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On July 11, 2003, newspaper headlines proclaimed the dramatic awakening of Terry Wallis, a 39-year-old Arkansas father who had been in a “coma” after suffering a head injury in a July 1984 car accident. He had been riding with a friend when their car plunged into a creek. When they were found under a bridge the next day, his friend was dead and Wallis was comatose. But now, 19 years later, he was talking. His ﬁrst words were “Mom” and then “Pepsi,” and, over the ensuing weeks, he began to speak with greater ﬂuency. He apparently had no memories of the intervening time. In his world, Ronald Reagan was still president. The media described his recovery as a “miracle,” and his doctors were stunned. What occurred seemed scientiﬁcally beyond the realm of possibility.
Despite the very unexpected (and as yet unexplained) nature of what happened to Wallis, we were, perhaps, less surprised than many people. For a decade we have been conducting research at the frontiers of understanding impaired consciousness and the ethical challenges posed by devastating brain injury. We have seen other patients like Wallis, whose improvements, although less heralded, also defy our understanding of impaired consciousness that follows brain injury. Our goal has been to understand both the mechanisms of recovery and biological differences between those patients who remain forever unconscious after catastrophic injury and those who regain at least limited awareness.
From our own research and that of a handful of other cognitive neuroscientists, we knew that the media’s portrayal of Wallis’s condition before he recovered was inaccurate, at best, and, at worst, seriously misleading. Although he was portrayed as being in an irreversible coma, or in a vegetative state, Wallis was in neither. He had not been in a coma immediately before his recovery, because “coma” describes a state of unconsciousness typically lasting only weeks from the time of injury. Comatose patients usually either recover or slip into various longer-term states of impaired consciousness. A review of literature about Wallis indicates that his behavior during the 19 years after the accident was also inconsistent with being in a vegetative state. He had been able to respond to simple questions with a nod of the head or with grunting sounds, indicating some level of awareness and interaction with his environment—neither are seen in the vegetative state. These behaviors, noted before his dramatic recovery, suggest a state that scientists are only beginning to characterize: the minimally conscious state.1
The importance of these distinctions cannot be overstated. Identifying those patients with severe brain injuries who have a chance of recovering is the ﬁrst step in deciding who may beneﬁt from the therapeutic approaches now being developed that might help them to regain function and independence. Having said that, we come face to face with a puzzling paradox: Why has this progress in understanding impaired states of consciousness been met by a surprising lack of interest—not to say an attitude of dismissal—on the part of the scientiﬁc community and society at large?
Our Hidden Epidemic of Traumatic Brain Injury
At the outset, we should appreciate that what happened to Wallis when he was 20 years old is an all-too-common story. Although most of us do not think about traumatic brain injury (TBI) until a family member is touched by its tragedy, its incidence is staggering. TBI is the leading cause of long-term disability in children and young adults and, in the United States alone, has 1.5 to 2.0 million victims a year. Motorcycle, automobile, and sporting accidents are among the most frequent causes. The toll of TBI is still more graphically demonstrated when we consider that head trauma has left between 2.5 and 6.5 million people in the United States with some degree of permanent impairment. The yearly cost for new cases of TBI is between $9 and $10 billion, and lifetime costs per individual have been estimated to be between $600,000 and $1,875,000.
Even these numbers, however, fail to do justice to the burden of TBI. Lives are suddenly and irrevocably altered by severe head trauma. If a patient is lucky enough to survive the acute phase of injury and intensive care, but remains severely impaired, he may face years of rehabilitation on the road to recovery. Unfortunately, rehabilitation services are often limited, and third-party payment depends on evidence of the patient’s continual improvement and on demonstration of what is called “medical necessity.” Some patients move from hospital to rehabilitation facility and then return to a life that is markedly different from their former existence. Such was the experience of Trisha Mellie, whose autobiography, I Am the Central Park Jogger, tells the story of a young investment banker attacked while jogging in 1988 and her recovery from that nearly fatal attack. Mellie describes how she had to relearn all the tasks she had once mastered as a child and to develop new strategies to compensate for her loss of cognitive function. Even more daunting, she had to grapple not only with memory loss but with the realization that her injury had changed who she was as a person.
