material had, as a core property, “resonances,” and, further that predictable, quantifiable rules governed such neuronal “resonators” to manage and “integrate” the activity of the brain. A basic set of resonator properties, dispersed throughout the pluripotential cerebral cortex, rather than highly localized and specific functions, made the brain work.
Revisiting these diverse (and vying) mechanistic and holistic, local and diffuse characterizations of how the brain worked to produce consciousness puts into perspective the responses to brain death after 1968, and the clinical challenges it faced. Later responses criticized brain death criteria as not engaging with the conceptual groundwork necessary to explain how brain, consciousness, and organism were related. These responses, characteristic of the bioethics literature on brain death, lose some credibility around their claim to introduce a new conversation about the necessary conceptual groundwork when seen as yet another one of recurring attempts to do just that. The pre-1968 conversation was tied to testable methods in ways that the later bioethical conversation was often not. This underscores and helps explain the difficulties faced by the post-1968 critical community to make instrumental use of their conceptual critique to learn more, to improve care, or to focus on the sort of core questions about what nature means and what science can do—questions that Jonas, and also Beecher, engaged.
As I suggested in Chapter Two, Jonas and Beecher—frequent exemplars of the oft-characterized divide between medical facts and ethical values that ostensibly called for bioethics—were similarly engaged with the project of how to take on the limits of dualism and to source values in nature. Beecher, though, saw no credible path of action coming from Jonas’s and others’ various critiques of the hubris reflected in setting man apart from nature via medical technologies. The neuroscientific study of consciousness briefly reviewed here, and especially the next chapter’s analysis of its use in medical settings, are as yet underused opportunities to historically trace how medical facts might help broker and operationalize that project.
Jasper and Penfield, along with Cobb, were supported by the Rockefeller Foundation in a funding initiative intended to no less than do battle with that dualism—to unite psychiatry with medicine. The aim was for the neurosciences to describe brain function in ways that could be used to solve problems. For these clinicians and researchers, the actionability of some of the new models of how the brain worked was a key attraction. Restricting consciousness to a small part of the subcortical brain lent itself to a more targeted experimental approach. “This notion of the whole brain acting as a whole is, to my thinking and experimenting, rather sterile,” remarked Jasper. “It gives us no possible conception of a real mechanism of integration. It leaves us completely without experimental approach to these problems.”53 EEG lent tangibility to brain action that could be translated into other experimental programs and then into potentially therapeutic action.
The complex link between these experimental paradigms and their actual use through the work of medicine can be seen in how the structures of the lower brain were described not only as parts of consciousness in terms, for example, such as in selecting among an array of sensations and ordering the sequence and objects of attention, but also as the building blocks of emotional experience, and in what those distinctions even meant. After reducing consciousness to snapshots of awareness, why not explain the dimensional and personal aspects of consciousness within these same events? Penfield, for example, elaborated on the emotional regulatory functions of temporal lobes, whose role in storing memories and mediating emotion was included in his centrencephalic ensemble. Philip Bard and Martin Macht also associated emotion more closely with these structures. They described the ability of decerebrate cats to roam freely, displaying stereotypically aggressive postures or other seemingly emotional reactions which, as Bard and Macht demonstrated, were only pseudo-affective—only having the outward form or appearance of an emotional experience. But at the 1959 CIBA Symposium, when Magoun asked them whether they therefore felt emotions could be localized to the brainstem or midbrain, Bard responded by raising a point central to later debates over brain death and to the comparisons of anencephalic, persistently vegetative, and brain-dead patients in those debates: “I am not prepared to say whether a decerebrate animal possesses subjective experience or not; we have no way of telling that” (emphasis mine).
Others seemed to be suggesting that the evidence indicated that they did have a way “of telling that.” Penfield described how cortical stimulation can lead to vocalizations of crying while the patient reported not actually feeling sad, implying that the cortex provided just the form, and not the substance, of emotion. Magoun made this explicit: “If this were a response evoked by stimulating the cortex, I would not expect it to be associated with an affective experience.” Chimed in Penfield: “I think the cortex is utilizing the mechanism in the brainstem.”54
By the late 1950s, several summary reviews, conferences, and textbooks appeared that reflect the established presence of RAS as a key focus of research into brain function and consciousness, including Magoun’s book The Waking Brain.55 The “real significance” of EEG patterns “in terms of intra-cortical activity and of behavior” was “not completely known as yet.” How much RAS was an active “director of attention with the actual work of consciousness” as opposed to a passive, though necessary, relay for attention, remained in dispute.56 The process of establishing boundaries and differentiating roles between RAS in particular and associated midbrain structures, especially the thalamus and other midbrain centers, was often inconsistent. Thus, despite generating great creativity and opportunity, the value of EEG for clarifying the functional correlates of cortical activity was mixed.57 While an appreciation of arousal and selective attention sequencing and coordination for consciousness was a lasting contribution of this work, it soon faded as a central aspect of consciousness studies, replaced by other methods of mapping the recruitment and activity of brain regions. But, during the 1950s and 1960s, the EEG and the map of consciousness it suggested provided critical working knowledge for several neurologists—Schwab and Adams prominently among them—to describe and manage patients in coma. The ambiguity of Bard’s response, yet the repeatedly confirmed and tangible connections between brainstem and cortex, together lent confidence, but also the “whole brain” scope, to the eventual criteria, reinforced through experience with its use in care.
How readily were ideas based on EEG recordings from brain-lesioned cats applied to cases like the following reported in 1952?
