Emotions, Pain and Optical Illusions: Some Fascinating Insights into How the Human Brain Works
In this article I will discuss three areas which are of particular interest in modern neuroscience.
Pain because of its pervasive nature in so many diseases in addition to being an unnecessary form of suffering, which with sufficient knowledge could be all but eliminated by modern medicine. Neurological pathologies as they are becoming increasingly prevalent as life expectancy increases, and also because of how much they tell us about the brain. Finally perception, not only because it is a topic everyone can engage with in the form of illusions, but also because of the more difficult philosophical questions it raises as well as some unanswered scientific questions.
In order to discuss pain, we must first establish exactly what pain is. This seems incredibly trivial, since we’ve all experienced pain and we all have a very good idea what pain feels like. However, in scientific terms pain is much harder to describe. It is not simply the result of physical damage: there are well documented cases of people experiencing severe injury such as losing a limb but not noticing until they have looked down and seen the damage. Equally there are cases of people experiencing pain in limbs which have been amputated, “phantom limb pain”, despite the fact they no longer even have a limb to be damaged. The International Association for the Study of Pain uses the following definition: “Pain is an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage.” This definition acknowledges that pain is not just a sensory experience, but also emotional, with emotional state having a quite remarkable impact on the perception of pain levels.
But why do we experience pain? Most people will have very negative associations with pain and it seems as if we would be better off without it. In fact, there are a group of people who suffer from what is known as congenital analgesia, a lifelong condition causing the inability to experience pain. Instead of having any kind of advantage, sufferers experience many problems including biting off the tip of their tongue, being unable to notice infections and suffering burns and fractures at a very high rate. In these situations a healthy individual would sense pain and take action to prevent serious damage occurring, for example by withdrawing their hand from a very hot surface. In contrast, a person with this condition will not respond until they receive alternative sensory information, such as seeing their skin blister in response to the heat. Minor injuries also tend to become exacerbated without the ability to experience pain; if a healthy individual damages a joint it will become sore and they will avoid placing excessive strain on it. Without painful feedback the joint would continue to be used until serious damage occurs.
Of course pain is not always useful. For a terminally ill cancer patient pain is of little benefit and instead brings a great deal of suffering. Equally, pain is of little use to someone undergoing minor surgery or simply experiencing a sore throat and therefore drugs have been developed to reduce pain: anaesthetics. However, in these two cases very different types of anaesthetic are used as two very different effects are required. Local anaesthetics are used for localised pain such as a sore throat or minor surgeries, as they only act on the area to which they are applied and have minimal side effects. They work by exploiting how pain signals are carried through nerves to the brain. Nerves conduct an electrical signal by opening voltage-gated ion channels, in particular the sodium channel. This allows sodium ions to enter the nerve and create a positive internal voltage. Local anaesthetics block this channel and prevent sodium entering, therefore preventing a signal being carried down the nerve.
In the case of cancer patients local anaesthetics are less appropriate, as their pain is much more diffuse and chronic. Therefore their pain is managed with opioids, with the most frequently used being morphine. These act in a variety of different ways, depending on the location within the body. For example, in the spinal cord they act to lower the excitability of neurons by opening potassium channels. These are the opposite of sodium channels as they let potassium flow out of the cell and therefore make the internal voltage less positive. Therefore, when opioids open these channels it becomes harder to conduct signals via these nerves.
The structure of morphine
There are a class of opioids which are naturally produced in the body, called endorphins. They produce similar effects to morphine both in terms of pain relief and the associated sensation of euphoria. They are released in a variety of situations, including during prolonged exercise of moderate to high intensity and are responsible for the effect known as “runner’s high”. Interestingly the time of release corresponds with the moment when muscles have used up their stored energy reserves and must start using fat supplies mobilised from other parts of the body. This switch between energy sources has also been associated with the sensation of “hitting the wall” and it is likely that the release of endorphins is intended to mitigate the associated pain.
As life expectancy increases, degenerative neurological conditions are rapidly becoming incredibly important. Patients suffering from a form of dementia such as Alzheimer’s are not only suffering a great deal from confusion and gradual deterioration, but also use a great deal of available healthcare resources. A large amount of research is going on to determine the cause of Alzheimer’s and how to treat it and progress is being made, but there is still no cure. The oldest hypothesis of the cause of Alzheimer’s is the cholinergic hypothesis: that the cause of AD is reduced synthesis of acetylcholine, a neurotransmitter. A neurotransmitter is a chemical that is used to transmit signals in the brain between neighbouring neurons and a particularly important one, which will be discussed later, is dopamine. However, the cholinergic hypothesis has been widely refuted; treatments based on this supposed deficiency have been largely ineffectual. The amyloid hypothesis suggested that the deposition of “plaques” in the brain led to the development of Alzheimer’s, with these plaques being composed of short sequences of cleaved protein (called beta-amyloid) forming an aggregate. These were then suggested to affect signalling processes in the brain which are normally involved in the destruction of unnecessary neuronal connections in early development.
