How Do General Anaesthetics Cause Loss of Consciousness - Essay Example

Anaesthesia, Conscious and Unconscious s For many years, general anaesthetic agentshave been used as medication to patients undergoing surgery. The anaesthetics lead to loss of consciousness to the subject of the surgical experiments. General anaesthetics agents are given in the form of liquids and gases. Liquids are injected to the human body into the veins whereas the gases are inhaled through the masks (Perry 2010, p. 56). Many studies have been conducted to explain how anaesthetic agents work, but, the mechanisms behind the whole processes remain unknown. However, all theories have proven that anaesthetics interrupt the flow of information along the nerves. Usually, the general anaesthetics are used during long surgical operations that are also very painful. For example, during hysterectomy, hernia repairs, removal of gall bladder and more (Perry 2010, p. 67). Positron Emission Tomography (PET) is one the research conducted in search for the effects of anaesthetics in humans.The PET study covers the activity of both inhibitory and excitatory neurons that describe the conscious states of mind (Alkire, Haier and Fallon 2000, p. 371). Other studies have identified that general anaesthetics affects the thalamus, cerebellum, midbrain reticular formation, occipital cortex and basal forebrain. Research has revealed that the anaesthetics suppress the thalamocortical circuits, which interfere with the transfer of signals across the neural networks (Squire 1996, p. 114). These agents thalamocortically suppresses the regions of the brain differently although some theories tend to assume that the agents affect the entire brain, mostly focusing on the midbrain reticular formation and thalamus. The general anaesthetics do not affect the brain activities the same way. They affect different regions of the brain thus producing different states of unconsciousness. While humans are asleep, the flow of blood in the thalamus reduces, which means low metabolic rates which lead to unconsciousness. On another hand, anaesthesia involves artificial suppression of the metabolism processes in the thalamus, which make human beings unconscious, as well. Theories of Anaesthetic Effect on Human Brain In their PET studies, Dr.Alkire, Fallon and Haier used 11 unconscious brains and 11 conscious brains. They used two anaesthetic agents, which include the isoflurane and the halo-thane. They recorded the regional uptakes of fluorodeoxyglucose (FDG) in each human brain of the subjects of the study. Then, they compared FDG uptake patterns of the unconscious subjects with the conscious subjects(Alkire, Haier and Fallon 2000, p. 372). The inferences of the metabolic activities in specific regions of the brain were then taken. In their analysis, the researchers conclude that the different neural discharge and regional metabolism activities in all the subjects well describe the conscious state of brain. According to Alkire et al., (1997, 1999a),the isoflurane and the halothane decreases the glucose metabolisms in the primary parts of the brain such as the thalamus and cortex.Upon the decrease of the metabolic rates, the subjects lose consciousness. The researchers gearing the PET study conclude that the two anaesthetic studies affect the regional metabolism in nearly identical ways (Alkire, Haier and Fallon 2000, p. 373). In another study altogether, researchers conclude that anaesthetic agents suppress the thalamocortical circuits that transfer signals in the human brain. In the study of the characteristics of the human brain in the conscious state, other theories are put across on the behaviour of neurons. There are two theories that describe the conscious state of mind. One theory suggests that particular regions of the brain undergoing the discharge activities support consciousness. On another hand, a theory put across tries to explain how consciousness of the brain is supported by the organization of the signalling processes taking place in several neurons. Although the two theories contradict in description, they give a clear view on the parts of brains that contribute the conscious states of mind (Alkire, Haier and Fallon 2000, p. 378). In summary, consciousness is achieved when the metabolism rates in the major regions of the brain such as thalamus are normal. The supporting systems of the brain consciousness include the neuron networks. Neurons refer to the small veins that transmit neural signals from other body parts to the brain and the vice versa. Normal metabolism, neural discharge and signal transmission processes also sustain the conscious state of the human brain. Loss of Consciousness Loss of consciousness emerges when there are disruptions of the neural signalling systems in the brain caused by anaesthetic agents. Examples of general anaesthetics include the halothane, isoflurane, propofol and ketamine (Perry 2010, p. 78). Unconsciousness is brought about by suppression/interference of production of neural signals, disruption of neural processes that interpret the neural signals and blockage of transmission of neural signals. Traditionally, researchers concluded that the general anaesthetic agents reduce the neural metabolism activities that are required to support the signalling processes. The theories put across describe the anaesthetic agents’ impacts on the flow of blood in the brain (Squire 1996, p. 118). The agents affect the signal-suppressions on individual neurons as well as the neural populations. Thalamus is an organ located centrally in the human brain. Upon