Massage & Bodywork

March/April 2013

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Resources Bellato, E. et al. "Fibromyalgia Syndrome: Etiology, Pathogenesis, Diagnosis, Treatment." Pain Research and Treatment (2012). Gudin, J. "Expanding Our Understanding of Central Sensitization." Medscape Neurology 6, no. 1 (2004). International Association for the Study of Pain. "Classification of Chronic Pain." Accessed February 2013. FreeBooks/Classification_of_Chronic_Pain/default.htm. Multidisciplinary Panel On Neuropathic Pain. "Role of Central Sensitization in Chronic Pain." Accessed February 2013. Staud, R. et al. "Temporal Summation of Second Pain and its Maintenance are Useful for Characterizing Widespread Central Sensitization of Fibromyalgia Patients." The Journal of Pain 8, no. 11 (2007): 893–901. is already vulnerable to dysfunction. In addition, central sensitization easily leads to anxiety, depression, and poor sleep—all of which can exacerbate pain. The result is an endless loop of pain and reactive behaviors that reinforce pain. Mechanisms of Central Sensitization You may remember from anatomy classes that all of the peripheral sensory neurons enter the spinal cord via the dorsal aspect. Within the dorsal horn of the spinal cord, short sensory axons have synapses with tracts of neurons carrying messages up to the thalamus and cortex, where sensation is perceived. Nociceptors (pain receptors) release excitatory neurotransmitters to stimulate the next neurons in the pathway. When enough nociceptors are signaling loud enough to pass the message to the neurons of the ascending tracts, those postsynaptic neurons may also become highly sensitized. Studies show that even a short-term stimulus can cause a long-lasting change in the chemical environment of the dorsal horns. This allows the CNS to distort and amplify the severity and duration of pain. Further, remember that each dermatome has some amount of overlap of nerve root supply; the same is true to an even greater extent for myotomes and sclerotomes. As neurons from multiple levels are recruited 44 massage & bodywork march/april 2013 to relay messages about pain, the brain perceives that the pain is spreading. But what starts the whole process of this type of chronic pain? And what maintains it? Consider a typical sprained ankle. The initial injury leads to inflammation and the secretion of potassium ions, substance P, bradykinin, prostaglandins, and other proinflammatory chemicals that support and prolong inflammation and the sensation of pain. Nociceptors that might otherwise have been silent may be activated in this chemical environment. So far, this is a healthy process. Pain tells us about damage—that we need to treat this part of the body carefully. Under normal circumstances, we heal, the pain signals stop, and all is well. But if the injury or problem is severe, all the sensory neurons— not just the nociceptors—can begin to behave like pain sensors. They pour pain-related excitatory neurotransmitters into the dorsal horn, the ascending tracts become highly sensitized, and the brain interprets it all as pain. Meanwhile, mechanisms that would limit pain sensation languish: inhibitory interneurons stop working, and the secretion of gammaaminobutyric acid, an inhibitory neurotransmitter, is suppressed. Chronic pain is such a common and serious problem that the National Institutes of Health present it as a freestanding disorder, rather than as a complication of some underlying condition. Nonetheless, many other problems list chronic, hard-to-treat pain as a major symptom, including: • Complex regional pain syndrome. • Fibromyalgia. • Neuropathic pain, including diabetic neuropathy and postherpetic neuralgia. • Postsurgical complications. • Rheumatoid arthritis and osteoarthritis.

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