Autonomic activation and pain in response to low‐grade mental stress in fibromyalgia and shoulder/neck pain patients

Nilsen, Kristian Bernhard; Sand, Trond; Westgaard, Rolf H.; Stovner, Lars Jacob; White, Linda R.; Leistad, Rune Bang; Helde, Grethe; Rø, Magne

doi:10.1016/j.ejpain.2006.11.004

Cited by 67 publications

(60 citation statements)

References 60 publications

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“…chronic generalized pain syndromes, such as fibromyalgia (Nilsen et al, 2007) and irritable bowel syndrome (Bach et al, 2006), as well as in other illnesses, like posttraumatic stress disorder (Otis et al, 2003) and depression (Blackburn-Munro and Blackburn-Munro, 2001). …”

Section: Discussionmentioning

confidence: 99%

“…Stress exacerbates generalized pain syndromes such as fibromyalgia (Nilsen et al, 2007), irritable bowel syndrome (Bach et al, 2006), and interstitial cystitis (Temml et al, 2007), and painful inflammatory diseases like rheumatoid arthritis (Zautra et al, 2007). However, mechanisms mediating the impact of stress on pain are poorly understood.…”

Section: Introductionmentioning

confidence: 99%

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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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Section: Discussionmentioning

confidence: 99%

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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show abstract

“…Sympathetic hyperactivation has already been shown in fibromyalgia, [6] migraine, [7] and chronic neck and shoulder pain. [8] The sympathetic and parasympathetic systems work together to maintain the harmony of the human physiology, but this state can be disrupted by the chronic pain.…”

Section: Introductionmentioning

confidence: 99%

Assessment of cardiac sympathovagal activity in the patients suffering from ankylosing spondylitis

Roy¹,

Singh²

2017

Natl J Physiol Pharm Pharmacol

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Background: Ankylosing spondylitis (AS) is an autoimmune disease which leads to the involvement of skeletal, cardiac, nervous tissues, and other systemic diseases. Aims and Objectives: This study was conducted to assess the cardiac sympathovagal responses in the AS patients using Valsalva maneuver (VM) and tilt-table test (TTT). Materials and Methods: A total of 30 AS patients having Bath AS Disease Activity Index of ≥4 were included in this study. The same numbers of age-and sex-matched controls were also selected. The blood pressure (BP) and electrocardiogram were recorded during VM and TTT. The Valsalva ratio and 30:15 ratio were calculated. Results: During VM, there is a statistically significant decrease in the Valsalva ratio in the cases (P < 0.05). After TTT, there is a significant decrease in 30:15 ratio and significant increase in systolic BP (SBP) in the cases (P < 0.05). Conclusion: The Valsalva ratio in the cases is decreased indicating the parasympathetic loss which is further supported by the decrease in 30:15 ratio observed after TTT. The increase in SBP in cases also supports the shifting of sympathovagal balance toward the sympathetic side.

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“…However, contradictory findings have also been reported. For example, altered cardiovascular responses to low-grade mental stress were found in fibromyalgia patients, whereas a group of subjects with neck-shoulder pain did not react significantly differently than healthy controls (Nilsen et al 2007). More recently, a study of individuals with trapezius myalgia showed an elevated heart rate at rest but no differences in stress responses compared with controls (Sjörs et al 2009).…”

Section: Autonomic Aberrations In Chronic Neck-shoulder Pain: Recent mentioning

confidence: 99%

Autonomic Regulation in Musculoskeletal Pain

Hallman¹,

Lyskov²

2012

Pain in Perspective

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Autonomic activation and pain in response to low‐grade mental stress in fibromyalgia and shoulder/neck pain patients

Cited by 67 publications

References 60 publications

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

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

Assessment of cardiac sympathovagal activity in the patients suffering from ankylosing spondylitis

Autonomic Regulation in Musculoskeletal Pain

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