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. with secondary sources of inflammation (fibrous bands or bulked, edematous, or transformed muscles), promoting a vicious cycle. This inflammation is unusual in that it does not respond to arachidonic cascade inhibitors, such as nonsteroidal anti-inflammatories or corticosteroids, and is largely cell-mediated in nature. This concatenation of observations emphasizes the importance and involvement of immune and supportive (glial) cells, which have been largely overlooked in generating these painful symptoms, swelling, adhesions, and concomitant disability. Over the last decade, white blood cells, Schwann cells in the periphery, and microglia centrally have been implicated in the development of chronic pain through their reactivity and secretion of neuropeptides and cytokines, some of which I have documented as being present in the adhesions investigated intraoperatively, as mentioned above. These molecules are part of tight, intermeshed networks that control local inflammation and pain, and can be destructive. Their presence and continued secretion to minimal stressors brings about a vicious cycle of immune-cell activation, swelling, fibrosis, and various pains and abnormal sensations.