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Loss of Consciousness

Ben Baldassare

This paper explores the phenomenon of consciousness in terms of loss of consciousness (LOC). A person might experience LOC as a result a mechanism such as head trauma, hypoxia, or anesthesia. The widely-accepted Glasgow Coma Scale (GCS) assesses a patient's level of consciousness by measuring responsiveness. It is, however, feasible to have a seemingly unresponsive conscious patient or a seemingly responsive unconscious patient. The other aspect of consciousness that can be measured is contents of consciousness, which can be determined by assessing a patient's awareness of his or her environment, often called orientation. While consciousness exists on a spectrum, instances where both level and contents of consciousness are completely absent allow us to better understand what it means to conscious. This paper examines some of the mechanisms that cause LOC to find similarities that might hint at what causes consciousness to occur by explaining what causes it to cease.

Consciousness is a phenomenon that has likely been discussed since the Fox P2 gene granted us the ability to talk 50,000 years ago. Ancient cultures often attributed it to the presence of a soul, an entity that enters the body at life's beginning and leaves it at life's end. This explanation, however, fails to explain what happens to the soul when we are rendered temporarily unconscious, such as after a significant blow to the head causes what we now call a concussion. Unlike sleep, which involves dreams, unconsciousness can produce a state that is completely devoid of experience. Other causes of LOC include general anesthesia, epileptic seizures, and hypoxia. Medics usually try to assess both level and contents of consciousness. The GCS, developed in the 1970s, attempts to classify level of consciousness by rating it on a scale of 3 to either 14 or 15 based on eye opening, verbal response, and motor response. Contents of consciousness can be measured by a patient's orientation to his or her environment, which tends to disappear in the order of time followed by place followed by person based on the severity of the condition, although the usefulness of measuring orientation has not been thoroughly verified (Alverzo, 2006). Simplified versions of these assessments, such as the AVPU scale, allow caregivers and emergency responders to more easilyalbeit less accuratelyassess these factors. General anesthesia, epileptic seizure, and concussion are three of the most common and most studied causes of LOC. Since they do not all involve the same physiological changes, it is reasonable to assume that not all unconsciousness is equivalent. Similarly, it is also worth distinguishing different types of persistent unconscious states, namely brain death, coma, and vegetative state (VS). Brain dead patients have no chance of recovery and are considered dead in most jurisdictions, while comatose and vegetative patients may regain consciousness at a later date (Bernat, 2009).

Long-Term Consciousness Disorders

While auditory stimulation will evoke responses from the brain stems of both comatose and vegetative patients (which is not the case with brain dead patients), electroencephalograms (EEG) reveal differences between the two, namely the presence of theta waves in VS patients and burstsuppression in comatose patients, although delta waves will often be present in patients with either condition. The main difference between the two is that comatose patients do not exhibit the physiological signs of sleep-wake cycles while VS patients do (Bernat, 2009). The presence of sleepwake cycles in VS patients shows that LOC is not the same thing as sleep, as these people be awake and still unconscious.

General Anesthesia and Epileptic Seizures

General anesthesia and epileptic seizures are both relatively easy to record in a clinical setting. The former is already routinely induced in hospitals while the latter occurs frequently enough in patients suffering for epilepsy that researchers need only wait for it to happen. It is generally considered unethical to intentionally concuss humans for the purpose of a science experiment, so research on concussion involves a mix of studies on animals and information gathered from patients admitted to hospitals for concussions. This means that the mechanisms of action for LOC due to general anesthesia and epileptic seizures have been studied more extensively, and their conclusions seem to have less controversy surrounding them. Propofol is often used in studies on anesthesia because its effects at different concentrations are well-established and easy to predict. This agent is thought to work on the GABAA receptor, among others. Anesthetized patients exhibit increased sigma waves and decreased gamma waves in EEG recordings, with overall brainwave power increased. Positron emission tomography (PET) data shows that propofol decreases overall cerebral blood flow, and that this decrease is most pronounced in the

