Relationship between sympathetic activity and pain intensity in fibromyalgia

Antonio Roberto Zamunér, Franca Barbic, Franca Dipaola, Mara Bulgheroni, Alessandro Diana, Fabiola Atzeni, Andrea Marchi, Piercarlo Sarzi-Puttini, Alberto Porta, Raffaello Furlan

Research output: Contribution to journalArticle

36 Citations (Scopus)

Abstract

Objective. Fibromyalgia (FM) is a syndrome characterised by chronic musculoskeletal pain, hyperalgesia on specific areas of tenderness (tender points) and by an autonomic nervous system dysfunction consistent with sympathetic overactivity. It is not known whether there is any relationship between the amount of cardiovascular sympathetic activity and the magnitude of pain. Our objective was to assess this potential relationship in patients with FM. Methods. Electrocardiogram, finger blood pressure, respiration and post-ganglionic sympathetic discharge activity (muscle sympathetic nerve activity, MSNA) were continuously recorded at rest in 25 patients with primary FMS. The autonomic profile was assessed by MSNA and spectral indices of cardiac sympathetic (LFRR) and vagal (HFRR) modulation and of sympathetic vasomotor control (LFSAP) computed by spectrum analysis of RR and systolic arterial pressure (SAP) variability. Cardiac baroreflex function was evaluated by the index α (αLF). Baroreceptor modulation of the sympathetic vasomotor control (sBRS) was assessed by the MSNA/diastolic pressure relationship. Results. Pain intensity was linearly correlated with LFRR/HFRR (r2=0.21; p=0.03), LFSAP (r2=0.26; p=0.02) and MSNA (burst rate) (r2=0.45; p=0.003). Pain intensity was inversely correlated with the aLF index (r2=0.24; p=0.02) and the sBRS (r2=0.28; p=0.03). Thus, the higher the sympathetic drive to the heart and vessels, the higher the magnitude of chronic pain. Also, the gains of both the cardiac and MSNA baroreceptor control were inversely related to the pain intensity. Conclusion. These findings raise the theoretical possibility that in FM patients the use of anti-adrenergic agents might lessen chronic pain intensity by reducing the underlying excessive sympathetic activity.

Original languageEnglish
Pages (from-to)S53-S57
JournalClinical and Experimental Rheumatology
Volume33
Publication statusPublished - 2015

Fingerprint

Fibromyalgia
Chronic Pain
Pain
Muscles
Pressoreceptors
Blood Pressure
Musculoskeletal Pain
Adrenergic Antagonists
Baroreflex
Autonomic Nervous System
Hyperalgesia
Adrenergic Agents
Fingers
Spectrum Analysis
Myocardium
Arterial Pressure
Electrocardiography
Respiration

Keywords

  • Fibromyalgia
  • Pain intensity
  • Sympathetic activity

ASJC Scopus subject areas

  • Rheumatology
  • Immunology
  • Immunology and Allergy
  • Medicine(all)

Cite this

Relationship between sympathetic activity and pain intensity in fibromyalgia. / Zamunér, Antonio Roberto; Barbic, Franca; Dipaola, Franca; Bulgheroni, Mara; Diana, Alessandro; Atzeni, Fabiola; Marchi, Andrea; Sarzi-Puttini, Piercarlo; Porta, Alberto; Furlan, Raffaello.

In: Clinical and Experimental Rheumatology, Vol. 33, 2015, p. S53-S57.

Research output: Contribution to journalArticle

Zamunér, AR, Barbic, F, Dipaola, F, Bulgheroni, M, Diana, A, Atzeni, F, Marchi, A, Sarzi-Puttini, P, Porta, A & Furlan, R 2015, 'Relationship between sympathetic activity and pain intensity in fibromyalgia', Clinical and Experimental Rheumatology, vol. 33, pp. S53-S57.
Zamunér AR, Barbic F, Dipaola F, Bulgheroni M, Diana A, Atzeni F et al. Relationship between sympathetic activity and pain intensity in fibromyalgia. Clinical and Experimental Rheumatology. 2015;33:S53-S57.
Zamunér, Antonio Roberto ; Barbic, Franca ; Dipaola, Franca ; Bulgheroni, Mara ; Diana, Alessandro ; Atzeni, Fabiola ; Marchi, Andrea ; Sarzi-Puttini, Piercarlo ; Porta, Alberto ; Furlan, Raffaello. / Relationship between sympathetic activity and pain intensity in fibromyalgia. In: Clinical and Experimental Rheumatology. 2015 ; Vol. 33. pp. S53-S57.
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AU - Zamunér, Antonio Roberto