As monumental a challenge as Mellie faced, another class of patients with TBI has sustained even greater impairment. This class includes people such as Wallis, who recover from their acute injuries and have (perhaps minimal) evidence of cognitive awareness but fail to meet the criteria for medical necessity required to qualify for intensive ongoing rehabilitation. Our health care system fails them and their families. After a brief period of coma rehabilitation—or none at all—they are exiled to nursing homes for what is often impolitely called “custodial care.” The experience of Wallis and his family is not unusual. His parents report that, after the accident, Terry was never seen by a neurologist. He was placed in a nursing home, and his family was told that an evaluation would be expensive. His father said to reporters, “They told us it would cost $120,000 just to evaluate him to see if he could be helped, and we didn’t have that kind of money.” The Wallis family applied for Medicaid to cover the cost of evaluation but was turned down. “They said the government will not put out that kind of money on no more chance than he’s got to re-enter the workforce,” reported his father.
Even if the government was correct that the cost of evaluation would be more than Wallis’s potential wages if he recovered, what is our ethical obligation to patients like him? We think society owes the many people with TBI, and their care givers, some intellectual curiosity about severely impaired consciousness, as well as the potential fruits of scientiﬁc investigation. In the light of new understanding of various brain states after injury, clinicians, patients, and their families need accurate information to make informed choices about care. But, sadly, many clinicians are themselves ill informed, so they are unable to discuss the options for treatment—or refusal of it—in a meaningful way. If a society must ration scarce resources, the decision about who to treat should be based on the best available science and an accurate assessment of diagnosis and prognosis. Such clinical precision seems to be the least that physicians should demand of themselves when caring for these patients.
States of Disordered Consciousness: A Primer
What brain states can follow head injury? The immediate consequence of a severe brain injury, like the one that Wallis sustained, is a loss of consciousness that results in a brain state known as coma, an “unarousable unresponsiveness.” The person does not respond to vigorous efforts to elicit a response of any kind—sound, movement, or eye-opening—and shows no variation in behavior, simply a sleeplike state with eyes closed.
The prognosis for someone in a coma very much depends on the person’s age, the amount of structural damage (as identiﬁed by brain imaging), and whether there is evidence of direct injury to the brainstem. From coma, very severe brain injuries can progress to brain death, a total loss of whole brain function, including brainstem activity. In other cases, the comatose state, if uncomplicated by other factors, is typically followed within 7 to 14 days by an indeterminate period during which an eyes-open, “wakeful” appearance alternates with an eyes-closed, “sleep” state. These alternating periods represent a limited recovery of cyclical change in arousal pattern and characterize the vegetative state (VS), as originally deﬁned by Bryan Jennett, M.D., and Fred Plum, M.D., in 1972.2 In all other respects, the vegetative state is similar to coma. Patients in vegetative states demonstrate no evidence of awareness of self or response to their surroundings. If the patient remains in a vegetative state for more than 30 days, he is deemed to be in a persistent vegetative state (PVS). Prospects for the recovery of consciousness become grim when the vegetative state becomes chronic or permanent, after three months in the case of anoxic injury, caused by oxygen deprivation, and a year following traumatic injuries.
In other cases, a patient may recover to the point of very limited but deﬁnitely observable responses to his environment. Such a patient is classiﬁed as in a minimally conscious state (MCS). In this condition, a patient exhibits bits of directed behaviors that are different from the reﬂexive behaviors seen in PVS patients. The difference is that MCS patients demonstrate unequivocal—albeit ﬂuctuating—evidence of awareness of self or the environment. Limited behavior exhibited by MCS patients can include basic verbalization, gestures, memory, attention, intention, and awareness of self and environment.