thalamus (Fiset, Paus, Daloze, Plourde, Meuret, Bonhomme, Hajj-Ali, Backman, & Evans, 1999). Because the thalamus regulates wakefulness, it would make sense that decreasing blood flow to it would result in a sleep-like condition. Indeed, the high amplitude delta waves and decreased gamma waves observed when consciousness was lost are similar to the EEG patterns seen during NREM-4, the deepest phase of sleep cycles (Fiset et al., 1999). That gamma waves decreased is particularly notable because these have been demonstrated to correlate with conscious experience, and may actually be the conscious pilot that was once called the soul. Multiple brain regions may demonstrate synchronized gamma waves, suggesting that those neurons are firing in sync with each other even though they may not be located next to or even near each other. This behavior occurs at the same time that the subject is conscious of experiences those regions are involved in processing (Hameroff, 2008). That gamma waves decrease when a patient is anesthetized provides further support for this theory. Neural synchrony, however, can also be present in unconscious brains, especially during an epileptic seizure. Seizures occur when neurons in one or more regions of the brain start firing in sync, and this synchronized activity might spread to other regions of the brain. Seizures can take multiple forms. Most people are familiar with the generalized tonic-clonic seizure (GTCS), or grand mal seizure, because its violent convulsions are dramatic enough to make for good television. Another type of seizure is the absence seizure, which is more common in children and which still involves a complete LOC but without the convulsions. A third type of seizure, the complex partial seizure, progresses unpredictably after onset and may or may not involve LOC. Other symptoms, such as hallucinations and convulsions, can sometimes arise during a complex partial seizure, but again this is not always the case (Cavanna & Monaco, 2009). The period of time when a seizure is occurring is referred to as the ictal period and is followed by a postictal period where the patient may remain unconscious for several minutes afterwards. Neuroimaging can reveal what changes occur in the brain during and after a seizure. An fMRI can determine which parts of the brain are responsible for each type of seizure by measuring increases

or decreases in brain activity in various regions. Researchers also look at EEG recordings during both the ictal and postictal periods. GTCS, absence seizures, and complex partial seizures begin with decreased activity in the medial prefrontal cortex and increased activity in the thalamus and upper brain stem. The EEG for a GTCS is characterized by high-frequency, high-amplitude, spiky brainwave activity, which contrasts against the slower and lower-amplitude neural activity that occurs during absence seizures. Absence seizure EEG recordings will show a rounded wave followed by a sharp spike followed by another rounded wave and another sharp spike, and so on. In complex partial seizures, brainwaves which are abnormal but rhythmic are localized and usually begin in temporal lobe from which they may or may not spread to other regions (Eugenio & Monaco, 2009). Both general anesthesia and epileptic seizures involve changes in the thalamus and upper brain stem, but general anesthesia decreases activity in that region while epileptic seizures increase it. In either case, this system is effectively disabled, thus causing LOC. Many theories of concussion also attribute it to effects on the ARAS, although it is not clear exactly how it is affected (Shaw, ????). Concussions are caused when intense acceleration damages the brain. Rotational acceleration which deforms the brainis more likely to cause this than linear accelerationwhich merely compresses the brain. Concussions involve not only LOC but also mild amnesia. Retrograde amnesia forgetting events that took place before the concussionmay decrease as a person recovers from a concussion, while anterograde amnesiarelating to events after the concussioncan be used to assess the severity of the concussion. The convulsive hypothesis compares concussions to epileptic seizures, which also involve amnesia. It identifies two phases of concussion: the convulsive period and the paralytic period. These are compared to the ictal and postictal periods of epileptic seizures, respectively. The hypothesis argues that the convulsive period is so brief that it is often overlooked, and experiments on animals have in fact identified seizure-like convulsions. This theory attributes concussion to excitation of the ARAS neurons, contrasting the reticular hypothesis which claims that the neuronal activity in that area is depressed due to cellular damage. The medical community has yet

to determine if either hypothesis is correct. The advantage of the convulsive hypothesis is that it explains the LOC as well as the amnesia resulting from concussion. Epileptic seizures interrupt the learning centers of the brain, which could result in the observed amnesia (Shaw, ????). Perhaps both hypotheses have some validity, as acceleration could cause the neurons to fire and then shut down, explaining why the convulsive period is so much shorter in concussions than in epileptic seizures.