A schoolgirl … [with] a sudden episode in which she lost consciousness for an hour, simultaneously she developed the further ocular signs and marked rigidity (recalling the decerebrate state … in subsequent months, had three essentially similar attacks … in each there was excessive sleepiness of several days’ duration … Magoun and his school argue from [their] results that Bremer’s conception is no longer tenable unless the concept of deafferentation be enlarged to include the reticular formation in its scope … by offering a constant background excitation directed towards the hemispheres … It is a speculation to be proved or disproved by pathological study.58
Such speculation caught the attention of leaders of twentieth-century neurology. Hugh Cairns addressed this topic in the Victor Horsely Memorial Lecture, which also appeared in the medical journal Brain in 1952.59 He credited Moruzzi and Magoun’s work for forcing a change in ideas regarding the residence of consciousness in the cortex, and for the rejection of Jackson’s belief that it was centered there: “However … I must make clear what degree of ‘consciousness’ I consider is possible in the brain-stem and thalamus. The evidence, which is far from complete, comes from human anencephalic and hydrocephalic monsters who survive long enough to develop reactions.”60 Cairns noted that these patients, one surviving four decades, were able to eat, have preferences, go through sleep cycles, and show alertness, all with brainstems that functioned with only some or no remaining cortex. If coma did occur, it at times resembled sleep behaviorally and electroencephalographically, though without arousal; while at other times it appeared as something different, an unresponsiveness distinct from normal sleep. It was not clear then how a centrencephalic or reticular consciousness was appreciable or knowable in such patients and, consequently, whether Magoun’s question to Bard and Macht was answerable or not. The relationship between RAS, cortex, and other regions and functions could be observed and mapped, but the translation of that mapping into conclusions about experience in general, or the anencephalic’s experience in particular, was still elusive and may always be. Was Fessard’s “experienced integration” enough of a phenomenon to be considered human consciousness?
Percival Bailey surveyed the implications of EEG-based research for treatment and patient care in his1955 presidential address before the American Neurological Association.61 Bailey, a leading figure in early to mid-twentieth-century neurology,62 remarked that Penfield’s centrencephalon “may be more fundamental … more concerned with the primitive emotions, but the cerebral cortex (Jackson) is the highest level of the nervous system, the crowning glory of Homo sapiens.” Consciousness boils down to the cortical “kaleidoscopic play which we call the mind.” Consciousness without the cortex “must lead as dim and tenuous an existence as that of the shades in Hades. The cerebral cortex alone is capable of that bewildering play of intricate mental processes which is characteristic of human mentality.”63 Penfield’s or Lindsley’s “integration” was different from Bailey’s. For the latter, brainstem (or thalamic) integration merely supported consciousness, whereas Penfield might consider this integration central to a concept of consciousness.
Citing a case of akinetic mutism of one year’s duration with a completely absent EEG but diffusely injured neocortex, Bailey concluded, “It now appears that consciousness cannot be localized in the brainstem. It seems that one could no more localize consciousness than any other function of the nervous system. It must be looked upon as a machine.”64 In this case, holism and mechanism reinforced each other. Consciousness was present everywhere, and thus could be disrupted in a myriad of ways. The machine was not a pluripotential whole, like Lashley’s, but at least a functionally unified one. Moruzzi and Magoun found “a regulating control” of reticular formation over cortex; Jasper revealed how the thalamus was included in that mechanism; and Bremer showed how the cortex also exerted influence over how these lower structures worked. This was how Bailey briefly summarized the state of EEG work on consciousness, attention, and awareness, at the time when Schwab first used EEG to support turning off a respirator. Bailey used that data to show just how dubious any localization of consciousness was. However, if consciousness was specifically understood as willful action and self-understanding, it remained in the cortex.
These distinctions began to matter at the bedside, and not just to Schwab. In another case report published in 1952, a five-year-old girl operated on for congenital hip displacement had a cardiac arrest mid-operation. She was given open cardiac massage and an intracardiac epinephrine injection with successful resuscitation after about five minutes. For decades, five minutes had been well known as a critical time window for cortical nerve cell survival. Almost two hours later, the EEG
“was practically a flat line, unmarked by any significant activity … At that time the patient was breathing spontaneously. Two hours and forty minutes after the accident, bursts of high amplitude and mixed frequency were noted in the EEG … The patient eventually died seventeen hours after the anoxic episode.”
It does not appear that she was placed on a respirator. This girl was included as one case in a report of six cardiac arrests during operations. Two had flat EEGs and both died, leading to the tentative conclusion that “it seems to us that the EEG could be of some value in determining the prognosis after episodes of cerebral anoxia.”65
Cardiac arrests in the operating room were an initial opportunity to connect EEG changes, prognoses, and mechanisms of injury and recovery.66 Initially, however, conclusions as to the significance of EEG changes in coma, in particular a “flat-line,” were cautious:
Recovery without evidence of residual abnormalities is possible from almost any type or degree of electroencephalographic disorder. However, if the electroencephalographic activity has continued flat for over four hours there is a strong presumption that this cortical damage may not be completely reversible.67
Intensive care for life support was still new at this time. By 1950 the use of respirators was still limited, as was active cardiac massage and cardiac stimulatory medication for patients with cardiac arrest.68 A small cadre of experts in coma emerged after expanded use of more mobile and effective positive pressure respirators for polio in particular, as described earlier, in the Danish epidemic of polio in the early 1950s. Many of the leaders of this successful public health effort founded some of the first “intensive care units.” Beyond diseases of the respiratory mechanism, such as polio and myasthenia gravis, they spread the use of respirators to management of head trauma, cardiac arrest, respiratory illness, postoperative care, and so on.