To know that a patient has emerged from MCS, we must observe consistent functional communication. Crossing this threshold requires more than the ability simply to follow commands. For example, a patient may be able to correctly identify a printed “yes” or “no” on a card held up by an examiner but not be able to answer questions reliably using such signaling. The patient would be considered only at the borderline of emergence from MCS.
In Terry Wallis’s case, we see him emerging from MCS after he passed through an initial coma and a period in the vegetative state. Although Wallis has often been described as vegetative right up until he began to speak, in fact he had been able (possibly within the ﬁrst year after his accident) to respond to simple questions with a nod of his head or grunting—hallmarks of MCS. If so, his pattern of recovery is wholly consistent with scientiﬁc understanding of the recovery of consciousness from a vegetative state resulting from traumatic brain injury.
Because the progression from PVS to MCS may take months following a traumatic brain injury, physicians who do not fully understand what is happening, and rely solely on their observations of a patient, can have unnecessarily negative expectations for the patient’s recovery. Information about the patient’s underlying brain function, gained from neuroimaging, may change those expectations. New neuroimaging techniques may eventually become an important adjunct to careful neurological examination and lead to much earlier identiﬁcation of patients like Wallis who may be able to emerge from MCS. Just as surely, though, they might tell us that no further recovery can be expected, even if a patient exhibits some limited behavior above a vegetative level. Having more knowledge, sooner, will bring hope to some and despair to others.
Seeing into the PVS Brain
The ﬁrst brain-imaging studies of PVS patients were done by Fred Plum, M.D., David Levy, M.D., and their colleagues in the early 1980s using a technique called ﬂuorodeoxyglucose positron emission tomography (FDG-PET). This imaging technique measures how much energy the brain is consuming. Plum and Levy discovered that overall brain-tissue metabolism in PVS patients was half or less than half of normal.
On the basis of their work, we can now pose a critical question: What functional activity might remain in severely injured brains? Seeking an answer, together with Plum, we have collaborated with research groups at the New York University Center for Neuromagnetism (directed by Urs Ribary, Ph.D., and Rodolfo Llinas, M.D., Ph.D.), and the Memorial Sloan-Kettering Center (directed by Brad Beattie, Ph.D., and Ron Blasberg, M.D.). To try to size up the remaining functional activity in several PVS patients, we used three neuroimaging techniques: magnetic resonance imaging (MRI), magnetoencephalography, and quantitative PET analysis.3 What we have discovered is new evidence that the persistently vegetative brain can harbor still functional, but isolated, networks and that these networks, at times, can generate recognizable fragments of behavior.
We became interested in the possibility of this residual function through the case of a 49-year-old woman who had suffered a series of cerebral hemorrhages as a result of malformed blood vessels in her brain. Despite some two decades in PVS, this woman occasionally uttered single words (typically expletives) without any external stimulus. MRI imaging showed that her right basal ganglia and thalamus were destroyed, and FDG-PET measurements conﬁrmed a marked overall reduction of more than 50 percent in overall brain-tissue metabolism, which is consistent with what we know of cerebral metabolism in PVS. What was intriguing, though, was that several isolated, relatively small regions in her left hemisphere showed higher levels of metabolism. These regions, in the normal adult brain, are associated with language functions. Two other patients we studied also revealed isolated metabolic activity in the brain that could be correlated with other unusual patterns of behavior. It seems, then, that residual cerebral metabolic activity that remains after severe brain injuries is not random; it is tied to local cerebral networks that have been preserved and to patterns of neuronal activity.
The work of other scientists helps to ﬁll in the picture. Using a different PET technique, David Menon, M.D., and his colleagues in Cambridge, England, found that a patient who was recovering from PVS into MCS had isolated neural networks that responded to human faces. Steven Laureys, M.D., and his colleagues in Belgium have examined functioning in the PVS brain by comparing its responses to simple auditory and other stimuli with its baseline resting state. For both types of stimuli, these PVS patients demonstrated a loss of brain activation in so-called higher-order regions —regions outside of their primary sensory cortices.4 This seems to indicate that there is a wholesale disconnection between functions in the PVS brain that prevents basic sensory input from being processed anywhere but the earliest cortical levels. This evidence is consistent with our own results and supports the conclusion that residual cortical activity seen in PVS patients does not signify any awareness.
