ABSTRACT
This chapter considers how the brain, mind, and body play significant roles in the pathoetiology of soft-tissue pain, particularly fibromyalgia syndrome. The terminology central sensitivity syndromes has been used most particularly by M. B. Yunus. Any factor that would increase or decrease the functional aspects of pain transmission or pain modulation in the neuromatrix would be able to influence pain sensitivity. The concept of dysfunctional pain modulation encompasses two aspects: the development of central sensitization secondary to neurochemical and neuroanatomical changes initiated and induced by pain, and dysfunctional inhibition, the inability of the normal inhibitory descending antinociceptive pathways to effectively inhibit nociception. Central sensitization with regions of secondary hyperalgesia have been felt to be associated with myofascial trigger points. The concept of the limbically augmented pain syndrome is considered to be a clinical manifestation of corticolimbic sensitization secondary to kindling mechanisms in the supraspinal structures that effect both nociceptive processing and affective regulation.