AU - Barbic, Franca

AU - Dipaola, Franca

AU - Bulgheroni, Mara

AU - Diana, Alessandro

AU - Atzeni, Fabiola

AU - Marchi, Andrea

AU - Sarzi-Puttini, Piercarlo

AU - Porta, Alberto

AU - Furlan, Raffaello

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N2 - Objective. Fibromyalgia (FM) is a syndrome characterised by chronic musculoskeletal pain, hyperalgesia on specific areas of tenderness (tender points) and by an autonomic nervous system dysfunction consistent with sympathetic overactivity. It is not known whether there is any relationship between the amount of cardiovascular sympathetic activity and the magnitude of pain. Our objective was to assess this potential relationship in patients with FM. Methods. Electrocardiogram, finger blood pressure, respiration and post-ganglionic sympathetic discharge activity (muscle sympathetic nerve activity, MSNA) were continuously recorded at rest in 25 patients with primary FMS. The autonomic profile was assessed by MSNA and spectral indices of cardiac sympathetic (LFRR) and vagal (HFRR) modulation and of sympathetic vasomotor control (LFSAP) computed by spectrum analysis of RR and systolic arterial pressure (SAP) variability. Cardiac baroreflex function was evaluated by the index α (αLF). Baroreceptor modulation of the sympathetic vasomotor control (sBRS) was assessed by the MSNA/diastolic pressure relationship. Results. Pain intensity was linearly correlated with LFRR/HFRR (r2=0.21; p=0.03), LFSAP (r2=0.26; p=0.02) and MSNA (burst rate) (r2=0.45; p=0.003). Pain intensity was inversely correlated with the aLF index (r2=0.24; p=0.02) and the sBRS (r2=0.28; p=0.03). Thus, the higher the sympathetic drive to the heart and vessels, the higher the magnitude of chronic pain. Also, the gains of both the cardiac and MSNA baroreceptor control were inversely related to the pain intensity. Conclusion. These findings raise the theoretical possibility that in FM patients the use of anti-adrenergic agents might lessen chronic pain intensity by reducing the underlying excessive sympathetic activity.

AB - Objective. Fibromyalgia (FM) is a syndrome characterised by chronic musculoskeletal pain, hyperalgesia on specific areas of tenderness (tender points) and by an autonomic nervous system dysfunction consistent with sympathetic overactivity. It is not known whether there is any relationship between the amount of cardiovascular sympathetic activity and the magnitude of pain. Our objective was to assess this potential relationship in patients with FM. Methods. Electrocardiogram, finger blood pressure, respiration and post-ganglionic sympathetic discharge activity (muscle sympathetic nerve activity, MSNA) were continuously recorded at rest in 25 patients with primary FMS. The autonomic profile was assessed by MSNA and spectral indices of cardiac sympathetic (LFRR) and vagal (HFRR) modulation and of sympathetic vasomotor control (LFSAP) computed by spectrum analysis of RR and systolic arterial pressure (SAP) variability. Cardiac baroreflex function was evaluated by the index α (αLF). Baroreceptor modulation of the sympathetic vasomotor control (sBRS) was assessed by the MSNA/diastolic pressure relationship. Results. Pain intensity was linearly correlated with LFRR/HFRR (r2=0.21; p=0.03), LFSAP (r2=0.26; p=0.02) and MSNA (burst rate) (r2=0.45; p=0.003). Pain intensity was inversely correlated with the aLF index (r2=0.24; p=0.02) and the sBRS (r2=0.28; p=0.03). Thus, the higher the sympathetic drive to the heart and vessels, the higher the magnitude of chronic pain. Also, the gains of both the cardiac and MSNA baroreceptor control were inversely related to the pain intensity. Conclusion. These findings raise the theoretical possibility that in FM patients the use of anti-adrenergic agents might lessen chronic pain intensity by reducing the underlying excessive sympathetic activity.

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