In 1959, several papers by French investigators appeared that described a unique form of coma for which medical intervention was considered futile. Mollaret and Goulon coined the subsequently widely repeated term coma dépassé, or “beyond coma,” to describe this state. In a continuous scale of comas—separated by degree of impaired responsiveness to the environment including reflexive, vegetative, and basic metabolic functions (respiration, circulation, thermal regulation)—coma dépassé was at an extreme end, absent all functions, the “total abolition of the vegetative functions of life.”69 This condition was found to have widespread necrosis—the essential effacement of the normal cellular components of the brain—as its pathology.70 Jouvet argued that isoelectric EEGs could “permit the affirmation of the death of cortical and diencephalic formations” and suggest futility of further treatment.71 Fischgold and Mathis published a review of 155 coma patients that attempted to find associations between clinical signs and EEG. Fischgold had been studying EEG and coma since at least the 1940s, and had devised the numbered (I through IV) scale of increasing severity of coma used by Jouvet. Stage IV described disruption of vegetative functions, the need for artificial life support, isoelectric EEG, and 100 percent mortality.72
That description, “beyond coma,” is only comprehensible within the preceding decades of work on EEG and consciousness. Coma dépassé truly went beyond the nimble mechanisms or desynchronization paradigms with which Jouvet was so familiar. Those moving parts were gone. To these observers, coma dépassé’ described the end of discernible function of the nervous system as they understood it. It was beyond anything that had before appeared with beating heart and expanding lungs. Yet coma dépassé did not immediately translate into death. In part, this was because not all experts accepted the opinion of the authors that coma dépassé represented the absolute nonfunctioning of the brain, let alone the nervous system. Schwab’s work was part of a process that unfolded over decades to capture and verify what the loss of these electrical signals meant.
Fred Plum—who emerged in the early 1960s as an international authority in coma—also became curious as to which signs reliably captured the degree of both nervous system and brain function loss in these patients. Plum authored the first comprehensive manual for the examination of the comatose patient, The Diagnosis of Stupor and Coma, which was published in 1966.73 Working with polio patients at a respiratory care unit he had developed in Seattle, Washington, Plum became an expert in the management of hypoxia and respiratory insufficiency.74 He then began admitting head trauma patients and others unable to breathe on their own into his convalescent polio unit, as the other hospital departments offered no similar intervention. The concentration of respirator use and expertise further expanded its application to a wide range of otherwise rapidly lethal conditions. But soon thereafter, by the mid-1950s, concern appeared in medical journals about sustaining otherwise unsalvageable patients in coma.
At the international meeting of transplant physicians and jurists sponsored by the CIBA foundation in 1966, several European transplant centers revealed that they were each using fairly comparable criteria with which to harvest organs from patients. They did so bolstered by the fact that at autopsy the brains and spinal cords of potential donors were similar to nervous systems in corpses over a week old.75 This physical appearance was a striking and repeatedly invoked proof of brain death, the confirmation of a nonfunctioning brain. Beecher’s friend and Committee member Joseph Murray commented at the CIBA gathering:
I knew they were dead because I’d be waiting for them, I’d stop the post-mortem by taking out the kidneys, but I’d hang around for the rest of the post-mortem, and by the time they took the skull off the brain was just, uh, like oatmeal, no sulci, nothing there, just gone. So, I knew the patient had been really dead, in essence, long before we harvested the organ.76
But what were external, reliable signs of such extensive death of the brain that didn’t require an autopsy to see? Many observers, including Fischgold, felt Mollaret and Goulon’s coma dépassé might not mean irreversibility of brain damage, let alone death of the body, but was a particular state whose prognostic meaning could vary.77
So by 1968, at the threshold of defining brain death, one group of neurologists wrote that “the neurologist today appears practically without useful semiotic elements” to predict outcome in traumatic coma. Locating the level of the lesion through physical examination “does not reveal any prognostic meaning.”78 Part of this confusion lay in reconciling physical findings (i.e., unresponsiveness) and EEG findings; even patients with severe coma and extensive central nervous system loss at autopsy could still have EEG activation or reactivity.79 Thus, while one review of almost two hundred cases of comatose patients with EEG found that “at times the isoelectric record … will raise the issue of the advisability for continued efforts to maintain life,” EEG findings and physical findings still had to be interpreted in the context of each other: “When there is a marked discrepancy between the clinical and electrical signs—i.e., a relatively normal record with normal reactivity in a deeply comatose patient—the EEG should suggest a brain stem lesion.”80 But what did that suggest? Doubt and uncertainty about what EEG was describing captured a key problem for the EEG lab: Did the electric window into coma provide a picture of the status of mechanisms of consciousness and/or brain function, or was it simply an indication of the extent of cell death from which those inferences about brain function could not yet reliably be made?
So, as Schwab started to gather material for what would be a series of studies in the 1960s for his criteria, the “flat line” was still without stable meaning. In large part, this was because of inconsistent definition, as some took flat line to simply mean low amplitude, which explained why “10 percent of all adults” were described as having flat-line EEGs the year the flurry of French reports appeared.81 Fischgold reflected the feelings of many when asserting that:
“Flat EEG trace” does not signify death of the brain … but does have prognostic significance if it persists for hours or days in a subject who is at normal body temperature in the absence of anesthesia … Thus, prolonged electrical silence of the EEG, although it does not necessarily signify death of brain cells, acquires a grave prognosis.82
Through the 1950s and 1960s, some physicians increasingly raised questions about the connections between EEG and consciousness, and the significance of absent electrical activity. One patient could be reported to have a “flat electroencephalogram” for twenty-eight days and eventually fully recover.83 Another, with atrophy of most of the reticular substance, had a relatively normal EEG despite quadriplegia and absent response to painful stimuli.84 A published review of five coma patients concluded that “our observations seem to justify the assumption that no one established relationship exists between the intensity of coma and the recorded cerebral-electrical activity.”85 The authors tried to reconcile their findings with the patterns of lesions in the cats of EEG brainstem researchers. Some patients fit those patterns while others did not. Given the complexities of the tiny universe of the pontine and midbrain space, perhaps “the nervous structures involved in the regulation of the electroencephalographic activity and in the mechanism which gives rise to the state of consciousness are different or that these structures have different functional activities.”86
In another case, a patient with a brain stem infarct had a waking EEG but was unresponsive to stimulation and demonstrated partial loss of cranial nerve reflexes. This situation seemed to resemble cat experiments in which, at a particular midbrain transection, electrocortical activity and actual apparent awareness appeared to become disconnected, as they did here.87 Similar findings in cats that showed persistent desynchronized unresponsiveness with transection at the midpontine pretrigeminal level generated interest and curiosity.88 Desynchronization, usually associated with alertness, could apparently persist in cats without a synchronizing mechanism. Similar findings were detected in some unfortunate humans: “The question arises whether the patients and animals with such midpontine lesions are really conscious or not. Although ocular movements of the midpontine cats are suggestive of wakefulness this does not necessarily prove that the animals actually are conscious.”89 Magoun’s question circled back to the bedside.
