Introduction
Acute pain after an injury is a common experience. However, chronic pain can be debilitating and is becoming an extremely costly major health problem. US costs due to all forms of chronic pain are estimated at $90 billion a year due to lost income, disability and direct patient care costs. Some types of chronic pain are increasing, for example, the lifetime prevalence of recurrent low back pain may now be as high as 80%. Improving understanding about the nature of pain and how acute pain can become chronic is very important.
The original simple explanation of pain saw it as a direct consequence of specific injury: nerve impulses from the injury site travel to the brain and pain is experienced. In this explanation, pain experienced is directly proportional to the severity of the injury. When dealing with acute and localized injuries, this explanation may be accurate enough. However, a number of clinical observations challenged this initial description. First, pain experienced seems to depend on factors other than severity of injury. For example, some people report little pain from severe injuries (e.g., soldiers severely injured in combat, athletes hurt during competition) while others report great pain from a minor or undetectable injury. In other cases, such as phantom limb pain, there is no clear source for the pain (phantom limb pain even persists after the remaining nerve supply has been removed surgically), or, as in most cases of low back pain, clear anatomical abnormalities may not be evident (recent studies suggest that X-rays, CT scans and MRIs could not distinguish most low back pain patients from controls).
"Gating" of Pain
A more contemporary explanation of pain accounts for these observations. Many clinicians and scientists now see pain as the result of a gate-like mechanism that controls how nerve impulses reach the brain and are interpreted. The crucial notion (first put forward by Melzack and Wall in 1965) is that the messages transmitted to your brain from the injury site are also affected by messages that come down from your brain. Messages from your brain result in the intensity of the nerve impulse from the injury site being altered or sometimes even blocked completely. This explains how pain experienced can differ based on the situation and other variables. Factors which affect the pain "gate" have been explored in detail. Physical factors which increase pain experienced include: extent of the damage (including inflammation and scarring); dysfunction of artery or muscle system (inherited), and muscle tension. Emotional factors which increase experienced pain include: anxiety, anger and depression. Lastly, specific psychological factors that can increase pain include: degree of focus on the pain, boredom, beliefs about the meaning of the pain, and a sense of poor control over the pain.
Reducing Pain
Pain can be reduced by interventions designed to address each of these factors.
For the physical factors involved in the pain: 1) medication (such as analgesics, anti-inflammatories, sedatives, etc.); 2) counter-stimulation (such as by TENS devices, heat, massage, etc.); 3) surgery (severing nerve fibers, etc.), and
4) reduced muscular tension. Medication may result in pain reduction initially, but after continuous use tolerance develops, pain may not be sufficiently controlled and side effects increase. While rest is useful for acute injury, with chronic pain, long term inactivity and isolation can lead to boredom, depression and muscular atrophy in addition to preoccupation with pain sensations (nothing else to focus on) which may make chronic pain more severe. Surgery is not always useful or feasible. It may also result in new physical problems (more scar tissue, etc.) and the original pain may continue. Emotion-centered interventions that can improve pain include: 1) relaxation, 2) anxiety reduction, and 3) improving mood (reduced depression and negative mood). Psychological techniques that can help decrease pain include: distraction, external focus of attention (outside your body), being engaged in other activities, cognitive strategies to reduce pain intensity; and active coping including pain control.
Again, pain experienced is not strictly a function of physical changes. You may feel frustrated if physical methods have not addressed your pain, especially if those you have consulted have suggested the pain is "all in your mind" or psychosomatic. Remember, all pain is experienced in the brain. Whether you have just stubbed your toe or are experiencing chronic headache, the messages go up the spinal cord to the brain where the signals are interpreted as pain. When the pain is chronic, your emotional and behavioral reactions may make it worse and may keep the pain "gate" open.
Managing Pain
In cases where the pain experienced is chronic and variable, the relationship between injury or disease (if any) and the pain experienced is complex. The experience of pain is a complex psychological phenomenon. The situation and meaning of the pain has a tremendous influence on the duration and intensity of the pain and distress experienced.
Looking at the list of factors that make pain worse, you can see that most of them arise as a consequence to prolonged pain. A vicious cycle may develop whereby isolation and inactivity contribute to anxiety, depression and muscle tension, which leads to increases in pain, which in turn causes more inactivity, depression, muscle tension and so on. Reactions to continuous pain can make it worse. Normally when you hurt yourself, pain causes you to stop what you are doing, leave the situation, and rest. This aids healing. With chronic pain, however, continual withdrawal from activities is boring and depressing, your fitness level decreases and you tire more easily (with one week of immobility a muscle may lose a third of its size and power). Undistracted, you focus on your pain and perceive it as more intense and your tolerance decreases. Medication you take may produce side effects, become habit forming, and not work as well (after a time they inhibit or even stop your own production of natural endorphins - morphine-like substances that help reduce your awareness of pain). Anxiety about your pain and situation may increase, muscles may become tense, and you may become depressed and less willing to become active, uncertain what to do, and, ultimately, feel helpless and defeated.
Fortunately, cognitive behavioral pain management programs (see Gatchel and Turk, 1996; Philips & Rachman, 1996) are designed to teach alternative ways of dealing with pain that help "close the gate" and reduce distress, anxiety and depression by increasing understanding and control over the problem, encouraging activation and breaking the cycle of factors which is maintaining the pain at high levels. Such self-management programs have been successful in reducing experienced pain in many cases where physical interventions have not succeeded.
To sum up, chronic pain is a common and costly phenomenon. Pain experienced is not simply a function of tissue damage. Factors which influence pain can lead to a vicious cycle in the case of chronic pain. Cognitive behavioral pain management programs can address these factors and have been shown to be effective treatments for chronic pain.
Dr. David Aboussafy, Ph.D.
UCounsel Corporation
Vancouver Hospital and Health Sciences Center
University of British Columbia
Further Information and Support
For more information, contact David Aboussafy, Ph.D. at [email protected] or
[email protected] or see the Chronic Pain Course at UCounsel.com
References
Gatchel, R.J. & Turk, D.C. (1996). Psychological Approaches to Pain Management. New York: Guilford.
Philips, H.C. & Rachman, S. (1996). The Psychological Management of Chronic Pain. New York: Springer.
Melzack, R. (1993). Pain: Past, present and future. Canadian Journal of Experimental Psychology, 47, 615-629.
Melzack, R. & Wall, P. (1988). The challenge of pain. Middlesex, England: Penguin Books.
Turk, D.C., Meichenbaum, D., & Genest, M. (1983). Pain and behavioral medicine: A cognitive behavioral perspective. New York: Guilford Press.