Purpose: Chronic pain, due to its persistent harassment effect on the nervous and immune systems, is most likely associated with central sensitisation, i.e., intense pain is perceived as the result of alteration to the level of spinal and brainstem cellular networks. Sleep is under the control of brainstem, thalamic and hypothalamic networks. Sleep is a state of lower pain perception that can become very instable in presence of too much interference such as noise, pain, etc (Lavigne, Pain 2000, 2004). Active during wake and pain states, serotonin and noradrenalin neurons are less active during non-REM sleep and nearly silent during REM sleep. This is an OVERVIEW presentation - following sections were fit for requirements of Abst submission Methods: The sleep of pain patients is characterized by high levels of recurrent brief arousals (3-15 second rises in brain with alpha EEG activity, motor and autonomic-cardiac activity) that result in fragmented sleep architecture and are the source of non-restorative sleep complaints (i.e., un-refreshing sensation). 50 to 70 % of musculoskeletal chronic pain patients report non-restorative sleep related complaints. The presence of restorative sleep seems to predict the resolution of chronic widespread pain (CWP; Davies, Rheumatol 2008). A circular model has been proposed to help explain the interaction between pain and sleep: a night with poor sleep can be followed by a day with more intense and variable pain, and a day with pain can be followed by non-restorative sleep. This model is influenced by the patient's life style, low level of physical fitness, presence of mild (i.e., sub-threshold for diagnosis and treatment) sleep breathing disorders (e.g., apnea/hypopnea; upper airway resistance) or periodic limb movements (PLM). Results: In normal and young subjects, sleep deprivation (4 hours instead of 8 hours) triggers mood alterations and complaints of pain after 3-4 days (Haack and Mullington, Pain 2005). In normal subjects, deprivation of sleep stages 3&4 and REM sleep enhances pain by reducing pain threshold or tolerance (Roehrs, Sleep 2006; Onen, J Sleep Res 2001). The duration of night sleep in most musculoskeletal CWP patients is about 60 minutes less (under 6 hours per night) than that of normal subjects (Okura, Sleep Med 2008; Edwards, Pain 2008). Female patients with CWP present twice as many sleep awakenings, 25% present less REM sleep duration and 40% lower slow wave power density during sleep. Female CWP patients also spend 2.6 less time in sleep stages 3&4 than CWP male patients. In patients with rheumatoid arthritis (RA), sleep duration is in the same range to the one of control subjects (Drewes 1988). Similarly to CWP patients, the presence of intermediate frequency of PLM (about 10 per hr of sleep in RA; control about 1-3 and PLM patients over 20) suggest that sleep fragmentation (with arousal and then Alpha EEG intrusions) may contribute to poor sleep quality perception and sleep instability (Drewes 1988, Okura 2008). Conclusions: The mode of action of medications known to improve both pain and sleep complaints (i.e., pregabalin and sodium oxybate in CWP and extended release of opioid or tramadol in OA patients) remains to be described (i.e., specific effect on sleep arousal-instability or continuity or circadian-homeostatic regulation or mood -sleep interferences). Research supported by CIHR, FRSQ, CFI and Canada Res Chair.
Lavigne, G. (2009). I-13 PAIN INTERFERENCES ON SLEEP IN OA PATIENTS: AN OVERVIEW. Osteoarthritis and Cartilage, 17, S5. https://doi.org/10.1016/s1063-4584(09)60018-2