inhalation of anaesthetic gases, the thalamus activities are affected, which in turn disrupts the entire neuron systems of the brain. Neural signals are not transmitted to a certain neural population thus causing unconsciousness. Signal suppression theories suggest that, under certain conditions such as the chlorase anaesthesia, increased rates of neural discharges will cause loss of consciousness. In the 1980’s, researchers discovered that, integration of the neural systems causes conscious awareness. Addition of chlorase reduces the products released by the cortex, and the reactions involved facilitate information processing that leads to conscious awareness. Additionally, in other studies, the chloralose agents have been identified as the most common general anaesthetics that cause high discharge activity. Propofol, chlordiazepoxide and chloralose have some effects on the brain activity. They suppress the cortical metabolism activities of some regions of mind that causes loss of consciousness (Alkire, Haier and Fallon 2000, p. 379). Blockage of the transmission of neural signals also causes loss of consciousness. Neural messages depend on the neural codes that are utilized in representation of information and the neurons that interpret them. Information is usually encoded in the profiles involved in the neural discharge activities. Upon inhalation or injection of general anaesthetics, there is changing of the rates of neural discharge activities that disrupt the entire neural network functioning leading to unconsciousness. Anaesthetic agents disrupt the discharge patterns that signal pain in the thalamus (Cariani 2000, p. 66). Virtually, the general anaesthetics disrupt neural processes, which in turn remove the mechanisms essential for interpretation of nerve impulse patterns. That is why one cannot feel pain during any operation. The disruption of the neural processes that support the interpretation of neural messages also results to unconsciousness. Some neurological studies reveal that cortical activities that constitute to consciousness include firing of neurons that are arranged in loops. Other researchers conclude that the neural basis for brain consciousness is constituted by the intrinsic thalamocortical processes of reverberation in the brain.The neural signalling processes ought to be self-regenerating and self-sustaining in conscious states of mind. However, anaesthetic agents disrupt these processes leading to failure of the neural systems, which no longer regenerate themselves. In this way, the on-going operations in the human body and the working memories supporting hearing seeing and hearing are not sustained leading to unconsciousness (Cariani 2000, p. 67). Theories Discussing Anaesthetic Effect at Molecular Level The effects of general anaesthetics can also be analysed using the molecular approach. Back in 1896, Hans Meyer suggested that anaesthetic agents contain hydrophobic liquids that are repelled by water. These liquid molecules are in turn attracted by the fatty molecules of the brain. According to Meyer, the bonding between the hydrophobic anaesthetic agents and the lipid molecules of mind contributes to unconsciousness (Scarc 2009). Charles Overton later developed the Meyer’s theory of hydrophobic effects of anaesthetic agents to the human mind. In his part, Overton developed the theory covering the gaseous and liquid forms of anaesthetics (Scarc 2009). Later in the early twentieth century, researchers scrutinized the Meyer-Overton discovering claiming that the lipid theory only focused on the lipid molecules of the brain. Instead, they proved that the anaesthetic agents interact and combine with all types of brain cells whether they contain fat proteins or not in order to produce the anaesthetic effect. Further criticisms of the Meyer-Overton lipid theory have rendered the theory obsolete (Scarc 2009). Volatile anaesthetic agents are the most commonly used anaesthetics during surgery because they are inhalable. These agents affect the nervous system, where they interfere with the nervous transmission processes. They reduce the release of the neurotransmitters in the central nervous system which means disruption of the transmission of sensory information to the cerebral cortex (Perkins 2005). Many methods developed in the study of the brain are based on the functioning of the ion channels in the lipid environments of the brain. For example, the EEG describes the interactions between the lipid molecules of agents such as the flulorane with the receptor proteins in the neurons of the thalamus region of mind. There have been difficulties in explaining how the anaesthetic agents work for the past decades (Warren 2014, p.134). The fact that anaesthetic molecules are volatile and do not bind easily to the lipid molecules of the brain makes it hard for thorough explanations of the great number of interactions that occur during an aesthetic state (Perkins 2005). Researchers have developed the lipid theories in explaining the effect of the anaesthetic agents at molecular level. As a result, they have developed the EEG, fMRI and the PET methods to expound more on how the human brain works. In summary, the general anaesthetics affect the thalamus part of the brain. The interference of the thalamocortical output causes unconsciousness. Loss of conscious depends on how the agents interact with the specific regions of mind. The regions include the thalamus, reticular nucleus and the cerebral cortex. Anaesthetic agents decrease the neural signalling rates, which also decreases the output to the cerebral