Acute pain: Pain that comes on quickly, can be severe, but lasts a relatively short time. (1)1
Addiction: A primary, chronic, neurobiologic disease whose development and manifestations are influenced by genetic, psychosocial, and environmental factors. It is characterized by behavior that includes one or more of the following: impaired control over drug use, compulsive use, continued use despite harm, and craving. (2)
Allodynia: Pain due to a stimulus that does not normally provoke pain. (3)
Allostatic load: The cumulative physiological cost to the body of chronic exposure to the stress response. (4)
Analgesia: Absence of pain in response to a stimulus that would normally be painful. (5)
Beliefs: Assumptions about reality that shape the interpretation of events and, consequently, the appraisal of pain. (6)
Biopsychosocial model: A framework that accounts for the biological, psychological, and social dimensions of illness and disease. The biopsychosocial model
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1 Numbers in parentheses indicate the respective references listed at the end of this glossary.
provides a basis for the understanding and treatment of disease, taking into account the patient, his/her social context, and the impact of illness on that individual from a societal perspective. The model states that ill health and disease are the result of interaction among biological, psychological, and social factors. (7)
Chronic pain: Ongoing or recurrent pain lasting beyond the usual course of acute illness or injury or, generally, more than 3 to 6 months and adversely affecting the individual’s well-being. A simpler definition for chronic or persistent pain is pain that continues when it should not. (8)
Cognitive-behavioral therapy: An empirically supported treatment focusing on patterns of thinking that are maladaptive and the beliefs that underlie such thinking. Cognitive-behavioral therapy is based on the idea that our thoughts, not external factors, such as people, situations, and events, cause our feelings and behavior. As a result, we can change the way we think to improve the way we feel, even if the situation does not change. (9)
Hyperalgesia: Increased pain from a stimulus that normally provokes pain. (10)
Interdisciplinary: Refers to efforts in which professionals from several disciplines combine their professional expertise and understanding to solve a problem.
Neuromatrix theory: Proposes that pain is a multidimensional experience produced by characteristic “neurosignature” patterns of nerve impulses generated by a widely distributed neural network—the “body-self neuromatrix”—in the brain. These neurosignature patterns may be triggered by sensory inputs, but they may also be generated independently of them. (11)
Neuropathic pain: Pain caused by a lesion or disease of the somatosensory nervous system. (12)
Nociception: The neural processes of encoding and processing noxious stimuli. (13)
Opioid: Any compound that binds to an opioid receptor. Includes the opioid drugs (agonist analgesics and antagonists) and the endogenous opioid peptides. (14)
Pain: An unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage. (15)
Pain catastrophizing: An individual’s tendency to focus on and exaggerate the threat value of painful stimuli and negatively evaluate his/her ability to deal with pain. (16)
Referred pain: Pain subjectively localized in one region although due to irritation in another. (17)
Self-efficacy: Beliefs that individuals hold about their capability to carry out actions in a way that will influence the events that affect their lives. (18)
Sensitization: An increased response of neurons to a variety of inputs following intense or noxious stimuli. (19)
REFERENCES
(1) American Chronic Pain Association. 2011. Glossary. http://www.theacpa.org/30/Glossary.aspx (accessed June 9, 2011).
(2) APS (American Pain Society). 2001. Definitions related to the use of opioids for the treatment of pain. http://www.ampainsoc.org/advocacy/opioids2.htm (accessed April 25, 2011).
(3) IASP (International Association for the Study of Pain). 2011. Pain terms. http://www.iasp-pain.org/AM/Template.cfm?Section=Pain_Definitions&Template=/CM/HTMLDisplay.cfm&ContentID=1728#Allodynia (accessed June 9, 2011).
(4) NIAAA (National Institute on Alcohol Abuse and Alcoholism). 2011. Glossary. http://pubs.niaaa.nih.gov/publications/arh312/177-179.pdf (accessed April 25, 2011).
(5) IASP (International Association for the Study of Pain). 2011. Pain terms. http://www.iasp-pain.org/AM/Template.cfm?Section=Pain_Definitions&Template=/CM/HTMLDisplay.cfm&ContentID=1728#Analgesia (accessed June 9, 2011).
