Biology and therapy of fibromyalgia: pain in fibromyalgia syndrome

Abstract

Fibromyalgia (FM) pain is frequent in the general population but its pathogenesis is only poorly understood. Many recent studies have emphasized the role of central nervous system pain processing abnormalities in FM, including central sensitization and inadequate pain inhibition. However, increasing evidence points towards peripheral tissues as relevant contributors of painful impulse input that might either initiate or maintain central sensitization, or both. It is well known that persistent or intense nociception can lead to neuroplastic changes in the spinal cord and brain, resulting in central sensitization and pain. This mechanism represents a hallmark of FM and many other chronic pain syndromes, including irritable bowel syndrome, temporomandibular disorder, migraine, and low back pain. Importantly, after central sensitization has been established only minimal nociceptive input is required for the maintenance of the chronic pain state. Additional factors, including pain related negative affect and poor sleep have been shown to significantly contribute to clinical FM pain. Better understanding of these mechanisms and their relationship to central sensitization and clinical pain will provide new approaches for the prevention and treatment of FM and other chronic pain syndromes.

Figure 1

Temporal summation of second pain (windup). When identical stimuli are applied to normal subjects at frequencies of ≥0.33 Hz, pain sensations will not return to baseline during the interstimulatory interval. Windup is strongly dependent on stimulus frequency and is inversely correlated with interstimulatory interval [75]. In contrast to normal subjects, FM patients windup at frequencies of < 0.33 Hz and require lower stimulus intensities [40].

Figure 2

Windup pain ratings of normal control (NC) and fibromyalgia syndrome (FM) patients. All subjects received 15 mechanical stimuli (taps (T)) to the adductor pollicis muscles of the hands at interstimulatory intervals of 3 s and 5 s. FM patients showed mechanical hyperalgesia during the first tap and greater temporal summation than NCs at both interstimulatory intervals. A numerical pain scale was used (0 to 100). The shaded area represents pain threshold.