Critically Assess How General Anaesthetics Cause Loss of Consciousness

A topic of discussion for years has been whether or not anesthesia causes loss of consciousness. Whether or not the use of general anesthetic in surgery can affect the conscious state. General anesthetic can be administrated in the form of liquids and gases injected into the body or inhaled through masks. Anesthesia is used as a method of pain relief. There have been theories that have emerged that aim to tackle how anesthetics interrupt the communication of information along the nerves. When we are under anesthetic during major medical procedures, we expect to no longer be consciously aware. It is hard to understand whether or not consciousness completely vanishes. Whilst the anesthesia may have an effect on the brain functioning and neuronal connections, it may not actually interrupt the relay of information through our brain and therefore our conscious awareness. There have been a growing number of studies that have set out to understand how general anesthesia affects our minds and consciousness, however this question still remains.

Thomas Nagel proposed the “what its like” notion. It explains our conscious awareness and “what its like” from our first person perspective explanation, no other person can fully experience “what its like” for me to see something I love, or when I smell a rose or experience something for the first time. Whilst I can say “what its like” to someone else, the person will not fully comorehend the same feelings or thoughts I felt during this experience (Nagel, 1974). It is still a mystery yet to be solved how consciousness in the brain works.

Position Emission Tomography (PET) describes a research method used to help understand the effect of anaesthetics on consciousness in humans; PET studies both the inhibitory and excitatory neurones that are involved in the conscious states of mind (Fallon, 2000). Further studies have identified an effect of anaesthesia on the thalamus, cerebellum, mid brain and occipital cortex and basal forebrain.

Dr Alkirie and colleagues conducted their PET studies on 11 unconscious brains and 11 conscious brains. In their study, they used two different anaestheticic agents- isoflurane and halothane. They recorded the regional uptakes of FDG in each brain and compared the conscious and unconscious brain uptake differences (Haier et al, 2000). Alkirie et al also localized the brains metabolic activities. The researchers concluded that different neural discharge and regional metabolism activities in all of the participants showed a conscious state of the brain. Alkirie and colleagues noted how isoflurane and halothane decreased the glucose metabolic activity in the primary parts of the brain- thalamus and cortex and upon decrease of metabolic rates, the participants lost consciousness. They conclude that the both anaesthetics affected the brain in near identical ways (Alkirie et al., 2000).

Anesthetics have different effects on various areas of the brain and may affect the persons ability to respond. Some anaesthetics deactivate the whole brain but disassciative anesthetics like Ketamine which only deactivate some regions can be more problematic. Ketamine when administered in low doses can cause out of body experiences known as depersonalization and can cause forgetfulness and loss of motivation to respond to commands. When Ketamine is administered at a higher dose, it can cause a person to take on a “characteristic state” where eyes remain open displaying a blank stare that shows no connection. Thanks to Neuroimaging studies, the data can show how metabolic changes are displayed in a complex pattern showing deactivation of areas of the brain including the basal Anglia. Ketamine administered at levels to induce unconsciousness can interrupt the working memory which would explain why patients cannot respond to commands as they would forget what they were asked to do almost immediately and cannot process the information to provide an action. Amnesia results from very low doses of anesthetics being administered. The isolated forearm studies show how paralysis is induced through use of a restraint called a tourniquent appled to the arm but allows the hand to move. These studies provide evidence to understand how patients under anesthesia can still communicate using hand gestures but after the operation deny this conversation having happened. Therefore restrospective oblivion can not provide enough evidence to explain the unconsciousness.

At different levels of anaesthesia between behavioural unresponsiveness and the induction of flat EEG, which indicates the brains electrical activity, criterion for the brain death, all conscious awareness must vanish. Use of brain function monitors can improve consciousness assessment during anaesthetic administration. An example being, the use of bi-spectral index monitors to record EEG signals over the forehead and reduce the complex signal into a single number that tracks the patient’s depth of anaesthesia. Devices as such can help to guide anaesthetic delivery and reduce cases of intraoperative awareness but indicate the presence or absence of consciousness.

Signal suppression theories suggest that under certain conditions such as the chlorase anaesthesia, increased rates of neural discharges with cause loss of consciousness. In the 1980’s researchers found that the integration of neural systems underlies conscious awareness. Use of chlorase anaesthesia reduces the products released by the cortex in the brain and the reactions involved in facilitating information processing leads to conscious awareness. Further studies have identified cholrase agents has the most common to discharge conscious activity. It suppresses the cortical metabolic activities of the brain regions that cause loss of consciousness (Fallon, 2000).

The suggestion of the thalamus as conscious switch was coined by investigating the reduced blood flow and thalamic metabolism when anaesthesia was administered to a patient. There are a growing number of studies that provide evidence to support the notion of the “conscious switch” in which these studies manipulate the thalamus. GABA agonists which mimic the anesthetic effect are injected into the intraluminal nuclei of a rat and effects show the rat falling asleep rapidly and EEG data shows how the electrical activity in the brain begins to slow. By injecting Nicole into the Thalmus of the Rat under anesthesia, they can be awakened. Any damage caused to the thalamus can induce a vegetive state which can only be recovered by restoring the connection between the cortex and thalmus (Perry., 2010). When the thalamus is stimulated by electrical activity, evuidence was found to show better behavioural responses suggesting that the patient was minimally conscious.

