What we do know is that the cramplike, diffuse muscle aching of fibromyalgia occurs when muscle receptors called nociceptors get turned on or turned up. Group III and group IV muscle receptors (nociceptors) are affected.

These nociceptors respond to mechanical or chemical stimulation. Substances released by the nerve endings sensitize the nociceptors. Once the nociceptors get fired up, neurons in the dorsal horn of the spinal cord also get turned on.

The messages between the muscles, spinal cord, and brain prolong the muscle pain. This creates a state of chronic muscle pain called hyperalgesia. Pretty soon, there are more receptors responding to normal stimulation as if it were noxious or painful.

The result is even more pain that can be great enough to travel to other areas of the body. This phenomenon is called referred pain. Motor control can get disrupted so that pain occurs at rest and becomes chronic (present all the time).

The actual process by which pain associated with fibromyalgia develops is very complex. Altered pain thresholds, involvement of neurotransmitters, and exaggerated responses of the nervous system may be part of the process. There remains much we don't know about this painful condition.