One common theme among these causes of LOC is that they all involve a disruption in the behavior of the ARAS in the brain stem and thalamus. It is possible that there could be instances of LOC without some sort of anomalous activity such as increased or decreased CBF in these regions, but no reports of this were found found. One possible exception could be VS, where sleep-wake cycles are preserved and sometimes these regions appear normal under an MRI, but in these cases, further examination using different methods identified that there was, in fact, considerable damage to the thalamus (Uzan, Albayram, Dashti, Aydin, Hanci, & Kuday, 2003). Further research should explore which types of damage will cause LOC and also explore whether or not it is possible to temporarily deactivate these regions completely. Another possible direction is to discover a method to induce LOC without affecting the brain stem or thalamus. It seems reasonable to conclude that these regions are at least partly responsible for generating and regulating the conscious pilot. Furthermore, the fact that by disrupting these regions,

consciousness can be shut down and then restored without the subject experiencing anything in the interim suggests that when we diewhen our consciousness is shut down permanentlywe will not experience any sort of an afterlife. Our ARAS will cease to function and we will cease to be.

Bernat, J. L. (2009). Chronic Consciousness Disorders. Annual Review of Medicine, 60(1), 381-392. Bui, E. T., Sourkes, M., & Wennberg, R. (2009). Generalized tonic-clonic seizure after a taser shot to the head.(Case study). CMAJ: Canadian Medical Association Journal, 180(6), 625(622). Cavanna, A. E., & Monaco, F. (2009). Brain mechanisms of altered conscious states during epileptic seizures.(Report). Nature Reviews Clinical Neurology, 5(5), 267(210). Dandurand, F., eacute, ric, & Shultz, T. R. (2002). Modeling consciousness. Behavioral and Brain Sciences, 25(03), 334334. Fiset, P., Paus, T., Daloze, T., Plourde, G., Meuret, P., Bonhomme, V., et al. (1999). Brain Mechanisms of PropofolInduced Loss of Consciousness in Humans: a Positron Emission Tomographic Study. The Journal of Neuroscience, 19(13), 5506-5513. Fiset, P., Plourde, G., & Backman, S. B. (2005). Brain imaging in research on anesthetic mechanisms: studies with propofol. S. Laureys (Ed.), Boundaries of Consciousness: Neurobiology and Neuropathology, 150, 245-250. Hameroff, S. (2010). The conscious pilotdendritic synchrony moves through the brain to mediate consciousness. Journal of Biological Physics, 36(1), 71-93. Hameroff, S., & Marcer, P. (1998). Quantum Computation in Brain Microtubules? The Penrose-Hameroff 'Orch OR' Model of Consciousness [and Discussion]. Philosophical Transactions: Mathematical, Physical and Engineering Sciences, 356(1743), 1869-1896. Mhuircheartaigh, R. N., Rosenorn-Lanng, D., Wise, R., Jbabdi, S., Rogers, R., & Tracey, I. (2010). Cortical and Subcortical Connectivity Changes during Decreasing Levels of Consciousness in Humans: A Functional Magnetic Resonance Imaging Study using Propofol. [Article]. Journal of Neuroscience, 30(27), 9095-9102. Owen, A. M., & Coleman, M. R. (2008). Detecting Awareness in the Vegetative State. [Article]. Annals of the New York Academy of Sciences, 1129, 130-138. Vardas, P. E., & Simantirakis, E. N. (2010). Transient loss of consciousness: an ongoing challenge. [Editorial Material]. Europace, 12(6), 774-775. Zhang, Y., Gao, J., & Wang, Y. (2009). Cerebral Ischemia Manifested as Recurrent Loss of Consciousness. [Meeting Abstract]. Cerebrovascular Diseases, 28(3), 213-213.