Pain is a type of sensation that can be sensible if we have external stimuli which will be harmful for us. It can because of both external stimuli and upon internal bodily damage. Pain is important in directing our attention toward a danger and holding it when a harmful stimulus is experienced. Therefore it is critical for survival. By taking into account this information, the current paper is aimed to evaluate importance of pain and the neural pathways & mechanisms involved in pain sensation in different contexts.
Although pain leads unpleasant emotion in reality this is the way which occurs to protect us from harmful stimuli. When Brand and Yancey (1997) write a book about pain they used The Gift Nobody Wants as a title of book which explains the phenomenon very well. Pain is a gift that we have to survive. To understand the value of the pain we need to look other side around. Therefore the case of Miss C., the woman who felt no pain will help us to understand the value of it.
As a child, she had bitten off the tip of her tongue while chewing
food, and has suffered third-degree burns after kneeling on a hot radiator to
look out of the window. When examined . . . she reported that she did not feel
pain when noxious stimuli were presented. She felt no pain when parts of her
body were subjected to strong electric shock, to hot water at temperatures
that usually produce reports of burning pain, or to prolonged ice-bath. . . .
A variety of other stimuli, such as inserting a stick up through the nostrils,
pinching tendons, or injections of histamine under the skin-which are
normally considered as forms of torture-also failed to produce pain.
Miss C. had severe medical problems. She exhibited pathological changes
in her knees, hip and spine, and underwent several orthopedic operations.
Her surgeon attributed these changes to the lack of protection to
joints usually given by pain sensation. She apparently failed to shift
her weight when standing, to turn over in her sleep, or to avoid
certain postures, which normally prevent the inflammation of joints.
Miss C. died at the age of twenty-nine of massive infectionsaˆ¦ and
extensive skin and bone trauma.
The case of Miss C. explicitly illustrate how important to feel pain is. After knowing the importance of to feel pain, in the second part of the article the neural pathways and mechanisms of the pain will be explained.
How we sense pain? Which neural pathways have an effect on the sensation of the pain? Firstly information from touch receptors in the head enters the central nervous system. This information enters the spinal cord and past through the brain via 31 spinal nerves consisting of pairs of 8 cervical nerves, 12 thoracic nerves, 5 lumbar nerves, 5 sacral verves and 1 coccygeal nerve (Figure 1). These nerves connect to a limited area of the body, usually to skin. The skin is connected to dermatomes-a single sensory spinal nerve (Kalat, 2007).
Pain sensation begins with a cutenous receptor which contains free nerve ending. Some of these receptors respond to acids and heat above 43°C. A special chemical which is found in hot pepper called capsaicin also activates these receptors. For instance, assuming that we touch hot pepper and then to our eyes, a burning sensation may be caused, indeed it causes pain. (Kalat, 2007) The animal studies showed that animal reacted this chemical by sweating or salivating (Caterina, Leffler, Malmberg, Martin, Trafton, Petersen-Zeitz, 2000).
The intensity of pain affects different neurotransmitters in the axons. While mild pains activate glutamate, strong pain activates not only glutamate but also substance P (Cao, Mantyh, Carlson, Gillespie, Epstein & Bashbaum, 1998). The study of DeFelipe, Herrero, O’Brien, Palmer, Doyle & Smith (1998) suggested that while mice having limited receptors for substance P reacted normally to mild injury, the reacted severe injury as if it was a mil done.
The cells in the spinal cord are pain sensitive and carry the information to different parts of the brain. Indeed there are a number of pathways in which pain sensation takes place. On pathway is from ventral posterior nucleus of the thalamus to somatosensory cortex. This cortex is responsible for detecting the location of the pain on the body. It responds both to painful stimuli and to signals that born of impending pain (Kalat, 2007). Another pathway is from reticular formation to central nuclei of thalamus, prefrontal cortex, cingulate cortex, hippocampus and amygdala (Figure 2). These areas not only reacts sensation but also unpleasant emotions (Hunt, Mantyh, 2001). For instance, the study of Singer, Seymour, O’Doherty, Kaube, Dolan & Frith (2004) suggested that we experience a “sympathetic pain” when we observe a loved-one experiencing pain. This pain shows up as activity in our cingulate cortex rather that somatosensory one.
