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Chronic Pain: A New Disease?
University of Tennessee
Dr. Brookoff is Clinical Associate Professor of Medicine, University of Tennessee College of Medicine, Memphis, and Associate Director,Comprehensive Pain Institute, Methodist Hospitals of Memphis.
Chronic pain continues to be perceived as a characterologic disorder rather than a serious, potentially fatal, medical disease. The general lack of understanding of how persistent pain becomes magnified and ingrained prevents many patients from receiving the level of care that they need to regain control of their lives and resume normal activities.
In the United States, nearly one third of the population experiences severe chronic pain at some point in life. It is currently the most common cause of long-term disability, partially or totally disabling upwards of 50 million people. As the population ages, the number of people needing treatment for chronic pain from back disorders, degenerative joint diseases, rheumatologic conditions such as fibromyalgia, visceral diseases, cancer, the effects of cancer treatment, and other syndromes will undoubtedly grow.
The good news is that safe and effective medical treatment for chronic pain is currently available. A major barrier to be overcome, however, is that chronic pain is often not viewed as a physical illness worthy of treatment. Recent studies demonstrating that specific changes occur in the peripheral and central nervous systems of patients with chronic pain provide the rationale for changing our approach to chronic pain syndromes and instituting more aggressive and comprehensive treatment.
Normal Pain Pathways
Pain serves as an important alarm that warns us of threatened or ongoing tissue damage. The ability to sense pain keeps us alive and functioning. When that ability is compromised--for example, by diabetes or other causes of sensory neuropathy--the risk of severe tissue damage and debility is greatly increased.
Tissue injuries trigger the release of chemicals that give rise to an inflammatory reaction that in turn triggers pain signals to the brain. These signals, in the form of electrical impulses, are carried by thin unmyelinated nerves called nociceptors (C-fibers) that synapse with neurons in the dorsal horn of the spinal cord. From the dorsal horn, the pain signal is transmitted via the spinothalamic tract to the cerebral cortex, where it is perceived, localized, and interpreted (Figure 1).
Figure 1 - Pain signalling between the brain and spinal cord.
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This complex nociceptive system is balanced by an equally complex antinociceptive system (Figure 2). Pain signals arriving from peripheral tissues stimulate the release of endorphins in the periaqueductal gray matter of the brain and enkephalins in the nucleus raphe magnus of the brainstem. The endorphins inhibit propagation of the pain signal by binding to µ-opioid receptors on the presynaptic terminals of nociceptors and the postsynaptic surfaces of dorsal horn neurons. The enkephalins bind to delta-opioid receptors on inhibitory interneurons in the substantia gelatinosa of the dorsal horn, causing release of gamma-aminobutyric acid (GABA) and other chemicals that dampen pain signals in the spinal cord.
Figure 2 - Diagram of the brain's own pain reduction systems.
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