Stress-induced hyperalgesia

Jennings, Elaine M.; Okine, Bright N.; Roche, Michelle; Finn, David P.

doi:10.1016/j.pneurobio.2014.06.003

Cited by 232 publications

(212 citation statements)

References 214 publications

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“…Exposure to chronic stress is more likely to result in stress-induced hyperalgesia or allodynia [561,562], possibly by inducing hypocortisolism that allows upregulation of pro-inflammatory cytokines, which then can sensitize nociceptors. Indeed, there are experimental human data suggesting that cortisol levels are causally involved in modulating pain sensitivity [563,564].…”

Section: Stress and The Stress Response Systems In Fmsmentioning

confidence: 99%

Fibromyalgia: A Critical and Comprehensive Review

Borchers

Gershwin

2015

Clinic Rev Allerg Immunol

225

217

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Fibromyalgia is a disorder that is part of a spectrum of syndromes that lack precise classification. It is often considered as part of the global overview of functional somatic syndromes that are otherwise medically unexplained or part of a somatization disorder. Patients with fibromyalgia share symptoms with other functional somatic problems, including issues of myalgias, arthralgias, fatigue and sleep disturbances. Indeed, there is often diagnostic and classification overlap for the case definitions of a variety of somatization disorders. Fibromyalgia, however, is a critically important syndrome for physicians and scientists to be aware of. Patients should be taken very seriously and provided optimal care. Although inflammatory, infectious, and autoimmune disorders have all been ascribed to be etiological events in the development of fibromyalgia, there is very little data to support such a thesis. Many of these disorders are associated with depression and anxiety and may even be part of what has been sometimes called affected spectrum disorders. There is no evidence that physical trauma, i.e., automobile accidents, is associated with the development or exacerbation of fibromyalgia. Treatment should be placed on education, patient support, physical therapy, nutrition, and exercise, including the use of drugs that are approved for the treatment of fibromyalgia. Treatment should not include opiates and patients should not become poly pharmacies in which the treatment itself can lead to significant morbidities. Patients with fibromyalgia are living and not dying of this disorder and positive outlooks and family support are key elements in the management of patients.

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Section: Stress and The Stress Response Systems In Fmsmentioning

confidence: 99%

Fibromyalgia: A Critical and Comprehensive Review

Borchers

Gershwin

2015

Clinic Rev Allerg Immunol

225

217

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“…Many studies have shown the positive correlation between preoperative anxiety and postoperative pain intensity as well as analgesic consumption [5][6][7][8][9]. The phenomenon that exposure to physical or psychological stressors can enhance nociception and pain sensitivity is described as stress-induced hyperalgesia (SIH) [10][11][12][13][14][15][16]. Although more and more attention has been paid to investigate this phenomenon, the potential underlying molecular mechanism has not been fully elucidated.…”

Section: Introductionmentioning

confidence: 99%

Glucocorticoid-Potentiated Spinal Microglia Activation Contributes to Preoperative Anxiety-Induced Postoperative Hyperalgesia

et al. 2016

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Clinically, preoperative anxiety adversely affected postoperative hyperalgesia. As stress-induced glucocorticoids (GCs) were reported to sensitize the activation of microglia, the present study investigated whether and how GCs and microglia played in the process of preoperative anxiety-induced postoperative hyperalgesia. The study used an animal model that exposed rats to single prolonged stress (SPS) procedure to induce preoperative anxiety-like behaviors 24 h before the plantar incisional surgery. Behavioral testing revealed that preoperative SPS enhanced the mechanical allodynia induced by plantar incision. SPS was also found to induce elevated circulating corticosterone levels, potentiate the activation of spinal microglia, and increase the expression of spinal proinflammatory cytokines. Inhibition of microglia by pretreatment with minocycline attenuated the SPS-enhanced mechanical allodynia, and this was accompanied by decreased activation of spinal microglia and expression of proinflammatory cytokines. Another experiment was conducted by administering RU486, the GC receptor (GR) antagonist, to rats. The results showed that RU486 suppressed SPS-induced and SPS-potentiated proinflammatory activation of spinal microglia and revealed analgesic effects. Together, these data indicated that inhibition of stress-induced GR activation attenuated the preoperative anxiety-induced exacerbation of postoperative pain, and the suppression of spinal microglia activation may underlie this anti-hyperalgesia effect. Pending further studies, these findings suggested that GR and spinal microglia may play important roles in the development of preoperative anxiety-induced postoperative hyperalgesia and may serve as novel targets to prevent this phenomenon.

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“…Migraine patients do not have any obvious injury (although inflammation may be present (41)), but perhaps more relevant is the proposal that chronic stress is a contributing factor to migraine (42). Extensive experimental preclinical studies of chronic stress have shown decreased pain thresholds or increased responses to painful stimuli in many models (40). Further, chronic stress in rats can change β-adrenergic receptor signaling rendering stimulation with epinephrine pro-nociceptive (43), and chronic stress induces visceral hypersensitivity that is attenuated in the presence of beta-blockers (30).…”

Section: Discussionmentioning

confidence: 99%

Meningeal norepinephrine produces headache behaviors in rats via actions both on dural afferents and fibroblasts

et al. 2015

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Background Stress is commonly reported to contribute to migraine although mechanisms by which this may occur are not fully known. The purpose of these studies was to examine whether norepinephrine (NE), the primary sympathetic efferent transmitter, acts on processes in the meninges that may contribute to the pain of migraine. Methods NE was applied to rat dura using a behavioral model of headache. Primary cultures of rat trigeminal ganglia retrogradely labeled from the dura mater and of rat dural fibroblasts were prepared. Patch-clamp electrophysiology, Western blot, and ELISA were performed to examine the effects of NE. Conditioned media from NE-treated fibroblast cultures was applied to the dura using the behavioral headache model. Results Dural injection both of NE and media from NE-stimulated fibroblasts caused cutaneous facial and hindpaw allodynia in awake rats. NE application to cultured dural afferents increased action potential firing in response to current injections. Application of NE to dural fibroblasts increased phosphorylation of ERK and caused the release of interleukin- 6 (IL-6). Conclusions These data demonstrate that NE can contribute to pro-nociceptive signaling from the meninges via actions on dural afferents and dural fibroblasts. Together, these actions of NE may contribute to the headache phase of migraine.

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Stress-induced hyperalgesia

Cited by 232 publications

References 214 publications

Fibromyalgia: A Critical and Comprehensive Review

Fibromyalgia: A Critical and Comprehensive Review

Glucocorticoid-Potentiated Spinal Microglia Activation Contributes to Preoperative Anxiety-Induced Postoperative Hyperalgesia

Meningeal norepinephrine produces headache behaviors in rats via actions both on dural afferents and fibroblasts

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