Cytokine abnormalities are associated with many symptoms of fibromyalgia, and may explain the onset and maintenance of central sensitization.
There is substantial evidence that central sensitization plays a significant role in the pathophysiology of fibromyalgia, but how does central sensitization originate?
Cytokine abnormalities may provide some basis for understanding the onset of central sensitization. As described in the publication summarized below, cytokine abnormalities may contribute to (or cause) the initial onset of central sensitization. Cytokine abnormalities may also be a significant contributor to fatigue, sleep impairment, pain, stress, and aching – all common symptoms of fibromyalgia.
Status of immune mediators in fibromyalgia.
Summary of the Abstract
The pathophysiology of fibromyalgia remains in question, as does the most effective means of treatment.
There are numerous hypotheses, including that cytokines may play a central role. Cytokines are involved in diverse processes, including fatigue, fever, sleep, pain, stress, and aching. Likewise, cytokine elevation may lead to long-term activation of spinal cord neurons with resulting central sensitization. Pain, stiffness, and depression in fibromyalgia might also be explained, at least in part, by activation of the inflammatory response system.