One additional observation may shed light on the signiﬁcance of residual islands of activity in the PVS brain. The observation involves one patient who had exceptionally widely preserved metabolism in the cerebral cortex, despite six years in a vegetative state after a trafﬁc accident. The patient’s behavior had been completely unremarkable. The unusual observation was that this patient’s cortical metabolism was near normal, except for marked reductions in the severely damaged region of the upper brainstem and central thalamus. We conjectured that this well-preserved cortical metabolism probably meant that there were many partially functioning brain networks. In other words—and this is crucial—nothing linked these islands of activity as before the injury. It is relevant that the upper brainstem and central thalamus regions were damaged in this patient because those regions have a critical role in the functional integration of parallel neural networks. In a different patient, who had recovered from a vegetative state, Laureys had identiﬁed a return of activity in these regions.
Inside the MCS Brain
Everything we had learned about the brains of PVS patients made us want to study what remaining cerebral activity might be found in MCS patients, particularly those recovering almost to the level of emergence from MCS. Patients who remain near this borderline raise different questions. What underlying mechanisms could be limiting their recovery of communication? In collaboration with Joy Hirsch, Ph.D., and her colleagues, we studied two such patients and compared what we found with our ﬁndings in PVS patients.5 Both MCS patients could intermittently follow simple commands with eye movements, occasionally made attempts to vocalize, and showed signiﬁcant ﬂuctuations in their responses. Would their brains respond to language? To test this, we played them taped narratives, spoken by a familiar relative. Tapes were played both as normal speech and backward.
We found that when the story was played forward, as normal speech, the two MCS patients showed activation of cerebral networks underlying language comprehension. The activation was similar to activation in normal subjects. Not so for the tape played backward. Normal subjects showed similar activation patterns for both, but the MCS patients failed to activate the language comprehension networks when they heard the tape reversed. This failure indicates to us that in some MCS patients there are forebrain networks that might be potentially functional, yet fail to establish the patterns of activity needed for consistent communication. The preservation of forebrain networks associated with higher cognitive functions, such as language, could provide a neurobiological basis for wide ﬂuctuations in behavior, such as was observed in Terry Wallis.
Obviously, these studies suggest the crucial importance of functional integration. Although these MCS patients demonstrated functioning forebrain networks and could respond to forward language, their overall resting cerebral metabolism was low, near PVS levels. To our surprise, we also found that these patients seemed to have intact integrative responses in both cerebral hemispheres. This leads us to believe that differences in the integration of functions, more than levels of resting brain activity, are what separate PVS from MCS.
Emerging from MCS
With this insight about what may be happening in the brains of some patients with severe brain injury, we can revisit the question: How could someone like Terry Wallis harbor residual cognitive capacities that lay dormant for so many years? One possibility is that, over time, as patterns of activation come and go in intact regional networks, one result may be improved awareness and cognition; but another result, exactly the contrary, may be the inhibition of recovery.
From a physiologic standpoint, several mechanisms may possibly be at work here, yielding changes in the capacities of patients who have complex brain injuries. How and to what extent these mechanisms may limit recovery, we do not know, as yet, but several observations are suggestive. It is relatively common, even after a localized stroke or brain injury, to have reduced cerebral metabolism in brain regions that are remote from the site of injury. The cause seems to be a loss of excitatory inputs from nerves at the site of the original injury. This process, which is reversible, results from a strong inhibition of the distant neurons brought about by a lack of incoming synaptic activity.
