Neuroendocrine Perturbations in Fibromyalgia and Chronic Fatigue Syndrome

Neeck, Gunther; Crofford, Leslie J.

doi:10.1016/s0889-857x(05)70180-0

Cited by 138 publications

(70 citation statements)

References 55 publications

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“…In addition, although there is debate regarding the precise pathophysiological classification of these syndromes, a blunted HPA axis has also been show in fibromyalgia, [161][162][163][164] irritable bowel syndrome 165,166 and chronic fatigue syndrome. 163,[167][168][169][170][171] Disruption of the HPA axis or glucocorticoid response at different levels can predispose to enhanced susceptibility to autoimmune and inflammatory disease. Thus, low circulating glucocorticoids or abnormalities of GRs leading to glucocorticoid resistance can reduce glucocorticoid inhibition of immunity and increase inflammatory susceptibility.…”

Section: Neuroendocrine Dysregulations In Autoimmune Diseasesmentioning

confidence: 99%

Brain-immune interactions and disease susceptibility

2005

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Many studies have established the routes by which the immune and central nervous (CNS) systems communicate. This network of connections permits the CNS to regulate the immune system through both neuroendocrine and neuronal pathways. In turn, the immune system signals the CNS through neuronal and humoral routes, via immune mediators and cytokines. This regulatory system between the immune system and CNS plays an important role in susceptibility and resistance to autoimmune, inflammatory, infectious and allergic diseases. This review focuses on the regulation of the immune system via the neuroendocrine system, and underlines the link between neuroendocrine dysregulation and development of major depressive disorders, autoimmune diseases and osteoporosis.

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Section: Neuroendocrine Dysregulations In Autoimmune Diseasesmentioning

confidence: 99%

Brain-immune interactions and disease susceptibility

2005

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“…Clinical studies of the role of stress in the pathogenesis of chronic pain syndromes have implicated the hypothalamopituitary-adrenal (HPA) axis in, for example, fibromyalgia and chronic fatigue syndrome (Crofford et al, 1996;Neeck and Crofford, 2000). Although better known for their antiinflammatory actions, glucocorticoids (principal stress mediators released by the hypothalamo-pituitary-adrenal axis) have recently been reported to enhance pain, both in animal models of peripheral neuropathy (Wang et al, 2004;Takasaki et al, 2005) and when used for the treatment of osteoarthritis in humans (Wollstein et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

Stress Induces a Switch of Intracellular Signaling in Sensory Neurons in a Model of Generalized Pain

Khasar¹,

Burkham²,

Dina³

et al. 2008

J. Neurosci.

159

169

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Stress dramatically exacerbates pain in diseases such as fibromyalgia and rheumatoid arthritis, but the underlying mechanisms are unknown. We tested the hypothesis that stress causes generalized hyperalgesia by enhancing pronociceptive effects of immune mediators. Rats exposed to nonhabituating sound stress exhibited no change in mechanical nociceptive threshold, but showed a marked increase in hyperalgesia evoked by local injections of prostaglandin E 2 or epinephrine. This enhancement, which developed more than a week after exposure to stress, required concerted action of glucocorticoids and catecholamines at receptors located in the periphery on sensory afferents. The altered response to pronociceptive mediators involved a switch in coupling of their receptors from predominantly stimulatory to inhibitory G-proteins (G s to G i ), and for prostaglandin E 2 , emergence of novel dependence on protein kinase C. Thus, an important mechanism in generalized pain syndromes may be stress-induced coactivation of the hypothalamo-pituitary-adrenal and sympathoadrenal axes, causing a long-lasting alteration in intracellular signaling pathways, enabling normally innocuous levels of immune mediators to produce chronic hyperalgesia.

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“…Since then, thyroid hormones (THs) were found to play significant roles in other chronic pain syndromes such as headache, arthritis, arthralgia, myopathies, and fibromyalgia. 28,29 A recent study found that hypothyroidism during pregnancy promoted hypersensitivity to noxious thermal stimulus. 30 Other studies have shown that THs are essential for the normal maturation of CNS and brain function at the anatomical, biochemical, and neurophysiological levels, 31,32 and that there is a connection between thyroid hormones and pain perception.…”

Section: The Thyrotropin Group (Trh Tsh T3)mentioning

confidence: 99%

Hormones in pain modulation and their clinical implications for pain control: a critical review

Chen¹,

Zhang²,

Wang³

2016

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Recently, more and more studies have found that pain generation, transmission and modulation are under hormonal regulation. Indeed, hormonal dysregulation is a common component of chronic pain syndromes. Studies have attempted to determine whether the relationship between the pain and its perception and hormones is a causative relationship and how these processes interrelate. This review summarizes and analyzes the current experimental data and provides an overview of the studies addressing these questions. The relationship between pain perception and endocrine effects suggests that hormones can be used as important biomarkers of chronic pain syndromes and/or be developed into therapeutic agents in the fight against pain.

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Neuroendocrine Perturbations in Fibromyalgia and Chronic Fatigue Syndrome

Cited by 138 publications

References 55 publications

Brain-immune interactions and disease susceptibility

Brain-immune interactions and disease susceptibility

Stress Induces a Switch of Intracellular Signaling in Sensory Neurons in a Model of Generalized Pain

Hormones in pain modulation and their clinical implications for pain control: a critical review

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