Comatose Awareness as Medical Science

Comatose Awareness

As medical science evolves, more is learned about the human body. With this knowledge, and the medical practices that naturally stem from this increased knowledge, often comes great moral debate. Of these, coma victims have received much debate, due to the still somewhat mysterious nature of the state. Whether or not medical intervention is appropriate for patients suffering from a persistent vegetative state is one of the most morally and legally debated topics in medicine today, spurred by cases such as Terri Schiavo. In Canada, Robert Kenneth Durksen, a 47-year-old Royal Canadian Mounted Police officer suffered from a coma brought on by severe brain injury in a plane crash in June of 1999. Durksen required intravenous hydration and nutrition to remain alive. Three months after remaining in a coma, his family sought the appointment of a public guardian, to make the decision whether or not to continue life support. The guardian turned to the courts, who eventually granted the application for the discontinuation of nutrition and hydration (Godlovitch, Mitchell, & Doig 1172).

Cases like Shiavo and Durksen put the morally quandaries regarding comatose victims to the forefront of the public's mind. Only by fully understanding the condition, and answering questions such as whether or not there is awareness in comatose patients, can the public make informed decisions, when these sensitive situations occur. This paper will give an overview of the comatose condition, followed by a review of literature regarding awareness in comatose patients, and then present conclusions drawn from this information, in hopes of shedding further light on such a delicate topic.

Comatose Overview:

The medical term comatose is derived from the Greek word koma, meaning a deep sleep. A comatose patient is in a deep state of unconsciousness that is characterized by the loss of reactivity to external stimuli and absence of spontaneous nervous activity, and cannot be awakened. Coma victims have usually experienced injury or disease of the cerebrum (Steinberg 18).

The origin of the injury affects the different patterns of coma. Losses of consciousness for short durations may be caused by concussions, whereas the lack of oxygen, or anoxia, may lead to a coma that lasts for several weeks or is fatal. Sudden loss of consciousness in some patients may be caused by a stroke, which is a rupture or blockage of the vessels that supply blood to the brain. In contrast, the gradual onset of comas is typically associated with metabolic abnormalities or cerebral tumors, with stages of lethargy and stupor occurring before true coma occurs. These metabolic comas are also more likely to have associated brain seizures, and typically leave papillary light reflexes intact (Steelman et al. 201). Patients suffering from coma due to physical causes usually do not experience this reflex.

The causes of coma are varied including, as noted, metabolic disorders or physical injuries to the brain from disease or trauma.

These can include acute neurological injuries such as hypoxia or stroke, or may be due to central nervous system diseases, metabolic abnormalities, or even severe intoxication, to name a few (Leviton 18). A coma like state may also occur in some psychiatric conditions, such as catatonic schizophrenia. In general, there is an impairment of the brainstem or the cerebral cortex functions. If the brainstem becomes compressed by swelling of other parts of the brain, such as occurs in encephalitis or following a concussion, coma can occur.

In addition, cerebral cortex disease can also cause coma. These "metabolic brain dysfunction such as hypoglycemia, endocrine disorders such as diabetes, brain tumors, drug overdose and poisoning, acute alcoholism, and oxygen deprivation" (Leviton 65). Many patients who suffer from epilepsy, narcolepsy, repeated incidents of low blood sugar, or reduction of blood supply to the brain, specifically the brainstem, may experience brief periods of coma.

Metabolic coma is often associated with diabetes, excessive alcohol ingestion, and barbiturate poisoning. Low insulin levels, in diabetics, allow the buildup of ketones. Ketones breakdown products of fat tissue that destroy the osmotic balance in the brain, which leads to brain cell damage. When coma is induced by excessive alcohol consumption, the patient may be treated by gastric lavage (stomach pump), during the early stages. A common cause of coma in suicide attempts is due to combined alcohol and barbiturate consumption, which produces a suppressed cerebral blood flow, resulting in anoxia. Gastric lavage shortly after barbiturate ingestion may remove sufficient quantities of the drug from the system to allow for recovery. The first step in treatment, for most metabolic comas, is to protect the brain cells and attempt to eliminate the cause of the coma. In many cases, assisted ventilation is needed. and, in most patients awaken from a coma within two to four weeks, despite the severity of the original injury (Leviton 65).

A considerable body of recent clinical data lends credence to the concept of coma actuarial tables, say Plum and Posner. In one study of 226 patients in coma, 54% died in the first month and 69% of those initially awake and responsive" recovered within a year. In another study of 500 coma patients, 76% died in the first month and 88% by the end of one year (Leviton 65).

