Chronic rhinosinusitis and sleep: a contemporary review

Abstract

Background: Patients with chronic rhinosinusitis (CRS) exhibit centrally mediated behavioral changes commonly referred to as "sickness behavior." Sleep alteration is a component of sickness behavior which is estimated to affect up to 70 million patients annually. Patients with CRS have poor sleep quality, and little is known about the underlying etiology and pathophysiology. This narrative review aims to further organize and present the current knowledge associating sleep and CRS.

Methods: A literature search was conducted of the OVID MEDLINE database using key search words including: "chronic rhinosinusitis," "sleep," "sleep disorders," and "sleep dysfunction." Additional keywords "nasal obstruction," "nasal polyp," and "fatigue" were identified and used to further delineate relevant articles.

Results: The articles that specifically addressed sleep and CRS were dissected and presented as follows: (1) chronic rhinosinusitis and sleep; (2) chronic rhinosinusitis and fatigue; (3) chronic rhinosinusitis, nasal obstruction, and sleep; and (4) pathophysiology of sleep in chronic rhinosinusitis (cytokines in both sleep and chronic rhinosinusitis and their association to the neuroimmune biology of chronic rhinosinusitis).

Conclusion: Patients with CRS have sleep dysfunction that is associated with their disease severity and overall quality of life. The etiology of sleep dysfunction in CRS is most likely multifactorial. Increasing evidence suggests sleep dysfunction in patients with CRS is partly due to the inflammatory disease process, and sleep physiology in patients with CRS may be actively regulated by the inflammatory component of the disease.

Trial registration: ClinicalTrials.gov NCT01332136.

Keywords: fatigue; review; rhinology; sinusitis; sleep.

Figure 1

Increased somnolence is an important component of sickness behavior and evidence demonstrates that inflammatory mediators are instrumental in eliciting these symptoms via central neuronal signaling. The pro-inflammatory cytokines interleukin (IL)-1β and tumor necrosis factor (TNF)- α released in chronic rhinosinusitis (CRS) are involved in the normal physiological regulation of sleep. The mechanisms by which local inflammatory cytokines might signal the central nervous system in patients with CRS to induce sickness behavior is unknown. However, preliminary evidence suggests they may: 1) Access or signal the brain via transport across the blood brain barrier (BBB), through the circumventricular organs (subfornical organ, vascular organ of the laminar terminalis, median eminence, intermediate and posterior lobes of the pituitary, pineal gland, subcommissural organ and the area postrema), 2) Act locally, as opposed to systemically, through the stimulation or alteration of afferent neuronal transmission, 3) Alter the level or activity of another substance that signals the brain, and/or 4) Act through direct passage across the BBB through molecular transporters. IL-1β, Interleukin-1 beta; TNF-α, tumor necrosis factor-alpha.