Like a “bell-ringing mechanism in a church”. That is how, in 1664, Descartes (Jackson, 2002) suggested pain should be visualized. This, however, is a very primitive description of the phenomenon of pain.
Injury or inflammation of a bodily tissue can lead to profound changes in the internal chemical environment. Damaged cells discharge their intracellular components, releasing substances, notably ATP, potassium ions (K+) and acetyl chloine (ACh). Some of these contents act on nociceptors directly, triggering an action potential which will end up in the brain. Other components released from the cells can sensitize the terminals, making them hypersensitive to further stimuli. This allows a pain signal to be transmitted when a seemingly insignificant concentration of, for example ATP (released in millimolar quantities), is introduced to the extracellular space.
Prostaglandins, of which many pain receptors are especially sensitive, are produced at the site of injury. Arachidonic acid is generated by the cells and this in turn is converted to prostaglandins. Cyclooxygenase-2 (COX-2) converts the acid to prostaglandin H which in turn can be converted to specific prostanoids, such as prostaglandin E2. As Woolf (2004) noted, prostaglandin E2 can be detected by prostaglandin E receptors, causing sensitisation without directly producing pain. He tells us how it takes bradykinin, taken up by its B2 receptor, to activate the notion of pain. This instance highlights how complex pain sensations can be, and, whilst we may wonder why such a mechanism is necessary, we can learn to exploit the system by producing painkillers that hinder a specific step, thus having a vast ‘numbing’ knock-on effect.
There are many heat-sensitive receptors in our b...
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Pain is neither objective nor seen or felt by anybody other than the person that is experiencing it. Pain is subjective, therefore there is no way to distinguish whether or not someone is hurting and the only and best measurement of pain is that what the patient says it is. In settings such as end of life care, patients present with many different disease processes and ultimately are there because they have an average of six months to live. Along with this stage in their lives, palliative care patients can encounter a myriad of symptoms, which can result in these patients experiencing tremendous physical and psychological suffering (Creedon & O’Regan, 2010, p. [ 257]). For patients requiring palliative care, pain is the most incapacitating of symptoms and in return unrelieved pain is the primary symptom that is feared most by these patients. So why has pain management not become the top priority when it comes to end of life care, considering this area is growing at an extraordinary rate as a result of an increasingly ageing population?
Each person will respond differently to the pain experience. Therefore, the individual’s attitudes, personal experiences and knowledge are also antecedents to the concept of pain. For instance, a person that has been exposed to severe pain knows the
The most common and well described pain transmission is “gate control theory of pain”. This theory was first proposed by Melzack and Wall in 1965 whereby they used the analogy of gate to explain the inhibition of pain which exists within the dorsal horn of the spinal cord. For instance, when tissue damage occurs, substances such as prostaglandin, serotonin, histamine and bradykinin are released from the injured cell. Individual usually consume or apply pain medications such as NSAIDs whereby these medications will cause electrical nerve impulse at the end of the sensory nerve fiber via nociceptor. Nociceptor is a pain receptor that is commonly found in the skin, cornea of eye and organ of motion such as muscles and ligaments. These nerve impulses
Have you ever wondered why when you stub your toe on the chair in the living room, it helps tremendously to yell out an expletive or two and vigorously rub the area? I may not be able to discuss the basis for such language in this paper, but we will explore the analgesic response to rubbing that toe, in addition to the mechanism of pain and alternative treatments such as acupuncture and transcutaneous electrical nerve stimulation.
Pain has been defined by Coates & Hindle as an unpleasant emotional and sensory experience which signals a potential or actual damage to tissues (2011, p. 213). Pain is a common human experience and can emanate from injury and illness. There are two main types of pain; acute pain is short-lived, lasting for minutes or several days and its onset often takes place rapidly. It results from the activation of pain nerve endings or nociceptors either by internal or external pain stimuli. On the other hand chronic pain is continuous and sometimes recurrent and can last for weeks, months or even years. Chronic pain is usually not located at or related to the tissue undergoing trauma (Draper & Knight, 2007, p. 104). Various theories have been proposed to explain the mechanism underlying the transmission and perception of pain.
department: Are we ever going to get better? Journal of Pain Research, 2, 5-10. Retrieved from http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3004630/
However, the authors mentioned that the opioids receptors are constitutively desensitized under normal condition in peripheral sensory neurons. Therefore, opioid receptors typically remain unresponsive to an agonist. Tissue damage or inflammation by inflammatory mediators can diminish this unresponsiveness as well as stimulates cAMP accumulation. PGE2 is synthesized in response to inflammation in peripheral tissue damage which stimulates cAMP accumulation. Therefore, PGE2 stimulation represent peripheral nociception in this
In the body, aspirin has two main actions. It can act as an anti-prostaglandin (anti-inflammation, fever-reducing, pain reliever) compound and also as an anti-platelet aggregation (blood thinner) agent. The molecule works by inhibiting cyclooxygenase (...
Nociception is the term commonly used to refer to the perception of pain. The receptors involved in pain detection are aptly enough referred to as nociceptors - receptors for noxious stimuli. (1) These nociceptors are free nerve endings that terminate just below the skin as to detect cutaneous pain. Nociceptors are also located in tendons and joints, for detection of somatic pain and in body organs to detect visceral pain. Pain receptors are very numerous in then skin, hence pain detection here is well defined and the source of pain can be easily localized. In tendons, joints, and body organs the pain receptors are fewer. The source of pain therefore is not readily localized. Apparently, the number of nociceptors also influences the duration of the pain felt. Cutaneous pain typically is of short duration, but may be reactivated upon new impacts, while somatic and visceral pain is of longer duration. (2) It is important to note that almost all body tissue is equipped with nociceptors. (1, 2) As explained above, this is an important fact, as pain has primary warning functions. If we did not feel pain and if pain did not impinge on our well-being, we would not seek help when our body aches. Hence, it makes evolutionary sense for the body to be so well equipped with nociceptors in almost all locations. The most notable exception to this logic is the brain. The brain itself has no nociceptors and therefore is pain insensitive. Why is this all-important structure not equipped with and therefore indirectly protected by nociceptors?
Staats, P.S., Hekmat, H., & Staats, A.W. (2004). The psychological behaviorism theory of pain and the
Somatic pain is that in which nociceptors in the cutaneous or deep tissues are activated by noxious stimuli. This is usually characterized by dull, aching pain which is well localized. This type of pain may be commonly experienced by individuals with metastatic bone pain or those who h...
Hemmings H.C.and Hopkins P.M., (2006) Foundations of Anesthesia 2sd ed. Elsevier. Hudspith M.J., Siddall P.J. and Munglani R. Physiology of Pain.
Tulunay, F. (2000). NSAIDs: behind the mechanisms of action. Functional Neurology, Suppl 15 (3) 202-207.
Potent pain medication contains the aspects of utilizing medications such as morphine or demerol, how the medications are dispensed, and t...
·Aspirin (salicylic acid acetate) is an anti-inflammatory (decreases swelling and inflammation), anti-pyretic (fever reducing), and anti-platelet (decreases platelets in the body to thin blood). Many heart treatment patients take an aspirin a day to prevent blood clotting. However, if aspirin is taken in large quantities over long periods of time, it may cause gastric ulcers or other internal damage. The molecular formula of aspirin is C9H8O4. Some examples of Aspirin are Bayer, Ecotrin, and Aspergum.