Parkinson’s disease is another important degenerative disease of the brain, but is better understood than Alzheimer’s. This understanding has led to innovative new treatments. At a very fundamental level Parkinson’s is caused by the death of dopamine-producing cells in the part of the brain called the substantia nigra.
This is part of a larger structure known as the basal ganglia, the role of which is to change the levels of motor neuron excitability. In Parkinson’s, motor neuron excitability is reduced over time, leading to classic signs such as the shuffling gait and the loss of arm swing while walking. There are two main pathways regulated by the substantia nigra, both of which are controlled by dopamine production. It is beyond this article’s scope to describe these pathways fully, but further detail can be found here. The influence of dopamine on either pathway is to create an overall increase in motor excitability; however, there are certain structures in the brain which these pathways travel through (the globus pallides) and when stimulated will also either increase or decrease excitability. It was then found that the symptoms of Parkinson’s could be alleviated by intentionally damaging (lesioning) the structures that had an inhibitory effect. More recently, technology has developed to allow for stimulation of the structures which have an excitatory effect, leading to the modern therapy of permanent brain implants in order to carry out what is known as “deep brain stimulation”.
A discussion of pathologies of the brain would be seriously incomplete without mentioning mental disorders. 10% of children have a mental health problem at any one time and depression affects 1 in 5 older people. Certain mental health problems also provide an interesting insight into how the brain functions. For example, phobias provide an insight into Pavlovian conditioning, addiction is related to “reward pathways” in the brain and schizophrenia is related to attention, specifically the brain’s ability to filter out unimportant stimuli.
In order to discuss phobias we must first examine emotional pathways in the brain and look at how emotion is generated. Traditionally it was assumed that emotion was very much a “top down” phenomenon, with an emotion such as fear being elicited in the brain and therefore causing associated physiological changes (increase in heart rate, blood pressure and stress hormones). However, James-Lange proposed an alternative theory, that emotional experience derives from feedback from the rest of the body. This theory was then backed up by an experiment by Hohmann in patients who had previously suffered damage in their spinal cord. Patients with the damage higher up their spinal cord were more disabled and thus received less information from the rest of their body. Hohmann demonstrated that there was a relationship between height of damage in the spinal cord (and therefore feedback from the body) and emotional response to certain stimuli, with decreasing response the higher the lesion. This evidence was complicated by the fact that patients who were injected with adrenaline did not necessarily display any kind of emotion, despite the physiological changes it caused in their body.
As a result a new model was proposed by Shachter & Singer, who suggested that mental processing and assigning context to the physiological changes in the body are as important as these changes occurring. They designed and performed a very elegant experiment to test their hypothesis. The basis of the experiment was injecting test subjects with adrenaline, but giving different test groups different information. One test group was told they were going to experience the effects of adrenaline (palpitations and flushing), while the two other groups were either uninformed or deliberately misinformed about the adrenergic effects. Members of all three groups were then exposed to one of two situations, in which an actor pretended to be either incredibly angry or euphoric. Test subjects were subsequently interviewed about their reaction to these situations. The idea was that the groups who had not been informed that their physiological changes would be due to the adrenaline would then mistakenly attribute them to the emotional situations they were in and as a result experience a stronger emotional response. Their experimental data strongly supported their theory, with those attributing their emotion to the adrenaline actually experiencing a much less strong emotional response than those receiving a placebo. However, those receiving adrenaline while not aware what they had taken experienced a stronger emotional response than those receiving the placebo as they attained the increased physiological response.
One of the drawbacks of this system of dependence on physiological feedback to elicit emotions is the delay between a stimulus and the associated emotion, due to the time taken for physiological changes to occur. This is overcome by a process known as conditioning, where the brain learns to associate a stimulus with an emotion. The idea of conditioning was famously demonstrated by Pavlov using dogs. By ringing a bell before feeding these dogs he could train them to expect food and therefore salivate simply by ringing a bell. The same mechanism may underlie phobias and has been tested in animal models by exposing the animal to a harmless stimulus followed by a harmful one, resulting in the animal expressing a fearful response to the harmless stimulus. Some functional brain imaging studies have shown greater than average activity in the area of the brain associated with fear (the amygdala) in phobia sufferers, even when looking at non-phobic but otherwise fear-inducing images. Interestingly, the type of phobias that are most common suggest that there is some evolutionary basis to phobias and fearful stimuli in general. Dog and snake phobias are relatively common, whereas knife and gun phobias are not. If you were to compare the number of negative experiences associated with knives compared to those with snakes you would expect the number of knife phobias to be far greater, therefore strongly suggesting that there is a hereditary/genetic component.
Perception can be defined as the organisation, identification and interpretation of sensory information in order to represent and understand our environment. When we are perceiving something we are not simply letting it stimulate our sensory nerves but also actively processing the information it has created based on a number of factors including previous experience and expectation. However, we may still be processing information which we do not perceive, as in the “cocktail party effect”. At a crowded (cocktail) party you will be generally oblivious to background conversation, but will still be able to pick up someone saying your name on the far side of the room. A great deal can be learned about perception by studying when perception fails to create an accurate interpretation of our environment, for example in optical illusions. A good example of this is the Hermann grid illusion. In this illusion grey blobs appear at the intersections between the white lines.