The effects of the anesthetic, Ketamine, instead of deceasing activity in the Thalamus they increase the metabolism. Different anesthetics can also trigger reduction in the thalamic activity which would induce sedation but not unconsciousness. An examples of these anesthetics include; Sevolflurane which can result in 23% reduced thalamic activity but this only happens when the patient is awake and still able to respond. There is also evidence of spontaneous thalamic firing happening when the patienrt is under anesthesia and this can be driven mainly by the cortical neurones- this response is known as indirect anesthesia effects. Deactivation of the cortex reduces thalamic netabolism and arousal as the celles involved project to the brain arousal centres. In animal studies, it has been showing that by removing the cortex, the anaesthetics electrophysical and metabolic effects on the thalamus can be diminished. When the thalamus is removed, the cortex still shows activated EEG which would allow us to understand that the thalamus is not the primary mediator of cortical arousal. However in a contrasting study, it was shown that when the electrodes were implanted deeper, the cortex EEG displayed a notably larger change and lost consciousness when 10 minutes later the EEG activity in the Thalamus was still active. During REM sleep, patients who suffer from epilepsy show how their cortical EEG was still active as if the patient were awake and thalamic EEG was shown to reduced in activity as if the patient were asleep. These findings help to understand the effects of anaesthetics on the thalamus and how it may actually be cortical activity rather than the previously suggested “conscious switch”. Furthermore it shows how the thalamus is not the “dynamic core” of consciousness.

In epileptic patients during REM sleep, the cortical EEG was activated as if awake but the thalamic EEG showed slow wave activity as if asleep. Therefore this helps to show that the effect of anaesthetics on the thalamus may instead be a representation of the cortical activity rather than a consciousness switch and thalamic activity may actually not be a sufficient basis for consciousness.

Hans Myer suggested that anaesthetics contain hydrophobic liquids repelled by water. These liquid molecules are attracted to the fatty molecules of the brain. Meyer suggested that the bond between the hydrophobic anaesthetic agents and the lipid molecules of mind contributes to unconsciousness (Sarc, 2009). Charles Overton went on to build upon Meyers Theory of the hydrophobic effects of anaesthetic agents to the human mind. The Meyer-Overton theory was criticised claiming that the theory only focused on the lipid molecules of the brain. The idea was supported when it was shown how the anaesthetic agents interacted and combined with all types of brain cells whether they contained fat proteins or not in order to produce the anaesthetic effect. Further criticisms of the Meyer-Overton theory have rendered the theory obsolete (Sarc, 2008).

Volatile anaesthetic agents are the most commonly uses anaesthetics during surgery because they are inhalable. These affect the nervous system and neurone transmission process. To reduce the release of neurotransmitters in the central nervous system which means a disruption of the transmission of sensory information the cerebral cortex (Perkins, 2005). There are a number of methods that have been developed to study the brains functioning of the ION channels in the lipid areas of the brain. An example being, the EG describes the interactions between the lipid molecules of anaesthetics such as fluorine with the receptor proteins in the neurons of the thalamus region. There has been much difficulty over the years to explain how the anaesthetics have effect on the brain (Warren, 2014). Anaesthetic molecules are so volatile and do not bind easily to the lipid molecules of the brain makes it difficult for through explanations to allow us to fully understand the number of interactions that occur under anaesthetic state (Perkins, 2005). This allowed researchers to develop the lipid theories to explain anaesthetic agents at a molecular level and develop EEG, fMRI and PET to give a visual explanation of how the human brain works.

In order for us to understand the neurons that are responsible for the conscious state of mind, monitoring activities have been developed. 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). 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).

The use of fMRI suggests how the thalamus operates in two different firing modes- single spiking and burst firing modes. Sensory information first reaches the thalamus before it reaches the cerebral cortex. Sensory information can only be passed by the thalamus is in single spike firing mode. When the thalamus is in burst firing mode, the thalamus cannot pass information, which means someone is asleep or under anaesthetic. Anaesthesia therefore causes a reduction of glucose metabolic rates in the thalamus and conversion of single spike to burst firing mode (Hutt, 2011). In EEG, general aneasthetic lead to the conversion of the beta waves to spindles and later to delta waves resulting in an unconscious state being entered (Franks, 2008).

Isoflurane is one of the most volatile anesthetics to hyperpolarize the brain cells in the thalamus resulting in them being in bursting state (Franks, 2008). This leads to the sensory information that originates in other parts of the body to not pass through the thalamus to reach the cerebral cortex. Isoflurane can be used during surgery that will last for a long period or cause a lot of pain. Not all anesthetics work in the same way- injectable anesthesia such as, propfol, interfere with the actions of the GABA receptors in contrast to the volatile anesthetics which instead hyperpolarize the thalamus cell directly in turn interfering with the transmission of sensory information (Franks, 2008).

In most studies, the general anesthetics have been assumed to induce sleep and disrupt the entire neural system of the brain. The particular brain regions affected by the general anesthetics are yet to be discovered (Bear, Connors and Paradiso 2007).

Therefore to conclude, the effect of general anesthetics on the human brain has been explained over the course of varying theories. There is no single theory that can specifically identify the specific regions of the brain under anesthesia and more work needs to be carried out to fully understand the conscious state of mind and which areas of the brain controls consciousness. Any new emerging research constantly builds upon the previous research and provides a further stepping stone to finally cracking consciousness.