Increased Neural Sympathetic Activation in Fibromyalgia Syndrome

Abstract

Fibromyalgia (FM) is a syndrome characterized by widespread musculoskeletal pain, although the mechanisms underlying the pain have not been fully elucidated. FM patients describe a number of nonspecific symptoms, such as anxiety, depression, fatigue, unrefreshing sleep, and gastrointestinal complaints, which appear after a flu-like illness, or after physical or emotional trauma in half of the patients, and are often exacerbated by exertion, stress, lack of sleep, and weather changes. There may also be symptoms of orthostatic intolerance, which suggests underlying abnormalities in cardiovascular neural regulation. Research suggests that various components of the central nervous system are involved, including the hypothalamic-pituitary-adrenal (HPA) axis, pain-processing pathways, and the autonomic nervous system (ANS). This review discusses the general aspects of the altered HPA and ANS, sympathetic overactivity, and alterations in cardiovascular autonomic responses to gravitational stimuli.

Is the Transcranial Magnetic Stimulation an Adjunctive Treatment in Fibromyalgia Patients?

“…A number of hypotheses have been proposed regarding the pathophysiology of FM, which includes dysfunction of pain modulatory systems within the central nervous system, neuroendocrine dysfunction, and dysautonomia (3)(4)(5). However, there is no concept that provides a full explanation of the pathogenesis of the disease.…”

Etiopathogenetic mechanisms of fibromyalgia syndrome

“…On the whole, however, there is no evidence to support any structural abnormality in the endocrine organs which comprise the HPA axis; thus, it seems that the changes found in hormone production under activation of the axis are functional in patients with FMS (82). Dysregulation of the HPA axis can potentially account for several symptoms in FMS, including fatigue, primarily, as well as depression and sleep disturbance; these symptoms are often present in subjects with a reduced activity of the axis (as in withdrawal from glucocorticoid therapy, or in Addison's disease) or in individuals with genetically altered HPA axis function (83). A link with pain is also present.…”

“…Increased central levels of CRH also produce analgesia in animals (85). Activation of the HPA axis stimulates the release of the opioid beta-endorphin, corticotrophin, and cortisol, which, thanks to its anti-inflammatory properties, has the potential of reducing pain (83), though it should be underlined that in FMS, specifically, corticosteroids are not effective (86).…”

Fibromyalgia syndrome: the pharmacological treatment options

“…The hypothesis that pain, anxiety, chronic stress and depression share common pathogenetic backgrounds which are represented by neurotransmitters and immune response is noteworthy. As such, depression must be considered as a systemic disease that is related not only to neurotransmission imbalance, but also to other neurotrophic, neurosteroidal, CNS hormonal modifications and diffuse, autonomic, immunologic, and metabolic somatic changes (8,21). According to this hypothesis, antidepressants restore neurotransmitter levels and modulate receptor expression in the hypothalamus, which normalizes hyperactivity of the hypothalamic-pituitary-adrenal (HPA) axis (18, 1).…”