Abstract
Fibromyalgia syndrome (FMS) is characterized by pain referred to deep tissues. Diagnosis and treatment of FMS are complicated by a variable coexistence with regional pain, fatigue, sleep disruption, difficulty with mentation, and depression. The widespread, deep pain of FMS can be a consequence of chronic psychological stress with autonomic dysregulation. Stress acts centrally to facilitate pain and acts peripherally, via sympathetic vasoconstriction, to establish painful muscular ischemia. FMS pain, with or without a coexistent regional pain condition, is stressful, setting up a vicious circle of reciprocal interaction. Also, stress interacts reciprocally with systems of control over depression, mentation, and sleep, establishing FMS as a multiple-system disorder. Thus, stress and the ischemic pain it generates are fundamental to the multiple disorders of FMS, and a therapeutic procedure that attenuates stress and peripheral vasoconstriction should be highly beneficial for FMS. Physical exercise has been shown to counteract peripheral vasoconstriction and to attenuate stress, depression, and fatigue and improve mentation and sleep quality. Thus, exercise can interrupt the reciprocal interactions between psychological stress and each of the multiple-system disorders of FMS. The large literature supporting these conclusions indicates that exercise should be considered strongly as a first-line approach to FMS therapy.
Highlights
Clinical diagnosis of fibromyalgia syndrome (FMS) has relied heavily upon tender point counts, a convenient evaluation of pain sensitivity that has come under scrutiny in terms of reliability and validity [1]
Pain from vasoconstriction and muscular ischemia can explain the referral of FMS pain to deep tissues
FMS patients complain of chronic pain referred to deep tissues and commonly present with depression, fibrofog, and sleep disruption
Summary
Clinical diagnosis of fibromyalgia syndrome (FMS) has relied heavily upon tender point counts, a convenient evaluation of pain sensitivity that has come under scrutiny in terms of reliability and validity [1]. When psychological stress and peripheral vasoconstriction become chronic and establish muscular ischemia, with sensitization of nociceptors [38, 39], muscular pain is evoked [9]. The most thoroughly studied form of central sensitization is temporal summation (windup), a form of central synaptic magnification that requires repetitive or tonic nociceptive input to central neurons [43] This phenomenology has led to proposals that central sensitization underlies FMS pain [42] and is responsible for the widespread cutaneous hyperalgesia that accompanies regional pain conditions [44]. The stress and autonomic dysregulation that accompany localized chronic pain can account for widespread hyperalgesia [58, 60,61,62,63,64,65,66, 66,67,68] and development of FMS pain after onset of a regional pain condition [50]
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