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The role of sleep in pain and fibromyalgia

Key Points

  • Abnormal pain processing is an important pathophysiological feature of fibromyalgia, and nonrestorative sleep is a common clinical and diagnostic feature

  • Polysomnography has demonstrated that patients with fibromyalgia have reduced slow-wave sleep and α-intrusion (α-waves during non-REM [rapid eye movement]), although these sleep disturbances are not unique to fibromyalgia

  • In healthy individuals. sleep deprivation can induce fibromyalgia-like symptoms and is associated with impairment in descending pain modulation

  • Population studies implicate poor-quality sleep as a risk factor for the development of widespread pain, and sleep disturbances can cause depression

  • Sleep dysfunction might have bidirectional roles in the pathophysiology of fibromyalgia

Abstract

Fibromyalgia is a common cause of chronic widespread pain, characterized by reduced pressure pain thresholds with hyperalgesia and allodynia. In addition to pain, common symptoms include nonrestorative sleep, fatigue, cognitive dysfunction, stiffness and mood disturbances. The latest research indicates that the dominant pathophysiology in fibromyalgia is abnormal pain processing and central sensitization. Neuroimaging studies have shown that patients with fibromyalgia have similar neural activation to healthy age-matched and gender-matched individuals; however, they have a lower pressure-pain threshold. Polysomnography data has demonstrated that these patients have reduced short-wave sleep and abnormal α-rhythms, suggestive of wakefulness during non-REM (rapid eye movement) sleep. Sleep deprivation in healthy individuals can cause symptoms of fibromyalgia, including myalgia, tenderness and fatigue, suggesting that sleep dysfunction might be not only a consequence of pain, but also pathogenic. Epidemiological studies indicate that poor sleep quality is a risk factor for the development of chronic widespread pain among an otherwise healthy population. Mechanistically, sleep deprivation impairs descending pain-inhibition pathways that are important in controlling and coping with pain. Clinical trials of pharmacological and nonpharmacological therapies have shown that improving sleep quality can reduce pain and fatigue, further supporting the hypothesis that sleep dysfunction is a pathogenic stimulus of fibromyalgia.

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Figure 1: Nociceptive pathways in the dorsal horn.
Figure 2: Centres in the brain involved in descending inhibitory pathways.
Figure 3: Regions of the brain in which healthy individuals have more activity than patients with fibromyalgia.
Figure 4: Sleep cycles in a healthy individual with high-amplitude, low-frequency δ-waves during stage 3 and 4 SWS.
Figure 5: Hypothesis of the role of sleep in the pathogenesis of fibromyalgia.

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Correspondence to Ernest H. S. Choy.

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The author has served as a member of advisory boards, as a consultant and at speaker's bureaus for Eli Lilly, Jazz Pharmaceuticals, Pierre Fabre Medicament, Pfizer and UCB.

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Choy, E. The role of sleep in pain and fibromyalgia. Nat Rev Rheumatol 11, 513–520 (2015). https://doi.org/10.1038/nrrheum.2015.56

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