Literature Review Regarding Comas and Coma Awareness:

Davis and Gimenez define coma as "an unarousable, unresponsive state without eye opening, verbalization, or ability to follow commands" (202). The researchers note that coma can occur due to a variety of local or diffuse injuries that disrupt reticular activating system (RAS) of the brainstem. RAS maintains arousal, the foundational element of information processing. More complex cognitive processes, including the sustained attention or concentration that is necessary for learning, cannot occur without arousal. When coma occurs, it disrupts the arousal mechanism and interferes with the individual's ability to respond to external stimuli. According to Davis and Gimenez, comas of the duration of 24 hours or more have been linked to poor recovery and impaired functional outcomes.

Facklemann explores the case of Karen Ann Quinlan, a young woman who died while comatose in the mid-1980s. Quinlan had been drinking gin and tonics with friends in 1975, while taking the tranquilizer Valium, and on the painkiller Darvon. The near-lethal combination stopped Quinlan's heart and respiration. Paramedics revived Quinlan, but she had already lapsed into a coma; her brain damaged by the lack of oxygen due to the cardiopulmonary event. After a court-ordered removal of the ventilation system, Karen continued to breathe without assistance. She progressed through normal sleep/wake cycles, with her eyes opening in the morning, but no other responses were experienced. A decade later, Quinlan died of massive infections (10).

Following her death, an autopsy was performed on Quinlan and her brain preserved in formalin. Three years later Hannah Kinney, a pathologist as Children's Hospital in Boston, was asked to study Quinlan's brain. Her research yielded surprising results. Previous studies had shown that people in comas typically showed extensive damage to the cerebral cortex, where memory, thought, language, and intellect are thought to occur. Quinlan's cortex was relatively intact. Instead, the damage was to the thalamus, where all sensory input, other than smell, goes through the thalamus before going to the cortex. This finding indicates that not only can damage to the cortex lead to coma, but also injury to the thalamus as well, and that the thalamus may be significantly linked to human awareness (Fackelmann 10).

Steinberg discusses whether vegetative and minimally conscious states expose the cerebral substrates of awareness. He notes that scientists are still unsure of why some patients awaken from comas, while others never do, citing the case of Terri Schiavo, who upon autopsy revealed a brain that had atrophied to approximately half of its normal weight, after 13 years in a coma, and that of Donald Herbert who after ten years in a coma awoke asking to speak to his wife. However, despite the many mysteries, Steinberg notes that brain-imaging technology is finally revealing some clues. Brain-imaging scans have already demonstrated the relationship between consciousness disorders and disrupted neural connections and decreased cerebral metabolism. It is hoped that someday these scans will be able to track and predict a patient's awakening (17).

Steinberg further cites Adrian Owen's research, a cognition and brain sciences expert, at the MRC Cognition and Brain Sciences Unit in Cambridge, UK. In this study, a comatose patient was scanned with positron emission tomography (PET). The scan indicated that certain regions of the brain of the comatose patient reacted similarly to spoken English sentences as that of fully conscious subjects. Functional magnetic resonance imaging (fMRI), nine months later demonstrated that the comatose patient's cortex had responded partially to semantically ambiguous sentences, which is thought to indicate higher levels of speech comprehension (See Figure 1). The researchers speculated that with the patient entering a minimally conscious state after these tests, that they may have picked up on his emergence from the perpetually vegetative state (17).

However, as Steinberg notes, there still are doubts in the scientific community about imaging's potential to elucidate consciousness. Although new information correlates fMRI with neuronal firing, scans typically detect hemodynamic, not neuronal, activity. They do not show what people perceive, and, in the end, this is what consciousness is (18).

According to Steinberg, PET studies of vegetative patients have indicated "that the primary sensory cortices respond to pain and sounds, but that higher-order associative cortices do not. For minimally and fully conscious people, in contrast, sounds activate associative areas as well" (18).

A study of minimally conscious patients exposed patients to recorded narratives. Similar brain activity was found in both healthy control subjects and the patients. However, when the recording was played backwards, only the healthy controls' cortices were activated, indicating that only fully conscious brains are engaged by ambiguous stimuli.

