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Influence of autonomic nervous system dysfunction in the genesis of sleep disorders in fibromyalgia patients

1, 2, 3, 4, 5, 6, 7, 8, 9

 

  1. Respiratory Unit, Centre for Sleep and Respiratory Disorders, University Hospital Luigi Sacco, Milan, Italy. rizzi.maurizio@asst-fbf-sacco.it
  2. Department of Biomedical Sciencies, University Hospital Luigi Sacco, Milan, Italy.
  3. Department of Biomedical Sciencies, University Hospital Luigi Sacco, Milan, Italy.
  4. Respiratory Unit, Centre for Sleep and Respiratory Disorders, University Hospital Luigi Sacco, Milan, Italy.
  5. Respiratory Unit, Centre for Sleep and Respiratory Disorders, University Hospital Luigi Sacco, Milan, Italy.
  6. Respiratory Unit, Centre for Sleep and Respiratory Disorders, University Hospital Luigi Sacco, Milan, Italy.
  7. Respiratory Unit, Centre for Sleep and Respiratory Disorders, University Hospital Luigi Sacco, Milan, Italy.
  8. Orthopaedic and Trauma Unit, Santissima Trinità Hospital, Cagliari, Italy.
  9. Rheumatology Unit, ASST-Fatebenefratelli-L. Sacco University Hospital, Milan, Italy.

CER10178
2017 Vol.35, N°3 ,Suppl.105
PI 0074, PF 0080
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PMID: 28681708 [PubMed]

Received: 13/12/2016
Accepted : 05/04/2017
In Press: 29/06/2017
Published: 29/06/2017

Abstract

OBJECTIVES:
Fibromyalgia (FM) is characterised by chronic musculoskeletal pain, autonomic nervous system (ANS) dysfunction, and disturbed sleep. The aim of this study was to evaluate the influence of ANS dysfunction on the genesis of sleep disorders.
METHODS:
Fifty female FM patients and 45 healthy subjects matched for age, gender and body mass index underwent a clinical, polysomnographic and autonomic profile evaluation at rest and during a tilt test in order to determine muscle sympathetic nerve activity (MSNA), plasma catecholamine levels, and the spectral indices of cardiac sympathetic (LFRR) and vagal (HFRR) modulation computed by means of the spectrum analysis of RR during sleep.
RESULTS:
The FM patients had a higher heart rate (HR), more MSNA and a higher LF/HF ratio, and lower HFRR values at rest (p<0.05), and showed no increase in MSNA, a smaller decrease in HFRR, and an excessive rate of syncope (46%) during the tilt test. Their sleep was less efficient (p<0.01), and they had a higher proportion of stage 1 non-REM sleep (p<0.001), experienced many arousals and periodic limb movements (PLMs) per hour of sleep (p<0.001) and a high proportion of periodic breathing (PB%) (p<0.0001). Their cyclic alternating pattern (CAP) rate was significantly increased (p<0.001). During sleep, they had a higher HR and LF/HF ratio, and a lower HFRR (p<0.001). The number of tender points, CAP rate, PB% and PLMI correlated positively with HR and the LF/HF ratio, and negatively with HFRR during sleep.
CONCLUSIONS:
Our findings seem to show that sleep causes the same effects as a stressful test in FM patients. A vicious circle is created during sleep: pain increases sympathetic cardiovascular activation and reduces sleep efficiency, thus causing lighter sleep, a higher CAP rate, more arousals, a higher PLMI, and increasing the occurrence of PB, which gives rise to abnormal cardiovascular neural control and exaggerated pain sensitivity.

Rheumatology Article