Patients with “akinetic mutism” especially seemed to resemble Bremer’s cat transection experiments. The term itself is attributed to a description in a paper by Cairns of a patient in 1941:
The patient sleeps more than normally, but he is easily aroused. In the fully developed state he makes no sound and lies inert, except that his eyes regard the observer steadily … Despite his steady gaze, which seems to give promise of speech, the patient is quite mute … Oft-repeated commands may be carried out in a feeble, slow and incomplete manner, but usually there are no movements of a voluntary character; no restless movements, struggling or evidence of negativism. Emotional movement is also in abeyance. A painful stimulus produces reflex withdrawal … [if] the stimulus is sustained, slow feeble voluntary movement may occur … but usually without tears, noise or other manifestations of pain or displeasure. The patient swallows readily, but has to be fed.90
Autopsy study of akinetic patients found extensive pontine and variable midbrain lesions, marring but not completely destroying the RAS:
As a result of the partial destruction of the reticular formation, the reticular activating system may energize the neuronal activity derived from external or internal stimuli to a degree sufficient to maintain movements of the eyes but not sufficient to maintain a degree of awareness permitting an intellectual command to be understood.91
The explanatory value and limits of “electricocentric life” developed substantially between Schwab’s first observations with Brickley in 1941, to the Report in 1968. Severely comatose patients at MGH called for methods to “see” the seemingly inaccessible status of brain function in terms of the possibility for consciousness, the sustainability of physiological survival, and the permanence of either. EEG was a tangible window on the comatose brain, but also became central to efforts to develop those methods because of three results of these decades of EEG research. First was an empirical warehouse upon which to believe that EEG as a technology captured mechanisms that were reliably reproduced and had certain correlates to functioning of brain regions,; second, a working set of models and vocabulary to use to interpret but therefore to also test against more common clinical ways of knowing such as neurological and physical examinations; and third, to have models that also had problems—that highlighted key unanswered questions that shaped the scope of work and the limits and cautions in the use of these signs. Which mattered more—cortical EEG activity or brainstem function? Loss of working consciousness, of arousal mechanism, or overall loss of functioning brain cell mass? Was, as the Macy participant asked, “an isolated cortex useless to an animal”?
In his use of EEG to advise colleagues about continuing treatment and refine his criteria, Schwab had to consider—and his work was framed by—these questions. The prevailing position of the Committee was that the most reliable determination of certain incapacity for consciousness and brain function that could be drawn from this research and clinical experience lay in what would come to be referred to as the “whole brain” criteria. This whole brain position was not itself a conceptual or ethical position, yet it described the conditions that Beecher considered to risk unethical experiment and incoherent acts of commission. It was not adopted as a metaphorical stand-in for a commitment to a certain philosophy of mind or to the relative value of consciousness to personhood, yet it did use accumulated experimental and empirical findings that resulted from testing or elaborating such ideas. The criteria would later be criticized as being conceptually underdeveloped, and offering little or no empirical support. But the “whole” approach instead reflects a typical building of medical facts from these sources.
In the context of managing these new kinds of comatose patients, EEG research could identify for Schwab and his colleagues only the scope of brain mechanisms to confirm as having failed in order to render the demise of the capacity for consciousness, but could not as yet reliably specify with adequate consensus and patient care experience the more specific part(s) of that mechanism that did so. Schwab could also only credibly use criteria that included a coincident set of signs of the body’s physiologic demise in these patients. The whole formulation allowed both, and had to allow for both. Within this point of view, deep within the building, testing, and use of medical knowledge in response to the severely comatose, such criteria described a set of tangible movements lost in death, as tangible as the loss of heartbeat.
1. Robert S. Schwab, Electroencephalography in Clinical Practice (Philadelphia: WB Saunders Co., 1951): 158–59.
2. Robert S. Schwab, “Manuscript Outline for Book Proposal, ‘Medico-Legal Aspects of Cerebral Death,’ ” 2. I am grateful for this and other papers belonging to Dr. Schwab obtained from his widow, Joan Schwab. This outline is undated, but likely circa 1970–72. Here Schwab also remarks that since 1954 “over 300 situations have arisen in our hospital where the presence or absence of an electroencephalogram is requested and if absent, and there is no breathing or reflexes, the patient can be declared dead. In these cases, 200 brains have been worked up in considerable detail and all of these cases showed marked dissolution and loss of structure,” 3.
3. Schwab, “Manuscript Outline.”
4. Robert S. Schwab, “The clinical application of electroencephalography,” Medical Clinics of North America (September 1941): 1477–89.
5. Schwab, Electroencephalography in Clinical Practice.
6. Schwab, “Manuscript Outline,” 2.
7. Robert Schwab, “The measurement of bodily currents,” Electrical Engineering 60 (1941): 919–23, 922.
8. S. A. Kinnier Wilson, “On decerebrate rigidity in man and the occurrence of tonic fits,” Brain 43 (1920): 220–68; 223–24; 226–27.