Figure 1:

Source: Steinberg 17)

Leviton concurs with Davis and Gimenez's work. Arousal is surmised to be linked with cognition. but, he cites Plum and Posner as noting that the limits of consciousness are difficult to define quantitatively and satisfactorily. Self-awareness is inferred by appearance and actions. Some degree of arousal is needed for cognition (65).

When physicians talk to their patients who are comatose as if they are aware, Leviton notes, they sometimes get startling results. He cites John La Puma MD, the Director of the Center for Clinical Ethics at Lutheran General Hospital in Park Ridge Illinois, and his experience with talking with comatose patients. La Puma assumed that comatose patients hear, and therefore talking with them would have potential therapeutic value. He noted that many had "normal physiological responses to auditory stimuli" (66), and therefore not talking to comatose patients may give the patients the notion that they are dead, or nearly dead, becoming a self-fulfilling prophecy.

In contrast, if comatose patients hear, then some cognitive functions may still be present, despite the brain damage. Although they may be physiologically helpless, they may not be as vegetative as the medical community has previously assumed. This, as Leviton notes brings up a significant moral dilemma for the medical profession. "If the patient indeed isn't hopelessly vegetative, then medical decisions about life support must include his views. Most M.D.'s don't want even to consider it" (67).

Leviton provides anecdotal evidence purported by La Puma. The doctor has noted several examples of patients that have emerged from comas and commented on what he had said to them. In addition, a patient that had been in a coma for fifty-three days had informed her doctor that when he was tending to her while unconscious, she would wonder why he never said hello to her, nor acted as if she were there (67).

Leviton also cites Glenn Johnson, PhD., who agrees with La Puma's methods. He concurs that if a comatose patient can hear there may be cognitive function, and perhaps speaking with them can coax them back to physical functioning. Johnson has used hypnotic imagery and suggestion to help ease comatose patients back to cognition and movement. Johnson worked with a patient who had been comatose for four months, believing that her negative expectations due to long-term inactivity were obstructing her success (68).

Johnson hypnotized the patient by speaking softly into the woman's ear, and asking her to focus on one idea. He described her condition, told her family was near, and that she was in a hospital being cared for and would be alright. Nearly immediately, Johnson noticed that the woman regained some control over her eye gaze. He worked with her until she had regained about 95% of her eye gaze and then proceeded with asking her to try to speak. A few days later, the woman did begin speaking and came out of her coma. She knew everyone's name, and recognized Dr. Johnson's voice (Leviton 69).

Although some coma experts dismiss these anecdotal accounts. First-hand accounts by patients who have recovered from comas, such as Mary Kay Blakely, note that some comatose patients report having been able to hear and feel while in the coma, but not able to respond. Blakely notes that her "body was like a broken transmitter, able to receive but not send messages" (qtd. Leviton 69).

Borthwick and Crossley with Johnson and La Puma. They put forth the idea that just because a patient could not communicate that he or she was aware, did not preclude awareness itself.

If people do not communicate awareness, why do we not begin from the standpoint that this a deficit in communication, rather than leaping to a conclusion that there is a deficit in awareness - a conclusion that should only be reached, if at all, when all other explanations have been exhausted? We should in the first instance attempt to remedy communication problems and only then consider whether awareness is irrecoverable (388).

The reported scans of a young British woman, performed by British and Belgian researchers, has made top news lately in this continuing search for answers. The researchers studying the unnamed patient who had suffered brain injury from a car accident scanned her brain and found possible signs of consciousness, much in agreement with Owen's findings. When the British and Belgian researchers asked the patient to imagine playing tennis or walking through rooms of her home, the activity patterns they found were similar to those of healthy person given the same task. Several months following the scans, the patient is beginning to recover (Goldberg C1).

The findings from this research, as noted previously, are in agreement with similar brain scan findings by Owen. This research indicates not only further support the use of brain imaging techniques to probe beneath the unresponsive surface of comatose patients, but also indicates that these patients have some level of awareness. Functional MRIs are the latest tool in this research, as Goldberg notes, transforming the snapshot abilities of traditional MRI, into motion images that can track reactions over time (C1).

More research is needed; however it is likely that brain scanning will become a routine tool for diagnosing comatose patients. Goldberg notes that cases like Terri Schiavo, and the public's outrage in the removal of her feeding tube, are an indication of the high stakes involved. However, the patient reported in the current research is significantly different from Schiavo, who had been in a coma for 15 years. it's noted that "patients in prolonged vegetative states whose brains are scanned do not show the British patient's type of activity" (C1).