Another mechanism that conceivably could affect the delicate balance of excitation and inhibition is abnormally increased synchronization of populations of neurons (such as is seen in epilepsy and other brain disorders). It is possible that, following structural brain injuries, such changes may arise in speciﬁc brain networks that play an important role in the functional integration of networks in the normal brain. An alteration of this kind could have played a role for Wallis, limiting his capacity for producing speech through active inhibition of language networks. While this explanation is, of course, speculation, some kind of functionally reversible process must play a role in such cases. Wallis’s doctors speculated that adding the antidepressant Paxil to his medications could have been connected in some way with his later recovery of speech, although he had taken Paxil for 18 months before his recovery. Did this antidepressant have a role in slowly changing his patterns of cerebral integration, and eventually unmasking residual function in his brain?
As neuroimaging is used to study additional patients with severe brain injuries, more questions will arise about the mechanisms underlying their functional disabilities. For patients like Wallis, neuroimaging could also reveal previously unrecognized residual capacities that can be at least partially restored by new kinds of therapy.
Exploring Deep Brain Stimulation
If some patients with severe cognitive impairment could be limited, in part, by a lack of functional integration among intact regions of their brains, we should look for ways to foster reintegration. Patients like Wallis who have recovered to functional levels that are near the threshold of emergence from MCS would be the ﬁrst likely candidates for new therapies to improve consistent communication. Of many new medical technologies, the most promise may lie in emerging techniques for deep brain stimulation.
Over the past 15 years, deep brain stimulation has advanced the treatment of drug-resistant Parkinson’s disease, sometimes dramatically, and is approved by the Food and Drug Administration for that use. More than 15,000 patients with Parkinson’s have been treated, to date, and new uses of deep brain stimulation are being investigated to help patients with chronic pain, epilepsy, and psychiatric disorders such as depression and obsessive-compulsive disorder.
In an interdisciplinary project with the Cleveland Clinic Foundation, the JFK-Johnson Rehabilitation Center, and the Columbia University Functional MRI Research Center, we have been planning how to use deep brain stimulation to raise the functional level of MCS patients. Our efforts follow some provocative work over the past two decades that studied this technique with patients in a vegetative state (including, in fact, Terry Schiavo). Speciﬁcally, there have been several attempts to use deep brain stimulation in regions of the central thalamus, an area with many connections to the cerebral cortex. Activating these brain regions with an electrical current induces many of the standard signs of arousal, conﬁrming experiments with animals in which electrical stimulation induced wakeful arousal. Unfortunately, in some 50 PVS patients studied worldwide, the stimulation evoked no evidence of sustained recovery of interactive awareness.
In contrast, deep brain stimulation did succeed in bringing about signiﬁcant physiologic responses in PVS patients, who had large increases in global and regional cerebral metabolism and changes in brain wave activity toward a more normal proﬁle for a wakeful state. The behavioral and physiologic arousal seen in all the patients demonstrated that, despite overwhelming brain damage, it was still possible to activate the cortex. It may be that, given the overwhelming brain injury in PVS, this increased activation was not enough to restore interactive awareness.
The areas electrically stimulated in these PVS patients are parts of the thalamus that are known to link a state of arousal with some aspects of moment-to-moment behavior. Here, then, is a new rationale for using deep brain stimulation in MCS patients who demonstrate limited integrative forebrain activity. Unlike the PVS patients—who initiate no behavior, follow no commands, and attempt no communication—MCS patients near the borderline of emergence typically have changes in cognitive functioning that come and go over hours, days, weeks, or even longer. This ﬂuctuation might be the result of unstable interactions of the arousal state with the organization and maintenance of behaviors, which these patients can initiate, but not sustain. If so, then deep brain stimulation of the central thalamus might improve integration in the damaged networks that underlie these limited behaviors. By contrast, functional and structural neuroimaging studies demonstrate these networks in patients with chronic PVS have been overwhelmingly damaged.
Before we can go beyond these planned pilot studies of deep brain stimulation in MCS patients, the criteria for selecting patients must be worked out, and important ethical questions considered.