cortex. Techniques Used in Study of Brain Activity In order to understand the neurons responsible for consciousness states of mind, one ought to incorporate theories that explain the monitoring activities of the brain. First, electroencephalography (EEG) is a process used to control the electrical activities of the neurons. EEG focuses on neuronal populations that are involved in signal transmission. The patterns of brain activities are drawn in conscious and unconscious states. Positron emission tomography (PET) involves detection of the gamma waves that are caused by positrons in the human brain. As stated earlier, PET also involves the measure of the metabolism rates. Use of fludeoxyglucose allows researchers measure the uptake of glucose in regions of the brain. Another method used in monitoring the brain activity is the functional magnetic resonance imaging (fMRI) (Franks 2008, p. 376). It involves the measuring of blood flows in the thalamus, neural nucleus and cortex. During sleep, the metabolism rates and blood flow greatly reduces in the thalamus (Bear, Connors and Paradiso 2007, p. 117). The method of fMRI suggests that the thalamus operate in two different firing modes, that is the single-spiking and the burst firing modes. Sensory information first reaches the thalamus before getting to the cerebral cortex. Sensory information only passed by the thalamus, when the thalamus itself is in single spike firing mode. In burst firing mode, the thalamus cannot pass information, which means someone is asleep or anaesthetic. Anaesthesia, therefore, causesa reduction of glucose metabolism rates in the thalamus and conversion of single spike firing to burst firing modes (Hutt 2011, p. 341). In the EEG, general anaesthetics lead to conversion of the beta waves to spindles and later to delta waves and this result to unconsciousness (Franks 2008, p. 376). Isoflurane is one of the most volatile anaesthetics that hyperpolarize the brain cells in the thalamus, putting them into a bursting state (Franks 2008, p. 378). As a result, sensory information originating from other parts of the human body does not pass through the thalamus to reach the cerebral cortex. Isoflurane can, therefore, be used during surgical procedures that take long periods or are very painful. It is important to note that general anaesthetic agents do not operate in similar ways. Injectable anaesthetics such as the propofol interfere with the actions of the GABA receptors whereas the volatile anaesthetics hyperpolarize the thalamus cells directly interfering with the transmission of sensory information. Ketamine is a general that blocks the flow of neural signals in the thalamus leading to unconsciousness. In sleep mode, the firing modes of the thalamic cells are in burst state, which limits the flow of sensory information (Franks 2008, p. 384). Thalamic switching is very important when describing the sleep and anaesthetic conditions of the human brain. Inputs from arousal and sleep nuclei control thalamic switching. In surgical procedures, the subjects are injected with general anaesthetics that operate within the specified period. Upon completion of surgery, the molar amounts of these agents are very low in the thalamus. As a result, the cells return to regular or normal modes leading to consciousness. Also, the metabolism rates return to normal since there is a regular flow of blood in the thalamus. In most studies, the general anaesthetics have been assumed to induce sleep and disrupt the entire neural system of the brain. The particular brain regions affected by the general anaesthetics are yet to be discovered (Bear, Connors and Paradiso 2007, p. 118). Conclusively, the effect of general anaesthetics on the human brain has been explained by many theories. There is no single theory, which explains the specific regions of the brain that is affected by these agents. However, studies conducted for the past centuries shows that the neural discharge, transmission and signalling systems are the key systems affected by the general anaesthetics. General anaesthetic agents do not suppress the neural processes in similar ways. Volatile anaesthetic agents produce different effects as compared to the liquid aesthetics. Most agents affect the thalamus part of the brain. The PET, fMRI and the EEG techniques are used to describe the brain activity in sleep and anaesthetic conditions. References List Alkire, M T, Haier, R J and Fallon, J H 2000, Towards a Unified Theory of Narcosis: Brain Imaging Evidence for a Thalamorcortical Switch as the Neurophysiologic basis of Anaesthetic–Induced Unconsciousness. Irvine, Academic Press. Bear, M F, Connors, B W, & Paradiso, M A 2007, Neuroscience: exploring the brain, Philadelphia, PA, Lippincott Williams & Wilkins. Cariani P 2000, Anaesthesia, Neural Information Processing, and Conscious Awareness, Boston, Academic Press. Franks N P 2008, General Anaesthesia: From Molecular Targets to Neuronal Pathways of Sleep and Arousal. London, Nature Publishing Group. Hutt, A 2011, Sleep and anesthesia: neural correlates in theory and experiment. New York, Springer. Perkins B 2005, How Does Anaesthesia Work? New York, Scientific American. Perry E K 2010, New horizons in the neuroscience of consciousness, Amsterdam, John Benjamins Pub. Scarc, P 2009, The Meyer-Overton Theory of Anaesthesia. London, Linus Pauling Squire, L R 1996, The history of neuroscience in autobiography. Washington D. C, Society for Neuroscience. Warren B 2014, Challenging concepts in anaesthesia: Cases with expert commentary, Oxford, Oxford University Press. Read More