Additionally microrecording and microstimulation experiments have demonstrated that humans and other species have neural structures that respond preferentially to noxious stimuli.(Grahek, 2007) These structures include fast A-a?† nerve fiber and slow C fibers.Indeed it can take more than a second for the nerve impulses conducted by C-fibers to reach the spinal cord from an injured foot, while the nerve impulses transmitted by A-a?† fibers from the same part of the body reached it long before The difference between those fibers is that while A-a?† nociceptive fibers corresponds to fast, sharp, pricking pain (first pain, or alarm pain), the activity of C-nociceptive fibers is related to slow, dull, or burning pain (second pain, or to speculate a bit, remembrance pain) (Grahek, 2007)
How pain is relieved and what are the ways that modulate pain is another issue that is going to be discussed in present paper. When we are aware of the pain, further pain messages accomplish little because opioid mechanism systems that respond to opioate drugs and similar chemicals put blocks on prolonged pain (Kalat, 2007). It has also been discovered that those opioates exert their effect by binding to certain receptors in periaqueductal area of the midbrain (Pert &Snyder, 1973) (Figure 3). Further discoveries also showed that these special receptors block the release of substance P. (Kondo, Marvizon, Song, Salgado, Codeluppi, Hua, 2005).
Endorphins-transmitters that attach to the receptors as morphine- are released by both pleasant and unpleasant stimuli and therefore relieve pain. (Kalat, 2007) They also have an effect on the further pain especially when it is inescapable (Sutton, Lea, Will, Schwartz, Hartley, Poole, 1997). It was also suggested by Zubieta, Ketter, Bueller, Xu, Kilbourn &Young (2003) that it was possible to decrease endorphin release if we brood about sad memories.
Another issue is related to how people differ in their way to feel pain. Why some injury hurts worse at the same time than others is related partly to genetic differences. However gate theory explains this difference clearly (Wei, Wang, Kerchner, Kim, Xu, Chen, 2001). The gate theory argued that spinal cord neurons not only receive message from pain receptors but also from touch receptors and axons descending from brain. These other inputs therefore close the Gates for the pain message. Indeed assuming that we have an injury, we can decrease pain by gently rubbing the skin around or by concentraing on something else (Kalat, 2007).
Using capsaicin is another way to modulate pain. As I mentioned earlier, by releasing substance P, it produces a burning or painful sensations. On the other hand it also causes cells to send pain message. That is if we rubbed capsaicin on a damaged shoulder, it produces a temporary burning sensation followed by a longer period of decreased pain (Karrer &Bartoshuk, 1991).
Placebos are widely used pain releasers used especially in experiments. Although a placebo does not have any pharmacological effect, it acts as if it has. In many experiments, while active treatment group receives a drug or treatment, the control group receives placebo. Although placebos do not have much effect, they sometimes relieve pain because pain decreased just because people expect it to decrease. (Hrobjartson & Gotzsche, 2001). The brain scans also displayed that placebos decrease the brain’s response to painful stimuli. Placebos are doing it by focusing on the emotion, not sensation. The activity eventuates in cingulate cortex, not in somatosensory cortex (Petrovic, Kalso, Peterson & Ingvar, 2002). The case is same with a hypnotized person, they feel pain but they do not react emotionally (Rainville, Duncan, Price, Carrier, Bushnell, 1997).
The body has not only mechanism for relieving pain but also has decreasing mechanisms. It is inevitable to feel pain if we touch light to a sunburned skin. Damaged and inflamed area in the body releases histamine, nerve growth factor and other chemicals helping to repair the damage but also magnify responses in closer pain receptors (Devor, 1996; Tominaga, Caterina, Malmberg, Rosen, Gilbert, Skinner, 1998).
Pain can sometimes be chronic after an injury has healed. It is unknown why this pain is developed in some people but the mechanism is partly understood. A barrage of intense stimulation of neuron can potentiate its synaptic receptors. Therefore same input may cause more vigorous response in the future. In fact this mechanism is central to learning and memory but it is also play a critical role in pain. (Ikeda, Heinke, Ruscheweyh, & Sankuhler, 2003).
To sum up, the information mentioned above explains the importance of pain and how it is essential for survival. Enhancing our knowledge of mechanisms playing active role in pain may help us to design studies and develop research questions in the future. Also there are some issue that have not been addressed such as memory. We know from the literature of trauma psychology that the way pain is felt and the way the situation is interpreted have an effect on the memory of a traumatic event. This may lead a researcher to focus on the the mechanisms involved in memory of the traumatic events that cause pain .
Figure 1: Spinal nerves in human central nervous system (Source: From James W. Kalat, Biological Psychology, 9th edition; 2007, 208)
Figure 2: Representation of pain in human brain.(Source: From James W. Kalat, Biological Psychology, 9th edition; 2007, 208)
Figure 3: The periaqueductal gray area, where electrical stimulation relieves pain. (Source: From James W. Kalat, Biological Psychology, 9th edition; 2007, 208)