A topic of discussion for years is whether or not anesthesia causes loss of consciousness. Whether or not the use of general anesthesia in surgery may affect the state of consciousness. General anesthesia can be administered as liquids and gases injected into the body or inhaled through masks. Anesthesia is used as a method of pain relief. Theories have emerged aimed at understanding how anesthetics interrupt the communication of information along nerves. When we are under anesthesia during major medical procedures, we expect to no longer be conscious of them. It is difficult to understand whether consciousness completely disappears or not. Although anesthesia can have an effect on brain function and neural connections, it cannot actually interrupt the relay of information through our brain and therefore our consciousness. More and more studies aim to understand how general anesthesia affects our mind and consciousness, but this question remains. Say no to plagiarism. Get a tailor-made essay on 'Why violent video games should not be banned'?Get the original essayThomas Nagel proposed the notion of 'what it looks like'. This explains our consciousness and "what it's like" from our first person perspective, no other person can fully experience "what it's like" for me to see something I like, or when I smell a rose or experience something for the first time. . Even if I can say “what it’s like” to someone else, the person will not fully share the same feelings or thoughts that I felt during that experience (Nagel, 1974). How consciousness works in the brain still remains a mystery to be solved. Position emission tomography (PET) describes a research method used to help understand the effect of anesthetics on consciousness in humans; PET studies both inhibitory and excitatory neurons involved in conscious states of mind (Fallon, 2000). Other studies have identified an effect of anesthesia on the thalamus, cerebellum, midbrain, occipital cortex, and basal forebrain. Dr. Alkirie and his colleagues conducted their PET studies on 11 unconscious brains and 11 conscious brains. In their study, they used two different anesthetic agents: isoflurane and halothane. They recorded regional FDG uptakes in each brain and compared differences in conscious and unconscious brain uptake (Haier et al, 2000). Alkirie et al also localized the metabolic activities of the brain. The researchers concluded that different neuronal firings and regional metabolic activities in all participants showed a conscious state of the brain. Alkirie and colleagues noted how isoflurane and halothane decreased glucose metabolic activity in primary parts of the brain-thalamus and cortex and that when metabolic rates decreased, participants lost consciousness. They concluded that both anesthetics affected the brain almost identically (Alkirie et al., 2000). Anesthetics have different effects on different areas of the brain and can affect a person's ability to respond. Some anesthetics deactivate the entire brain, but deterrent anesthetics like ketamine, which only deactivate certain regions, can be more problematic. When administered in low doses, ketamine can cause out-of-body experiences known as depersonalization and cause forgetfulness and loss of meaning.motivation to respond to orders. When ketamine is administered at a higher dose, a person may adopt a "characteristic state" in which the eyes remain open, displaying a blank stare that shows no connection. Through neuroimaging studies, the data can show how metabolic changes are displayed in a complex pattern showing deactivation of areas of the brain, including basal Anglia. Ketamine administered at levels causing loss of consciousness can interrupt working memory, which would explain why patients cannot respond to commands because they would almost immediately forget what they were asked to do and cannot process the information. to provide action. Amnesia results from the administration of very low doses of anesthetics. Isolated studies on the forearm show how paralysis is induced by the use of a constraint called a tourniquet applied to the arm but which allows the hand to move. These studies provide evidence to understand how patients under anesthesia can still communicate using hand gestures, but after surgery they deny that this conversation took place. Retrospective forgetting therefore cannot provide sufficient evidence to explain unconsciousness. At different levels of anesthesia, between behavioral insensitivity and the induction of a flat EEG, which indicates the electrical activity of the brain, the criterion for brain death, all consciousness must disappear. The use of brain function monitors may improve the assessment of consciousness during anesthetic administration. One example being the use of bispectral index monitors to record EEG signals from the forehead and reduce the complex signal into a single number that tracks the patient's depth of anesthesia. The devices themselves can help guide anesthesia delivery and reduce instances of intraoperative awareness, but indicate the presence or absence of awareness. Signal suppression