Mj. Lentz et al., Effects of selective slow wave sleep disruption on musculoskeletal pain and fatigue in middle aged women, J RHEUMATOL, 26(7), 1999, pp. 1586-1592
Objective. To determine whether disrupted slow wave sleep (SWS) would evoke
musculoskeletal pain, fatigue, and an alpha electroencephalograph (EEG) sl
eep pattern. We selectively deprived 12 healthy, middle aged, sedentary wom
en without muscle discomfort of SWS for 3 consecutive nights. Effects were
assessed for the following measures: polysomnographic sleep, musculoskeleta
l tender point pain threshold, skinfold tenderness, reactive hyperemia (inf
lammatory flare response), somatic symptoms, and mood state.
Methods. Sleep was recorded and scored using standard methods. On selective
SWS deprivation (SWSD) nights, when delta waves (indicative of SWS) were d
etected on EEG, a computer generated tone (maximum 85 decibels) was deliver
ed until delta waves disappeared. Musculoskeletal tender points were measur
ed by dolorimetry; skinfold tenderness was assessed by skin roll procedure;
and reactive hyperemia was assessed with a cotton swab test. Subjects comp
leted questionnaires on bodily feelings, symptoms, and mood.
Results. On each SWSD night, SWS was decreased significantly with minimal a
lterations in total sleep time, sleep efficiency, and other sleep stages. S
ubjects showed a 24% decrease in musculoskeletal pain threshold after the t
hird SWSD night. They also reported increased discomfort, tiredness, fatigu
e, and reduced vigor. The flare response (area of vasodilatation) in skin w
as greater than baseline after the first, and again, after the third SWSD n
ight. However, the automated program for SWSD did not evoke an alpha EEG sl
eep pattern.
Conclusion. Disrupting SWS, without reducing total sleep or sleep efficienc
y for several consecutive nights is associated with decreased pain threshol
d, increased discomfort, fatigue, and the inflammatory flare response in sk
in. These results suggest that disrupted sleep is probably an important fac
tor in the pathophysiology of symptoms in fibromyalgia.