Rheumatology 2000; 39: 1287-1289
© 2000 British Society for Rheumatology
Letters to the Editor |
A longitudinal study of clinical symptoms and sleep parameters in rheumatoid arthritis
1 Department of Internal Medicine M, Aalborg Hospital,
2 Department of Medical Informatics and Image Analysis, Aalborg University,
3 Department of Mathematics, Aalborg University,
4 Department of Clinical Neurophysiology, Aalborg Hospital and
5 Department of Rheumatology, Aalborg Hospital, Denmark.
SIR, Sleep complaints are reported by more than half of the patients with rheumatoid arthritis (RA) [1], and in several studies disturbances of the sleep architecture have been documented in these patients. In a previous paper we reported a close relationship between pain, morning stiffness and homeostatic sleep patterns [2]. To further elucidate this finding, the present study was conducted to follow up the clinical and ambulatory polysomnographic (PSG) parameters in the same patients. The dynamics of this study allowed us to extend the knowledge obtained in the previous study [2].
Thirty-five outpatients with RA [nine males and 26 females, mean age 50.6 yr (S.D. 13.9) and mean duration of disease 164.2 months (115.7)] were included. After a baseline PSG, the second recording was performed after a mean of 175.8 (70.9) days. The patients had a clinical examination in the evening before the sleep recordings and completed various questionnaires as in the previous study [2]. Medication was unchanged in the study period. All PSG data were scored manually and blindly in 30 s epochs according to standard criteria and the F1–A2 lead was selected for frequency analysis. The distribution of normalized power in the electroencephalography was calculated using autoregressive modelling. As the preliminary statistical tests indicated complex relationships between the individual variables, a graphical chain model was selected for final analysis and interpretation of data. Details regarding the model were given previously [2].
During the study period, a deterioration in disease activity was reflected in the Ritchie score (14.5 vs 16.7 at baseline and follow-up, P = 0.033) and the Health Assessment Questionnaire score (6.2 vs 7.0, P = 0.048), and a corresponding increase in erythrocyte sedimentation rate (24.0 vs 29.5, P = 0.023) was seen. The other clinical parameters were unchanged. Data from the Spiegel Sleep Questionnaire showed that sleep was more superficial and non-restorative at follow-up in comparison with the baseline. In terms of conventional sleep staging, patients spent more time in non-rapid-eye-movement (NREM) stage 1 (NREM1) at follow-up (17.2 vs 23.7 min, P = 0.008), but otherwise no differences in sleep stages or architecture were observed. Moreover, no significant differences were seen in the frequency analysis. Using likelihood-ratio tests in the selection procedures, a stable graphical model was computed (Fig. 1
). Morning stiffness, Ritchie score and pain showed significant interactions, and were related to the sleep parameters ‘wake’, NREM2 and slow-wave sleep (SWS; equivalent to NREM3 and 4 combined). The other variables did not influence the model and were excluded. Subsequent simulations in a causal probabilistic network model [2] showed that an increase in pain, Ritchie score and morning stiffness resulted in an increase in SWS and stage ‘wake’ and a decrease in NREM2. When a decrease in pain and stiffness was simulated, changes opposite to those described above were seen in sleep parameters. Thus, a deterioration in pain and morning stiffness was followed by an increase in SWS and stage ‘wake’ and vice versa, confirming the importance of sleep/wake interactions in RA.
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Most studies on the relationship between disease activity, pain and sleep disturbances have been cross-sectional, and few have followed the same patients for sufficient time to study simultaneous changes in clinical parameters and sleep. In an earlier report we found a relationship between morning stiffness, pain and sleep parameters [2], confirming the suggested relationship between daytime complaints and sleep patterns. In the present study an attempt was made to study these relationships further, as the follow-up design made it possible to evaluate dynamic time-dependent alterations in clinical parameters and corresponding changes in sleep structure. The relationship between pain and SWS is probably the most important finding in this study. A deterioration in disease activity was followed by an increase in SWS. This was also seen in patients with ankylosing spondylitis [3]. SWS is probably the most important part of sleep, being linked to homeostatic processes. Therefore, the increase in SWS may represent a bodily counter-reaction to the joint inflammation that is reflected in pain and stiffness. The simulations also showed that a deterioration in clinical activity was followed by an increase in the stage ‘wake’. Although pain may be the cause of periods spent awake, the awakenings may also lower the pain threshold and increase stiffness. Experimental and clinical studies have shown that fragmented sleep is non-restorative [4], and although time spent awake does not equal the number of arousals during sleep, the positive relationship between pain and time spent awake during the night may partly explain why sleep is reported to be non-restorative in RA.
In conclusion, this longitudinal study of clinical and sleep parameters in patients with RA showed a relationship between pain, morning stiffness and sleep architecture. Due to the homeostatic function of normal sleep, which is probably especially relevant in patients with chronic diseases, the covariation of sleep structure and clinical variables may indicate that attempts to improve sleep may be helpful in the treatment of the disease. The clinician should therefore address this topic when prescribing medication with the potential to alter sleep structure.
Notes
Correspondence to: A. M. Drewes, Department of Internal Medicine M, Aalborg Hospital, 9000 Aalborg, Denmark. 
References
- Drewes AM, Jennum P, Andreasen A, Sjøl A, Nielsen KD. Self-reported sleep disturbances and daytime complaints in women with fibromyalgia and rheumatoid arthritis. J Musculoskel Pain1994;2:15–31.
- Drewes AM, Svendsen L, Taagholt SJ, Bjerregård K, Nielsen KD, Hansen B. Sleep in rheumatoid arthritis: an ambulatory study of sleep/wake interactions. Br J Rheumatol1998;37:71–81.
[Abstract/Free Full Text] - Jamieson AH, Alford CA, Bird HA, Wright V. The effect of sleep and nocturnal movements on stiffness, pain, and psychomotor performance in ankylosing spondylitis. Clin Exp Rheumatol1995;13:73–8.[Medline]
- Bonnet MH. Performance and sleepiness as a function of frequency and placement of sleep disruption. Psychophysiology1986;23:263–71.[Medline]
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