9. Sherrington, “Decerebrate rigidity and reflex co-ordination of movements,” Journal of Physiology 22 (1897): 319.
10. Richard V. Lee, “Cardiopulmonary resuscitation in the eighteenth century: A historical perspective on present practice,” Journal of the History of Medicine (October 1972): 418–33.
11. Astley Cooper, “Some experiments and observations on tying the carotid and vertebral arteries, and the pneumogastric, phrenic, and sympathetic nerves,” Guy’s Hospital Report 1 (1836): 457–75.
12. Librio Gomez and F. H. Pike, “The histological changes in nerve cells due to total temporary anemia of the central nervous system,” The Journal of Experimental Medicine 11 (1909): 257–66, 257.
13. H. N. Simpson and A. J. Derbyshire, “Electrical activity of the motor cortex during cerebral anemia,” American Journal of Physiology 109 (1934): 99.
14. H. K. Beecher, F. K. McDonough, and A. Forbes, “Effects of blood pressure changes on cortical potentials during anesthesia,” Journal of Neurophysiology 1 (1938): 324–31; O. Sugar and R. W. Gerard, “Anoxia and brain potentials,” Journal of Neurophysiology 1 (1938): 558–72.
15. E. D. Adrian and H. C. Matthews, “The Berger rhythm: potential changes from the occipital lobes in man,” Brain 4, no. 57 (1934): 355–85.
16. For example, see a review by Morton A. Rubin, “The distribution of the alpha rhythm over the cerebral cortex of normal man,” Journal of Neurophysiology 1 (1938): 313–23.
17. Otniel E. Dror, “Techniques of the brain and the paradox of emotions, 1880–1930,” Science in Context 14, no. 40 (2001): 643–60.
18. David Milett, “Hans Berger: from psychic energy to the EEG,” Perspectives in Biology and Medicine 4, no. 44 (Autumn 2001): 522–42.
19. Roger Smith, “Representations of mind: C. S. Sherrington and scientific opinion, c. 1930–1950,” Science in Context 14, no. 4 (2001): 511–39.
20. G. Moruzzi and H. W. Magoun, “Brain stem reticular formation and activation of the EEG,” EEG and Clinical Neurophysiology 1 (1949): 455–73.
21. The reticular activating system was generally considered a collection of highly interconnected nerve fibers extending from the first section of the brainstem distinguishable from the top of the spinal cord, the medulla, through the next section, a “bulb”-like appearing pons, and into the midbrain. However, as will be discussed, there was also a system of fibers extending from the region of important nuclei further rostral (towards the head), the thalamus, with the cortex, the cerebral hemispheres often referred to as the thalamic reticular system. Connections between these two systems were a source of great interest and productive of varying hypotheses of the nature of arousal and consciousness, and “reticulum” was often used to describe both systems or parts of them. These terms were further complicated by the finding of regions within these areas that seemed to have more particular functions, and the literature frequently included reasonable complaints that general comments about “the reticulum” nonspecifically referred to the general region while perhaps describing more local effects. For characterizing the uses of these regions in reorienting versions of consciousness, the more general terms suffice.
22. D. B. Lindsley, L. W. Bowden, and H. W. Magoun, “Effect upon the EEG of acute injury to the brain stem activating system,” EEG and Clinical Neurophysiology 1 (1949): 475–86, 483.
23. Morruzzi and Magoun, “Brainstem reticular formation and activation of the EEG,” 468.
24. Among the work that factored in this discussion were Hess, American Journal of Physiology 90 (1929): 386; S. W. Ranson, “Somnolence caused by hypothalamic lesions in the monkey,” Archives of Neurology and Psychiatry 41 (Chicago, 1939): 1–23; Robert S. Morison and Edward W. Dempsey, “A study of thalamico-cortical relations,” American Journal of Physiology 135 (1942): 281–92; Dempsey and Morison, “The production of rhythmically recurrent cortical potentials after localized thalamic stimulation,” American Journal of Physiology 135 (1942): 293–300; Dempsey and Morison, “The interaction of certain spontaneous and induced cortical potentials,” American Journal of Physiology 135 (1942): 301; H. Jasper, J. Hunter, and R. Knighton, “Experimental studies of thalamocortical systems,” Transactions of the American Neurological Association 73 (1948): 210–12; Herbert Jasper, “Diffuse projection systems: the integrative action of the thalamic reticular system,” EEG and Clinical Neurophysiology 1 (1949): 405–20. Hess’s work on the thalamus was explicitly tied by his son and co-workers to the agenda of moving cortical function to these subcortical areas in K. Akert, P. Koella and R. Hess, “Sleep produced by electrical stimulation of the thalamus,” American Journal of Physiology 168 (1952): 260–67: “There have been numerous reports by Hess on the production of sleep in cats by electrical stimulation of the thalamus. These sprang from a concept developed in 1924 that the functional activity (‘Reactionsbereitschaft’) of the cerebral cortex is regulated by subcortical centers,” 260. However, it is important to note that Hess and Ranson’s prior work on the hypothalamic areas and supposed mechanisms of sleep were related to a view that part of the brain mediated the visceral stimuli shaping emotion, and thus when stimulated caused arousal. Thus, the elaborated roles of the thalamic areas in EEG research were ironically at first closely tied to afferentation models. They were also influenced by a prior fascination among earlier neurological investigators with animal, vegetative, and primitive influences on higher functioning, as suggested in the references to Reichardt’s work below. All of this is to note the shifting interplay and iterative use of concept and experiment in the neuroscience of consciousness that the medical literature has actually long incorporated. As I will elaborate further, the focus of bioethical critique on the conceptual aspects of these sorts of facts further separated, rather than more usefully integrated this sort of iteration.
25. Herbert Jasper, “Diffuse projection systems: the integrative action of the thalamic reticular system,” EEG and Clinical Neurophysiology 1 (1949): 405–20, 418.