theories suggest that under certain conditions such as chlorase anesthesia, increased rates of neuronal firing result in loss of consciousness. In the 1980s, researchers discovered that the integration of neural systems underlies consciousness. The use of chlorase anesthesia reduces the products released from the cortex into the brain and the reactions involved in information processing lead to awareness. Other studies have identified that cholrases are the most common agents for offloading conscious activity. It suppresses cortical metabolic activities in brain regions that cause loss of consciousness (Fallon, 2000). The suggestion of the thalamus as a conscious switch was coined by studying the reduction in blood flow and thalamic metabolism when anesthesia was administered to a patient. There are a growing number of studies that provide evidence supporting the notion of "conscious change" in which these studies manipulate the thalamus. GABA agonists that mimic the anesthetic effect are injected into the intraluminal nuclei of a rat and the effects show that the rat falls asleep quickly and the EEG data shows how the electrical activity in the brain begins to slow down. By injecting Nicole into the Rat's Thalmus under anesthesia, they can be awakened. Any damage to the thalamus can induce a vegetative state which can only be recovered by reestablishing the connection between the cortex and the thalmus (Perry., 2010). When the thalamus is stimulated with electrical activity, evidence showed improved behavioral responses suggesting that the patient was minimally conscious. The effects of the anesthetic, ketamine,instead of decreasing the activity of the thalamus, increase metabolism. Different anesthetics can also trigger a reduction in thalamic activity that would induce sedation but not loss of consciousness. Examples of these anesthetics include: Sevolflurane which can cause a 23% reduction in thalamic activity, but this only occurs when the patient is awake and still able to respond. There is also evidence of spontaneous thalamic activation when the patient is under anesthesia and this may be caused primarily by cortical neurons – this response is known as indirect anesthesia effects. Deactivation of the cortex reduces thalamic metabolism and arousal because the cells involved project to brain arousal centers. In animal studies, it has been shown that by removing the cortex, the electrophysical and metabolic effects of anesthetics on the thalamus can be diminished. When the thalamus is removed, the cortex still presents an activated EEG, which would allow us to understand that the thalamus is not the main mediator of cortical arousal. However, in a contrasting study it was shown that when the electrodes were implanted deeper, the EEG of the cortex showed a notably greater change and loss of consciousness whereas 10 minutes later the EEG activity in the thalamus was still active. During REM sleep, epileptic patients show that their cortical EEG was still active as if the patient was awake and the thalamic EEG activity was reduced as if the patient was asleep. These findings help to understand the effects of anesthetics on the thalamus and how it may actually be a cortical activity rather than the “conscious change” previously suggested. Furthermore, this shows that the thalamus is not the “dynamic core” of consciousness. In epileptic patients during REM sleep, the cortical EEG was activated as if they were awake, but the thalamic EEG showed slow wave activity as if they were asleep. Therefore, this helps to show that the effect of anesthetics on the thalamus may instead be a representation of cortical activity rather than a change in consciousness and that thalamic activity may actually not be a sufficient basis for the awareness. Hans Myer suggested that anesthetics contain hydrophobic liquids repelled by water. These liquid molecules are attracted to the fat molecules in the brain. Meyer suggested that the connection between hydrophobic anesthetic agents and lipid molecules in the mind contributes to unconsciousness (Sarc, 2009). Charles Overton continued by building on Meyers' theory of the hydrophobic effects of anesthetic agents on the human mind. The Meyer-Overton theory has been criticized, saying that it focused only on lipid molecules in the brain. The idea was supported when it was demonstrated how anesthetic agents interacted and combined with all types of brain cells, whether they contained fatty proteins or not, to produce the anesthetic effect. Other criticisms of the Meyer-Overton theory have made this theory obsolete (Sarc, 2008). Volatile anesthetic agents are the most commonly used anesthetics in surgery because they are inhalable. These affect the nervous system and the process of neuronal transmission. Reduce the release of neurotransmitters in the central nervous system, which means a disruption of the transmission of sensory information to the cerebral cortex (Perkins, 2005). A number of methods have been developed to study the brain function of ION channels in lipid areas of the brain. An example being, the EG describes the.