There are the unfortunate patients who develop pain hypersensitivity. These patients have a pain threshold that is lower than normal, and the duration of the pain response can become long-lived. There are two main mechanisms of pain hypersensitivity: peripheral sensitization and central sensitization. Peripheral sensitization is associated with inflammation and tissue damage, things found in a variety of rheumatic diseases. One notes an increase in the patient’s response to the peripheral ends of nociceptors, which are the nerve cell endings that transmit pain signals to the brain in response to noxious stimuli.
Peripheral sensitization is the result of changes in transduction proteins—the carriers of messages--that affect the excitability of nociceptors. Noxious stimuli, such as excessive heat, are transformed into an electric response in the nervous system via these proteins. Normally, we begin to find heat painful at approximately 108° Fahrenheit, but after peripheral sensitization, that threshold temperature may be much lower. In fact, the threshold may be so low that washing hands in warm water can be excruciating.
In contrast, central sensitization involves an increase in the excitability of neurons in the central nervous system, resulting in patients displaying what appears to be an exaggerated response to seemingly innocuous stimuli. Inflammation and actual damage to tissue are not essential in central sensitization. Conditions that have their origins through central sensitization include fibromyalgia, irritable bowel syndrome, and temporomandibular joint disorder, to name but a few. In central sensitization there appears to be a change in the relationship between the nociceptors that start the journey of pain, and the brain.
A variety of biochemical changes occur in the central nervous system; these changes can become permanent, and the pain hypersensitivity they produce may also be permanent. Central sensitization patients often experience significant pain in response to light touch, and hyperalgesia, pain sensitivity outside an area of inflammation, or prolonged sensations of pain long after the stimulus ends. These reactions and experiences demonstrate the plasticity in the central nervous system.
Unfortunately, basic surgical procedures can trigger chronic pain, even in the absence of stressors such as surgical complications. Patients may experience changes in their pain pathways that lead to long-lasting pain hypersensitivity. In a study of over 3,000 adults with knee osteoarthritis, a lower pain threshold was detected that was not clearly associated with actual damage of the joint; in some cases, this pain was not alleviated by joint replacement surgery.
It appears physical disease has a profound relationship to, and perhaps causes, changes in the nervous system. Once more it is the task of the health care professional to be mindful of the psychobiology of the human being. Perhaps with many of the physical diseases we treat, there is another affliction that needs simultaneous care, buried in a miasma of brain chemicals and psychological concerns. And we still know so little.