(6) Gatchel, R. J., Y. B. Peng, M. L. Peters, P. N. Fuchs, and D. C. Turk. 2007. The biopsychosocial approach to chronic pain: Scientific advances and future directions. Psychological Bulletin 133(4):581-624.
(7) Brown, B. T., R. Bonello, and H. Pollard. 2005. The biopsychosocial model and hypothyroidism. Chiropractic and Osteopathy 13(1):5.
(8) American Chronic Pain Association. 2011. Glossary. http://www.theacpa.org/30/Glossary.aspx (accessed June 9, 2011).
(9) (a) NAMI (National Alliance on Mental Illness). 2011. Treatment and services—cognitive-behavioral therapy. http://www.nami.org/Template.cfm?Section=About_Treatments_and_Supports&template=/ContentManagement/ContentDisplay.cfm&ContentID=7952 (accessed May 4, 2011).
(b) NACBT (National Association of Cognitive-Behavioral Therapists). 2011. Cognitive-behavioral therapy. http://www.nacbt.org/whatiscbt.htm (accessed May 4, 2011).
(10) IASP (International Association for the Study of Pain). 2011. Pain terms. http://www.iasp-pain.org/AM/Template.cfm?Section=Pain_Definitions&Template=/CM/HTMLDisplay.cfm&ContentID=1728#Hyperalgesia (accessed June 9, 2011).
(11) Melzack, R. 2005. Evolution of the neuromatrix theory of pain. The Prithvi Raj Lecture: Presented at the Third World Congress of World Institute of Pain, Barcelona 2004. Pain Practice 5(2):85-94.
(12) IASP (International Association for the Study of Pain). 2011. Pain terms. http://www.iasp-pain.org/AM/Template.cfm?Section=Pain_Definitions&Template=/CM/HTMLDisplay.cfm&ContentID=1728#Neuropathicpain (accessed June 9, 2011).
(13) Loeser, J. D., and R. D. Treede. 2008. The Kyoto protocol of IASP basic pain terminology. Pain 137(3):473-477.
(14) Katzung, B., A. Trevor, and S. Masters. 2009. Opiod analgesics & antagonists. In Basic and clinical pharmacology, 11th ed. McGraw-Hill Companies, Inc.
(15) IASP (International Association for the Study of Pain). 2011. Pain terms. http://www.iasp-pain.org/AM/Template.cfm?Section=Pain_Definitions&Template=/CM/HTMLDisplay.cfm&ContentID=1728#Pain (accessed June 9, 2011).
(16) (a) F. J. Keefe, J. C Lefebvre, J. R. Egert, G. Affleck, M. J. Sullivan, and D. S. Caldwell. 2000. The relationship of gender to pain, pain behavior, and disability in osteoarthritis patients: The role of catastrophizing. Pain 87(3):325-334.
(b) Rosenstiel, A. K., and F. J. Keefe. 1983. The use of coping strategies in chronic low back pain patients: Relationship to patient characteristics and current adjustment. Pain 17(1):33-44.
(c) Keefe, F. J., G. K. Brown, K. A. Wallston, and D. S. Caldwell. 1989. Coping with rheumatoid arthritis pain: Catastrophizing as a maladaptive strategy. Pain 37(1):51-56.
(d) Sullivan, M. J. L., S. Bishop, and J. Pivik. 1995. The pain catastrophizing scale: Development and validation. Psychological Assessment 7(4):524-532.
(17) MedlinePlus. 2011. Referred pain. http://www.merriam-webster.com/medlineplus/referredpain (accessed April 25, 2011).
(18) Smith, B. J., K. C. Tang, and D. Nutbeam. 2006. WHO health promotion glossary: New terms. Health Promotion International 21(4):340-345.
(19) Baranauskas, G., and A. Nistri. 1998. Sensitization of pain pathways in the spinal cord: Cellular mechanisms. Progress in Neurobiology 54(3):349-365.