WASHINGTON, D.C.–The experience of pain in patients with rheumatic diseases–and pain in other types of disorders–is much more complex than nerve endings on the skin getting the sensory input from a flame or another stimulus and the nervous system processing it as pain, recent research has shown.
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The central nervous system (CNS) is also heavily involved, and the understanding of this can lead to the treatment of pain that simultaneously resolves other symptoms that are also CNS regulated and that can help determine which drugs work in which people, experts said here at the recent 2012 ACR/ARHP Annual Meeting, held November 9–14.
The traditional notion of pain as just a peripheral, or strictly stimulus-driven, phenomenon is over, said Daniel Clauw, MD, professor of anesthesiology and medicine in the department of rheumatology at the University of Michigan, Ann Arbor. He is also director of the Chronic Pain and Fatigue Research Center there.
“There’s really two different parts of the pain system,” he said. “There’s a part of the pain system that is recognizing nociceptive input in the periphery—the classic sort of pain system that we’ve all learned about—but then the central nervous system can either turn up or turn down the gain and the extent to which the nociceptive input is felt by an individual.”
There can be a low-volume setting, with someone getting what might normally be painful stimuli but not actually feeling pain.
“Or they can have a very high-volume control setting, and they can be experiencing pain in spite of the fact that they don’t have any ongoing peripheral nociceptive input that we can identify by classic mechanisms, i.e., someone with a condition like fibromyalgia,” Dr. Clauw said.
Clifford Woolf, MD, PhD, director of the F.M. Kirby Neurobiology Center at Boston Children’s Hospital and professor of neurobiology at Harvard Medical School in Boston, who is credited with discovering and coining the term “central sensitization,” said that, “what’s fascinating is that many of the mechanisms that operate the human pain system and harness synaptic efficacy are very similar to the ones that operate and enable us to learn [and] retain information with memory.”
But one feature that differentiates central sensitization is “heterosynaptic facilitation.” This involves a “global increase in excitability of the neuron such that an input that was not activated before can now become enhanced.”
A simple example would be applying capsaicin to the skin, then applying secondary stimuli nearby. The capsaicin activates the nociceptors, producing a state of heightened excitability in the CNS, which can lead even a light touch nearby to be experienced as pain.