26. Martin Reichhardt, “Hirnstamm und Psychiatrie,” Monatsschrift für Psychiatrie und Neurologie 68 (1908): 470–506. (Translation in “Brain and Psyche,” trans. F. I. Wertham, Journal of Nervous and Mental Diseases 70 (1929): 390–96.)
27. W. G. Walter, G. M. Griffith, and S. Nevin, British Medical Journal i (1939): 107.
28. Lindsley et al., “Effect upon the EEG,” 485.
29. C. Judson Herrick, The Thinking Machine, 2nd ed. (Chicago: University of Chicago Press, 1932 [1929]).
30. Walter B. Cannon, “The James-Lange theory of emotions: a critical examination and alternative theory,” American Journal of Psychology 39 (1927): 106–24, and idem “Again the James-Lange and the thalamic theories of emotion,” The Psychological Review 38, no. 4 (July 1931): 281–95.
31. W. R. Hess, “Biological Order and Human Society,” in Biological Order and Brain Organization: Selected Works of W.R. Hess, ed. K. Akert (Berlin: Springer-Verlag, 1981): 3–15. This originally appeared as “Kollektive Ordnung in biologischem Aspekt in: Festschrift Max Huber (Late President of the International Red Cross) – Vom Krieg und Frieden (Zurich: Schulthess, 1944): 151–72.
32. See, for example, Christopher Lawrence and George Weisz, eds., Greater Than the Parts: Holism in Biomedicine 1920–1950 (New York: Oxford University Press, 1998); Anne Harrington, Reenchanted Science: Holism in German Culture from Wilhelm II to Hitler (Princeton: Princeton University Press, 1996).
33. Louise H. Marshall and Horace W. Magoun, eds., Discoveries in the Human Brain: Neuroscience Pre-history, Brian Structure and Function (Tatowa, N.J.: Humana, 1998).
34. Wilder Penfield, “The cerebral cortex in man: the cerebral cortex and consciousness,” Archives of Neurology and Psychiatry 40, no. 3 (September 1938): 415–42, 441–42.
35. Transcripts of these meetings were collected as Harold A. Abramson, ed., Problems of Consciousness, transactions of a conference sponsored by the Josiah Macy Jr. Foundation (NY: Corlies, Macy and Co, Inc.): vol. 1 (1951) for March 20–21, 1950 meeting; vol. 2 (1951) for March 19–20, 1951 meeting; vol. 3 (1952) for March 10–11, 1952 meeting; vol. 4 (1954) for March 29–31 meeting; vol. 5 (1955) for March 22–24, 1954 meeting.
36. While not one of the more active participants, Beecher generally spoke of the need for measurable indices of function or behavior for study of consciousness, and of the need to avoid researching subjective qualities. That conclusion was likely reinforced by his claims about the efficacy of pain medications, as discussed in Chapter Two. Beecher also maintained a friendly correspondence with Moruzzi, and each hosted the other. Beecher Papers, Box 2, folder 37.
37. Alexander Barry in “Closing Remarks,” in Problems of Consciousness, vol. 5, ed. Harold A. Abramson (1955): 155–61, 160.
38. Nathaniel Kleitman, in discussion of his presentation chapter “The Role of the Cerebral Cortex in the Development and Maintenance of Consciousness,” in Problems of Consciousness, vol. 5, ed. Harold A. Abramson (1955): 111–32, 122.
39. Stanley Cobb, Borderland of Psychiatry (Cambridge, MA: Harvard University Press, 1943), 100. For a biographic review of Cobb’s career, see Benjamin V. White, Stanley Cobb: A Builder of the Modern Neurosciences (Boston: Francis A. Countway Library of Medicine/University Press of Virginia, 1984).
40. Henry Alsop Riley in “Discussion on papers by Drs. Von Bonin, Magoun, and Jasper and associates,” in Archives of Neurology and Psychiatry, 67, no. 2 (February 1952): 167–71, 167.
41. This experiment and its pointing towards a centrencephalic model are most fully described in Wilder Penfield, “Mechanisms of voluntary movement,” Brain 77, no. 1 (March, 1954): 1–17.
42. E. D. Adrian, The Physical Background of Perception (London: Oxford University Press, 1947).
43. A. E. Fessard, “Mechanisms of Nervous Integration and Conscious Experience,” in Brain Mechanisms and Consciousness, ed. J. F. Delafresnaye (Oxford: Blackwell, 1954), 200–36, 202. In his preface to these remarks in the published version of the transactions, Fessard includes a line from Heidegger’s Being and Time, “Der Sinn des Daseins ist die Zeitlichkeit,” translated as “the whole sense of Being is Time”. References to phenomenological writings appeared not infrequently throughout this physiological and scientific literature regarding the nature of consciousness, though not in a systematic enough way to draw firm conclusions about possible connections between interpreting physiological data and these descriptions of experience. Perhaps more detailed biographies of individuals like Jasper, Moruzzi, Magoun, Lashley, Penfield, and Fessard might be useful in sorting through connections between culture and modeling consciousness, in particular connections to other areas of philosophy. That interaction has potential to inform as well the overall interest in this book on reconsidering how to leverage and improve the sourcing of values from the unique perspective of medical facts.
44. Stanley Cobb, “On the nature and locus of mind,” Archives of Neurology and Psychiatry 67, no. 2 (February 1952): 172–77, 176–77.
45. N. Weiner, Cybernetics: or Control and Communication in the Animal and the Machine (New York: John Wiley and Sons Inc., 1948).
46. Quoted in Cobb, “On the nature and locus of the mind,” 174. See Mary Brazier, “A neuronal basis of ideas,” Dialectica 4 (1950): 73.
47. Norbert Weiner, I Am a Mathematician: The Later Life of a Prodigy (Garden City, NY: Doubleday & Company, Inc., 1956), 269.
