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 By Lillian Chan & Y. Michael Chan Pain is probably the most common reason to seek medical attention. According to the International Association for the Study of Pain, this health issue accounts for more than 70 million health/medical visits each year in the United States. “Some visits follow trauma, infection, or acute illness; some relate to recurrent acute pain such as sickle cell crisis; many are due to chronic pain conditions such as neuropathies; while others may be associated with progressive diseases such as cancer,” it says. Definition The Association defines pain as “An unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage”. Pain is a perceived threat or damage to a person’s biological integrity. Pain experience The experience of pain is defined in terms of human consciousness. It is therefore a complex, subjective, perceptual, multilevel, multidimensional phenomenon. It is influenced by genetic predisposition, psycho-sociological expectations and conditioning, cultural and family dynamics, general health and mental conditions, nature and severity of the pain cause or illness, environmental factors, as well as personal meaning attributed to the experience. The list of determining factors goes on and on. As in any other experience of the human consciousness, pain is also a changeable and changing stream of awareness - improving or worsening, appearing or disappearing, amplified or forgotten; all can happen at a moment’s notice. Pain concepts “Pain is a more terrible lord of mankind than even death itself,” says Albert Schweitzer. “Pain is perfect miserie, the worst of evils, and excessive, overturns all patience,” says Milton in Paradise Lost. Ancient Egyptians believed pain was the spirit of the dead entering the body through ears or nose; ancient Indians thought it was from a frustration of desires, an ailment of the heart. Plato figured it was an emotional experience of the soul. Ancient Chinese attributed pain to Qi and blood (energy and nutrient) imbalance or insufficiency; whereas Hippocrates thought imbalance of the 4 humors caused pain. The court physician to Marcus Aurelius in Rome, Galen, who prescribed opium for pain, blamed pain on “hard nerves,” some types of peripheral nerves in the brain and spinal cord system. Decartes described pain as being transported by tube-like nerves connecting the skin to the brain. By the late 1800s, Scottish neurosurgeon Charles Bell, French physiologist Francois Magendie, German physiologist Johannes Muller, and British physiologist Charles S. Sherrington had formulated the dedicated neural pain pathway principle. They established that the function of pain is not to heal, but to provide warning of cells and tissues damage in the body. Pain is transmitted as nerve impulses by connecting peripheral receptors to spinal neurons, and to brain receptors. This pathway was thought to be like the telephone line exchange. In 1965, Canadian psychologist Ronald Melzack and British physiologist Patrick Wall developed the gate control theory. They established that the brain controls the amount of pain information it receives. There is a mechanism in the central nervous system that is closed to normal stimulation, and opened to pain sensations. The multiplicity of neural pathways has been demonstrated since then, and the involvement of simultaneous activities in various brain regions is being mapped. Now we know that the perception of pain is probably generated by the output of the neuromatrix, a pattern generating mechanism of the brain, as a function of the sensory inputs, together with information already stored in various regions of the brain. The role of conditioning and pain memory is being studied. It is clear that pain behaviour can be generated or perpetuated by learned cues in the environment, or by the expectation of pain. Injury not only produces pain, it also results in stress as the body tries to get back to the stable state of homeostasis. This process takes place at different parts of the body not just the injury site, and is influenced by many genetic factors that exist at the injury site (cytokine release), in the adrenal cortex (stress hormones), in the immune system, and in many areas of the brain. Components of pain Pain researchers Loeser and Melzack listed 4 broad categories as components of pain: nociception, perception of pain, suffering, and pain behaviour. Nociception - This is the detection of tissue damage by specialized transducer cells. These transducers are sensitive to inflammation and neural changes in their immediate environment. Non-steroidal inflammatory drugs (NSAID) such as aspirin and ibuprofen act by restoring nociceptive sensitivity to its resting state. Local and regional anesthesia can prevent nociception from becoming pain. Perception of pain - Although frequently triggered by a noxious stimulus, such as injury or disease, pain can occur without nociception. Lesions in the nervous system, as seen in diabetic neuropathy, spinal-cord injury or stroke, also generate pain. Pain due to nerve injury does not respond to analgesics such as morphine as efficiently as pain cause by tissue damage. When acute pain occurs, it is initially associated with specific autonomic and somatic reflexes, such responses disappear with chronic pain. With chronic pain there is frequently little or no relation between pain intensity and the extent of tissue injury. Suffering - It occurs when the physical or psychological integrity of the person is threatened. This is a negative response induced by pain, as well as by fear, anxiety, stress, loss of loved objects, and other psychological states. Pain behaviour - These are results from pain and suffering, and are the things a person can or cannot, does or does not, do. For example grimacing and lying down. Type of pain Transient pain - occurs in the absence of any tissue damage. It had evolved to protect the body from physical damage by the environment or by over-stressed body tissues. Acute pain - is elicited by substantial injury of body tissue and activation of nociceptive transducers at the site of tissue damage. The injury alters the response characteristics of the nociceptors, their central connections, and the autonomic nervous system in the region. Since the healing process usually takes a few days or a few weeks, pain that persists for months or years is not classified as acute. However, in malignant diseases, the invasion of the body tissues can produce continuous acute pain. The capacity to experience acute pain has a protective role: it warns us of imminent or actual tissue damage. By coordinating reflex and behavioural responses pain experience keeps such damage to a minimum. If tissue damage is unavoidable, changes in the peripheral and central nervous systems establish profound but reversible pain hypersensitivity in the inflamed and surrounding tissue. This process assists wound repair by avoiding contact of the damaged area until healing has occurred. Chronic pain - such as low back pain and fibromyalgia, are commonly triggered by an injury or disease. The injury may exceed the body’s capability for healing. It is also likely that stress, environmental and other affective factors may be superimposed on the original damaged tissue, and contributed to the intensity and persistence of pain. Chronic pain may continue when treatment stops. Psychological forms of therapy such as cognitive and behavioural treatment can also be used to reduce the effect of pain. Pain terms simplified
References Coghill, R.C. et al. Pain intensity processing within the human brain: A bilateral, distributed mechanism. Journal of Neurophysiology (1999) 82:1934-1943. www.wfubmc.edu/nba/faculty/coghill/coghill.html Loeser, J.D. and Melzack, R. Pain: an overview. Lancet (1999) 353: 1607-1609. Woolf, C.J. and Mannion, R.J. Neuropathic pain: aetiology, symptoms. Mechanisms and management. Lancet (1999) 353: 1959-1964 J.M. Besson, The neurobiology of pain. Lancet (1999) 353: 1610 Flor, H. et al. Phantom limb pain. International Association for the Study of Pain Clinical Update (2000) vol. VIII, #3 in www.iasp-pain.org |
 
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