At present, it seems that those who have recovered to functional levels near the threshold of emergence from MCS could be the ﬁrst candidates for new therapies to improve consistent communication. But new therapies for patients with severely impaired consciousness encounter challenges in the form of attitudes and preconceptions that could pose greater difﬁculties than the science. In particular, as we work with MCS patients, we will have to address two sources of skepticism: the right-to-die movement and the troubled record of psychosurgery.
Seeking a New Moral Warrant
The ﬁrst hurdle will be for our society to reexamine its attitudes toward patients with severe brain injury, attitudes shaped by the right-to-die movement. By taking to heart the possibility of new hope for these patients, we are asking for a moral warrant to intervene in patients who resemble those patients for whom the right to die was ﬁrst established in the 1960s and 1970s. This hard-won—and important—right was vouchsafed to patients closest to death and for whom, therefore, the withdrawal of life-sustaining therapy seemed justiﬁable: patients with permanent and irreversible loss of cortical function.
Because the futility of any potential treatment was pivotal in justifying the right to die for PVS patients, many physicians remain nihilistic about potential interventions in these patients with severely impaired consciousness. Why bother, they wonder, because these people are essentially dead? In ruminations like these, which underlie judgments but are seldom explicitly voiced, people echo perceptions that were critical in establishing the rights of patients to refuse life-sustaining therapies. In the seminal 1976 Karen Quinlan case, the New Jersey Supreme Court allowed the removal of life-sustaining therapy because Quinlan was in a vegetative state without, they held, any possibility of return to a “cognitive sapient state.” In 1968, a similar justiﬁcation was urged by Harvard anesthesiologist, Henry K. Beecher, M.D., when he advanced the concept of brain death, although that was in the context of seeking organs for transplantation. In both cases, however, the moral value placed on life and death hinged, in large part, on a person’s cognitive state.
We hope, of course, to intervene for patients who are in the minimally conscious state, not the hopeless condition of chronic PVS patients, but the various states are often conﬂated or simply confused or the crucial differences among them are considered unimportant. The sense of nihilism is so pervasive that even the delineation of MCS in the scientiﬁc literature has come under attack from some medical quarters.
We believe that reﬁning the deﬁnitions of brain states is value neutral, but many physicians have resisted this diagnostic clariﬁcation. Some proponents of the right to die have been concerned that this newly identiﬁed brain state might erode the hard-won right to forgo life-sustaining therapy. Disability advocates have also voiced their concern, worrying that adding MCS to the categories of impaired brain states could be used nefariously to equate higher functioning individuals with those in PVS, thus minimizing the value of their lives.
For the record: We support both the right to die and the right to appropriate medical care. We do not see these rights as mutually exclusive, and we view decisions to pursue or refuse care as a matter of ethically balancing the potential beneﬁts and burdens. What is interesting about the discord over MCS is not that the designation could justify either more treatment or less in any particular case, but, rather, how emotionally charged the entire issue has become. As a response to discussion of the designation’s scientiﬁc basis, the reactions seem way out of proportion. If nothing else, they are a cultural marker for our implicit assumptions about severe cognitive impairment.
The Specter of Psychosurgery
Progress in developing therapies for severe cognitive impairment will also be hampered by the association of deep brain stimulation with psychosurgery and the abuses that have marred its history. News stories about deep brain stimulation often allude to the crude and unjustiﬁable lobotomies performed by Walter Freeman, a neurologist who performed more than 3,000 procedures on mentally incapacitated patients, and to the specter of mind control. These fears harken back to the debate over psychosurgery in the late 1960s and early 1970s, when Spanish neurophysiologist Jose M. R. Delgado, M.D., advanced the use of an implantable electrode operated by remote control as a way to “psychocivilize society” and cope with the social unrest of the day. Delgado had already won some notoriety by using his “Stimociever” to halt a charging bull in a bullring in 1965. His work entered popular culture through novels and ﬁlms like Michael Crichton’s Terminal Man and Stanley Kubrick’s A Clockwork Orange.