48. Ibid., 291.
49. Lily E. Kay, “From logical neurons to poetic embodiment of mind: Warren S. McCullogh’s project in neuroscience,” Science in Context 14, no. 4 (2001): 591–614, 593. See also Michael Arbib, “Warren McCullough’s search for the logic of the nervous system,” Perspectives in Biology and Medicine 43, no. 2 (Winter 2000): 193–216. For a biography of his important and eccentric colleague Walter Pitts, see Neil R. Smalheiser, “Walter Pitts,” Perspectives in Biology and Medicine 43, no. 2 (Winter 2000): 217–26.
50. In the second edition of Cybernetics, Weiner essentially appends sections to his original work dealing with EEG phenomenon in a chapter on “Brain Waves and Self-Organizing Systems.” Cybernetics: or Control and Communication in the Animal and the Machine (Cambridge: MIT Press, 1969), 181–203.
51. See, for example, F. H. George, The Brain as a Computer (New York: Pergamon Press, 1961).
52. K. S. Lashley, Brain Mechanism and Intelligence: A Quantitative Study of Injuries to the Brain (Chicago: University of Chicago Press, 1929), 173.
53. In “General Discussion,” in Brain Mechanisms and Consciousness, J. F. Delafresnaye ed., 500.
54. Discussion in Philip Bard and Martin B. Macht, “The Behaviour of Chronically Decerebrate Cats,” in CIBA Foundation Symposium on the Neurological Basis of Behavior, eds. G. E. W. Wolstenholme and Cecilia M. O’Connor (Boston: Little, Brown and Co., 1958): 55–75, 72–73.
55. H. W. Magoun, The Waking Brain, 2nd ed. (Springfield, Ill: Charles C. Thomas, 1963 [1958]); Herbert H. Jasper, et al., eds., Reticular Formation of the Brain (Boston: Little, Brown & Company, 1958); GianFranco Rossi and Alberto Zanchetti, “The brain stem reticular formation,” Archives Italiennes de Biologie 9 (1957): 199–433.
56. Rossi and Zanchetti, “The brain stem reticular formation,” 404, 463, and 404.
57. Giusseppe Moruzzi, review of “Reticular formation of the brain,” EEG and Clinical Neurophysiology 11 (1959): 624–29.
58. Michael Jefferson, “Altered consciousness associated with brain-stem lesions,” Brain 75 (1952): 55–67, 59, 66.
59. Hugh Cairns, “Disturbances of consciousness with lesions of the brain-stem and diencephalon,” Brain 75, no. 2 (June 1952): 109–46.
60. Hugh Cairns, “Disturbances of consciousness with lesions of the brain-stem and diencephalon,” 113.
61. Percival Bailey, “Concerning the localization of consciousness,” Transactions of the American Neurological Association 80 (1955): 1–12.
62. Bonnie Ellen Blustein, “Percival Bailey and neurology at the University of Chicago, 1928–1939,” Bulletin of the History of Medicine 66 (1992): 90–113.
63. Bailey, “Concerning the localization of consciousness,” 9.
64. Ibid., 6.
65. Y. K. J. Gronqvist, Thomas Sheldon, and Albert Faulconer, “Cerebral anoxia during anesthesia: prognostic significance of electroencephalographic changes,” Annales chirurgiae et gynaecologiae Fenniae 41 (1952): 149–59, 155–56, 158.
66. J. Weldon Bellville, Joseph Artusio, and Frank Glenn, “The electroencephalogram in cardiac arrest,” JAMA 157, no. 6 (February 5, 1955): 508–10; J. Weldon Bellville and William S. Howland, “Prognosis after severe hypoxia in man,” Anesthesiology 18, no. 3 (May-June 1957): 389–97.
67. Bellville and Howland, ibid., 396.
68. One early report of such aggressive intervention is in J. C. Fox Jr., “Restoration of cerebral function after prolonged cardiac arrest,” Journal of Neurosurgery 6 (1947): 361, 1949. This paper is still cited in 1951 as the sole example of such resuscitative attempts for severe cerebral anoxia in a paper otherwise typical of period treatments of the subject in describing general typologies of different kinds of anoxic injury (e.g., “anoxic type,” “anemic type,” “stagnant type”), reiterating various theories about how this toxicity happens with a limited research base, and rehearsing well known relationships between limited time of complete anoxia and nerve cell death. See A. Theodore Steegmann, “Clinical aspects of cerebral anoxia in man,” Neurology 1 (1951): 261–74.
69. P. Mollaret and M. Goulon, “Le Coma Dépassé,” Revue Neurologique 101, no. 1 (1958): 3–15, 4.
70. P. Mollaret, Ivan Bertrand, and H. Mollaret, “Coma dépassé et nécroses nerveuses centrales massives,” Revue Neurologique 101, no. 2: 116–39. A pathology research literature would soon begin to develop, interested in the cellular events involved in the syndrome of a coma with loss of vegetative regulatory control. See W. Kramer, “From reanimation to deanimation,” Acta Neurologica Scandinavica 39, no. 2 (1962): 139–53.
71. M. Jouvet, “Diagnostic Electro-sous-corticographique de la mort du systeme nerveux central au cours de certains comas,” Electroencephalography and Clinical Neurophysiology 11 (1959): 805–8, 808.
72. H. Fischgold and P. Mathis, “Obnubilations, comas et stupeurs: ‘Etudes Electroencephalographique.” EEG and Clinical Electroencephalography Suppl 11 (1959), reported and abstracted in Daniel Silverman, “Retrospective study of EEG in coma,” Electroencephalography and Clinical Neurophysiology 15 (1963): 486–503.
73. Fred Plum and Jerome B. Posner, The Diagnosis of Stupor and Coma (Philadelphia: FA Davis Co., 1966).
74. See, for example, Fred Plum and August Swanson, “Abnormalities in central regulation of respiration in acute and convalescent poliomyelitis,” AMA Archives of Neurology and Psychiatry 80 (September 1958): 267–85.
