The Association of Sleep Disturbances with Lower Back Pain

Sleep is a complex and necessary physiological and behavioral process which the body undergoes in a rhythmic fashion. During sleep, important processes such as growth, healing, physical recovery, memory processing, information retention and emotional regulation occur. Sleep disturbance (SD) affects approximately 30-45% of the western population. These disturbances can be characterized by sleep initiation difficulty, sleep maintenance difficulty, poor quality sleep and decreased sleep. SD confers dysregulation to the above processes and manifests as impairments in cognition, decision making, psychomotor function, occupational efficiency, quality of life amongst many others. In addition, poor sleep has been associated as a risk for cardiovascular disease, immune suppression, dementia, metabolic syndrome, depression and chronic pain. This article will discuss the association between sleep disturbance and low back pain.

Several studies have documented the association between SD and chronic pain. Many patients who report chronic pain show sleep associated disorders such as insomnia, restless leg syndrome, and obstructive sleep apnea. There are several proposed mechanisms which conceptualize a vicious cycle whereby significant pain impairs sleep and poor sleep exacerbates pain. Previous studies have thought that both mechanisms exist in concert; however recent studies have shown a stronger impact from poor sleep exacerbating chronic pain in adult populations – i.e. studies show sleep deprivation can induce hyperalgesic pain responses in participants compared to healthy controls. These hyperalgesic responses can be reversed by sleep restoration.

The exact mechanism for pain exacerbation and SD is not clearly understood. A proposed mechanism looks at the biochemical and neurophysiological level with poor sleep directly increasing production of pro-inflammatory cytokines with inhibition of endogenous opioid production. Central pain modulation systems that are associated with chronic pain include wind up of wide-dynamic range neurons conferring decreased threshold to pain response from external stimuli. Sleep deprivation is proposed to aid in the wind up phenomenon of these wide dynamic range neurons which leads to development and maintenance of chronic pain states.

Klyne et al and Paul-Savoie et al both documented the association specifically with subjective sleep quality and low back pain through conditioned pain modulation through diminished descending pain inhibition. It is suggested that the dysregulation of endogenous biochemical and physiological mechanisms described in the paragraph above are responsible for this; however no study has specifically identified endogenous pathway dysregulation as the cause and further research is needed.

In summary, the association between SD and chronic pain has been previously described. There is a strong association between subjective low back pain complaints and sleep quality. The proposed mechanism for this is felt to be primarily due to SD causing dysregulation of endogenous biochemical and neurophysiological modulation pathways; however this has not been confirmed in current literature. Treatment of chronic pain often involves a multi-disciplinary approach and the article stresses the importance of addressing SD in management of chronic pain complaints.

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