Concerns about the ethics of psychosurgery moved the U.S. Congress to direct the National Commission for the Protection of Human Subjects of Biomedical and Behavioral Research to report on psychosurgery as part of the landmark National Research Act of 1974. The Commission did not ﬁnd that psychosurgery had been used for social control; in fact, it found enough evidence of potential efﬁcacy to recommend that the investigational use of some psychosurgical procedures proceed with appropriate regulation and oversight. This conclusion ran against popular opinion at the time, and popular opinion has never really changed.6
Moving Beyond Scientific Statis
Whatever the merits of deep brain stimulation in neurology and psychiatry (and we believe the merits are potentially great), public perception of its value and even its ethical standing is colored by the legacies of the right-to-die movement and psychosurgery. We believe that this perception does a profound disservice to some of our society’s most desperately burdened patients by contributing to their being marginalized and even abandoned. When patients with severe cognitive impairment across the whole spectrum of such conditions are perceived as beyond hope, any potential interventions that might be developed are automatically deemed ethically disproportionate.7 When this perception is combined with the problem that individuals with severe head trauma often lack the capacity to make decisions and, therefore, cannot give their own consent to enroll in clinical trials, you have a recipe for scientiﬁc deadlock.
Future Terry Wallises deserve better. They deserve protection from errors of commission, but equally of omission. They desperately need access to the fruits of science and all the assistance we can provide as they return from the limbo of impaired consciousness and try to reenter the world of human interaction.
The Hidden Epidemic of Traumatic Brain Injury in the United States
- 1.5 million TBI injuries occur every year.
- 50,000 people die from their injuries.
- 80,000 to 90,000 people experience long-term or lifelong disability as a result of their injuries.
- 2,000 people enter a persistent vegetative state following their injuries.
- One-third of all injury deaths are the result of a TBI.
- The cost of TBI is estimated to be more than $48 billion each year, including $10 billion for new cases.
The Most Frequent Causes of Traumatic Brain Injury in the United States
- Vehicle crashes: This includes motor vehicles, bicycles, recreational vehicles, and pedestrians.
- Firearms: Firearm use is the leading cause of death relating to a TBI, and 90 percent of people with a firearm-related TBI die.
- Falls: Falls are the leading cause of TBI among the elderly, and 60 percent of fall-related TBI deaths involve people over 75.
- Giacino, JT, Ashwal, S, Childs, N, et al. “The minimally conscious state: definition and diagnostic criteria.” Neurology 2002; 58(3): 349-353.
- Jennett, B. The vegetative state: medical facts, ethical and legal dilemmas. Cambridge University Press, 2002; Jennett, B and Plum, F. “Persistent vegetative state after brain damage. A syndrome in search of a name.” Lancet 1972; 1: 734-737.
- Schiff, ND, Ribary, U, Moreno, DR, et al. “Residual Cerebral Activity and Behavioural Fragments Can Remain in the Persistently Vegetative Brain.” Brain 2002; 125: 1210-1234.
- Laureys, S, Faymonville, ME, Peigneux, P, et al. “Cortical processing of noxious somatosensory stimuli in the persistent vegetative state.” Neuroimage 2002; 17(2): 732-741.
- Hirsch, J, Kamal A, Moreno, D, et al. “fMRI reveals intact cognitive systems for two minimally conscious patients.” Society for Neuroscience, Abstracts 2001; 271(1):1397.
- Fins, JJ. “From Psychosurgery to Neuromodulation and Palliation: History’s Lessons for the Ethical Conduct and Regulation of Neuropsychiatric Research.” Neurosurgery Clinics of North America 2003; 14(2): 303-319.
- Fins, JJ. “Constructing an Ethical Stereotaxy for Severe Brain Injury: Balancing Risks, Benefits and Access.” Nature Reviews Neuroscience 2003; 4: 323-327.