75. See J. Hamburger in “Discussion” of the paper, “Organ transplants: practical possibilities,” in CIBA Foundation Symposium Ethics in Medical Progress—With Special Reference to Transplantation, eds. G. E. W. Wolstenholme and Maeve O’Connor (Boston: Little, Brown, and Co., 1966): 65–77, 74. Hamburger was chief of the renal unit at Hopital Necker, Paris, and used criteria outlined by G. P. J. Alexandre, the head of renal transplantation at Hopital St. Pierre, Belgium, part of the University of Louvain. In addition to fixed dilated pupils, unresponsiveness, total areflexia, apnea, and a flat EEG, Alexandre added falling blood pressure, which required increased vasopressor drugs. With the latter, internal homeostasis was disappearing and thus patients meeting his criteria usually died on the respirator within hours. See CIBA Foundation., 69–70. Reports from yet another French hospital in Lyon added to these criteria absence of cortical circulation. Murray was an active participant in these discussions and very familiar with these practices.
76. Joseph Murray, interview with the author, February 18, 1998.
77. See H. Fischgold in “Introduction-Utilization of EEG Signs of Cerebral Hypoxia During Open Heart Surgery,” in Cerebral Anoxia and the Electroencephalogram, eds. Henri Gastaut and John Stirling Meyer (Springfield IL: Charles C Thomas, 1961), 229–30.
78. B. Bergamasco, L. Bergamini, and T. Doriguzzi, “Clinical value of the sleep electroencephalographic patterns in post-traumatic coma,” Acta Neurologica Scandinavica 44 (1968): 495–511, 495.
79. A. Bricolo, A. Gentilomo, G. Rosadini, and G. F. Rossi, “Long-lasting post-traumatic unconsciousness,” Acta Neurologica Scandinavica 44 (1968): 512–32; Alberto Fois, Erna L. Gibbs, and Frederic Gibbs, “‘Flat’ electroencephalograms in physiological decortication and hemispherectomy (recordings awake and asleep),” EEG and Clinical Neurophysiology 7 (1955): 130–34.
80. Daniel Silverman, “Retrospective study of EEG in coma.”
81. A. Adams, “Studies on the flat electroencephalogram in man,” EEG and Clinical Electroencephalography 11 (1959): 35–41, 40.
82. H. Fischgold, in discussion of Nenad Bokonjic, Fritz Buchtal, “Postanoxic unconsciousness as related to clinical and EEG recovery in stagnant anoxia and carbon monoxide poisoning,” in Cerebral Anoxia and the Electroencephalogram, eds. Henri Gastaut and John Stirling Meyer, 118–27, 128.
83. E. Bental and U. Leibowitz, “Flat electroencephalograms during 28 days in a case of ‘encephalitis,’ ” EEG and Clinical Neurophysiology 13 (1961): 457–60.
84. Arne Lundervold, Tormond Hauge, and Aagot Loken, “Unusual EEG in unconscious patient with brain stem atrophy,” EEG and Clinical Neurophysiology 8 (1956): 665–70. See also Arne Lundervold, “Electroencephalographic changes in a case of acute cerebral anoxia unconscious for about three years,” EEG and Clinical Neurophysiology 6 (1954): 311–15. Here, a thirteen-year-old boy with asphyxia went for two months without electrical activity on EEG, developed EEG responses to some stimuli at fifteen months, and showed seizure patterns over two years after. In this case, the author is puzzled as to what to call consciousness and how to describe it neurophysiologically. He offers Jackson, Jasper, and Magoun as possible helpful sources pointing to the frontal lobes, thalamus, and RAS, respectively, but leaves the question open and unresolved.
85. Carlo Loeb, Guido Rosadini, and G. F. Poggio, “Electroencephalograms during coma,” Neurology 9 (1959): 610–18, 615. See also, with similar conclusions, Carlo Loeb, “Electroencephalographic changes during the state of coma,” EEG and Clinical Neurophysiology, 10, no. 4 (November 1958): 589–606.
86. Loeb, Rosadini, and Poggio, “Electroencephalogram during coma,” 618.
87. Gian Emilio Chatrian, Lowell E. White Jr., and Cheng-Mei Shaw, “EEG pattern resembling wakefulness in unresponsive decerebrate state following traumatic brain infarct,” EEG and Clinical Neurophysiology 16 (1964): 285–89.
88. C. Batini, G. Moruzzi, M. Palestini, G.F. Rossi, and A. Zanchetti, “Persistent patterns of wakefulness in the pretrigeminal midpontine preparation,” Science 128 (1958): 30–32. These experiments are described in some detail by Antonio Damasio in The Feeling of What Happens (1999). While updating understanding of these findings in light of hypotheses regarding the functions of the particular nuclei cut, Damasio concludes also that despite wakefulness and possible attention, even with “intact all of the structures necessary to implement the proto-self,” one of Damasio’s core aspects of consciousness served up by more subcortical structures, “whether or not normal consciousness would still be possible is a question that cannot be decided … and certainly will never be answered in humans.” Antionio Damasio, The Feeling of What Happens: Body and Emotion in the Making of Consicousness (New York: Harcourt, Brace and Co., 1999), 257.
89. B. R. Kaada, W. Harkmark, and O. Stokke, “Deep coma associated with desynchronization in EEG,” EEG and Clinical Neurophysiology 13 (1961): 785–89, 788
90. H. Cairns, et al., “Akinetic mutism with an epidermoid cyst of the third ventricle,” Brain 64 (1941): 273–90, 273.
91. Humberto Craviato, Jacobo Silberman, and Irwin Feigin, “A clinical and pathologic study of akinetic mutism,” Neurology 10 (1960): 10–21, 20.