Sleep disturbance as a risk factor for developing chronic pain
The major question addressed in this project, with Clifford Woolf and Tom Scammell as co-PIs, is how sleepand its disturbances (specifically moderate sleep deficits) generally affect the function of the CNS. Thebiological need for sleep is quite clear – depriving sleep causes major cumulative deficits in attention, cognitionand many other brain functions – with death, after extreme levels of deprivation, but how exactly this occursand indeed what the benefit of sleep is at a neurobiological level, remains uncertain.As our model system, we are asking whether sleep disturbance is a risk factor for developing chronic pain andreciprocally, if promoting sleep reduces this risk, and whether chronic pain disrupts sleep architecture. We areseeking to reveal the reciprocal neurobiological interactions of pain and sleep, its mechanisms and clinicalimplications, testing the specific hypothesis that disturbances of sleep increase the susceptibility for developingchronic pain by virtue of increasing maladaptive neural plasticity. These findings should be generalizable toany disease state or condition where there is a deficit of sleep, something that is becoming increasinglycommon in children and adolescents – for example as a result of video games. For the latter the impact ofinadequate sleep is increasingly appreciated with effects on the ability to learn, concentrate and operate atmaximal cognitive capacity. We are generating models in mice where sleep is deprived without stress in amanner that mimics the increasing sleep deprivation present in the 21st century developed world, and our dataindicate that this has major consequence on pain sensation.