The process that underlies this is known as lateral inhibition, a form of sensory processing which occurs not just in vision but also in touch. Lateral inhibition functions to increase the resolution of vision by limiting the area which is stimulated by a point of light. Without lateral inhibition a single light source would stimulate a much larger area of the retina than is appropriate. Lateral inhibition allows cells which are stimulated to inhibit nearby cells, meaning any cells absorbing scattered light are inhibited from firing.
In the first diagram the signal intensity is relatively high in the area around the stimulus, so it would be harder to detect a second nearby point stimulus. In the second diagram the central stimulation inhibits the surrounding area, making a separate point of light easier to distinguish.
Visual perception is also designed to increase contrast between two neighbouring colours so that they can be distinguished. What this means is that the eye is not particularly good at perceiving absolute colour, but is very good at looking at colour compared to an adjacent object. This is the basis of many optical illusions, with perhaps the most dramatic being the grey square image shown below:
With the illusion completely assembled the squares A and B appear to be completely different shades of grey, yet at the start they are clearly identical. This is based on the simpler illusion of a solid grey bar or a greyscale background, as shown.
In this first image a plain grey bar is displayed. In this second image the same grey bar is shown superimposed over a greyscale background.
These two illusions show the importance of contrast in vision, but why is this the case? Contrast is important as the eye has to deal with a huge range of light intensities, ranging from a bright sunny day to a dimly lit room at night. In fact a white piece of paper can be 1 billion times brighter outside on a sunny day than on a moonless night. As a result there are many mechanisms to change the sensitivity of the eye, both physical (pupil diameter) and biochemical (receptor desensitisation). What this means is that the eye is quite poor at detecting absolute intensity, but compensates by instead looking at relative intensities, leading to the illusions above where a darker part of the background makes the same colour look relatively less dark.
While optical illusions are the most famous type of illusion other senses are also susceptible to illusions. One intriguing auditory illusion is known as Deutsch’s scale. This image neatly explains the basics of the illusion:
One melody is played exclusively in one ear and the other melody is played in the other. However, when it is listened to it is perceived as the descending scale being played in one ear and the ascending in the other, with statistically more right handers hearing the higher scale in their right ear. Even when the headphones are switched over the melodies are still perceived on the same sides. But why is this the case? A likely explanation is that in normal situations tones of a similar pitch tend to come from the same source, so we attribute the closely grouped tone sequences to one side or the other. However, this does not explain the statistical difference between left and right handed subjects and this remains a question to be investigated.
There are also tactile illusions, such as the cutaneous rabbit illusion. This illusion is brought about by tapping two skin regions in quick succession, for example the wrist and the elbow. Subjects will experience not only the rapid sequence of taps delivered, but also the sensation of a sequence of taps travelling between the two places being stimulated. The reason this is known as the cutaneous rabbit illusion is the hopping of the taps up the arm mimics the hopping of a rabbit.
One final illusion that offers a real insight into the function of the brain is one that has been described as the “induction of an illusory shadow person”, brought about by neurological stimulation. In an experiment performed on a woman who was being evaluated for epilepsy surgery, a very interesting and slightly disturbing outcome occurred. When a part of the brain known as the left temporoparietal junction was stimulated the subject reported perceiving the presence of a “shadow person” who would closely mimic her movements and would try to interfere with tasks she was given. This symptom is remarkably similar to that experienced by schizophrenics and was proposed to be due to the role of the temporoparietal junction in self-other distinction and the integration of multisensory body-related information. In this case the interference was likely to have caused this body-related information to be falsely attributed to this shadow presence.
What does it mean to perceive the colour red?
While the three topics of this article may seem disparate they are actually closely interrelated. Pathologies can affect perception, for example in schizophrenia, with malfunction in the brain sometimes giving significance to insignificant stimuli or creating the perception of another presence associated with hallucinations. Perception is a key part of pain, with the context and significance of pain widely varying its intensity and how much suffering it causes. In fact perception, when examined in detail, starts to create philosophical issues. There is an interesting thought experiment entitled “Mary the colour scientist”. In this thought experiment there is a woman called Mary who, for the purposes of the thought experiment, has been forced to learn about colour from a black and white room with a black and white television monitor. While she can receive data about what wavelength of light certain objects reflect and what colours these wavelengths are labelled as she has never seen these colours for herself. If she is then allowed to leave her room one day and experience the world for herself what difference does it make? Will Mary be able to learn anything new? What is the difference between consciously perceiving the redness of a sunset and it being unconsciously processed by the brain? This kind of question is probably best left to philosophers, but this has not stopped scientists contributing their opinions over the years.
I will conclude with this quote from the legendary physicist Erwin Schrodinger: “The sensation of colour cannot be accounted for by the physicist’s objective picture of light-waves. Could the physiologist account for it, if he had fuller knowledge than he has of the processes in the retina and the nervous processes set up by them in the optical nerve bundles and in the brain? I do not think so.”