Does Sleep Deprivation Aggravate Chronic Pain?
July 1, 2007 3 minutes read
Does Sleep Deprivation Aggravate Chronic Pain?
Abstract & Commentary
By Charles Pollak, MD, Professor, Clinical Neurology, Weill College of Medicine. Dr. Pollak is a stockholder for Merck, and is on the speaker's bureau for Merck.
Synopsis: Disturbance of sleep continuity, but not simple sleep deprivation, impairs pain inhibition and increases spontaneous pain.
Source: Smith MT, et al. The effects of sleep deprivation on pain inhibition and spontaneous pain in women. Sleep 2007. 30: 494-505.
Anyone with a toothache knows how difficult it can be to sleep. The same is true for back pain, fibromyalgia, or cancer pain, perhaps providing one reason why insomnia is common in the elderly. Less well known is the opposite effect, the augmentation of pain by sleep disturbance. Experiments designed to demonstrate that insomnia, for example, increases pain have indeed given inconsistent results. The present experiment, by contrast, clearly demonstrates that impairment of sleep continuity, though not simple sleep deprivation, impairs pain inhibition (to be explained) as well as increasing spontaneous pain.
The investigation was restricted to women, because female sex is associated with pain sensitivity and higher rates of chronic pain. A parallel investigation in males is in progress. Thirty-five women averaging 25 years of age participated. All were good sleepers and were healthy and did not abuse alcohol or other substances. They did not complain of pain or use analgesics. They were also screened for sleep disturbances, daytime sleepiness, psychiatric disorders, and acute pain. During the initial screening, they wore wrist actigraphs to provide measures of sleep and the circadian rhythm. During 7 subsequent experimental days, sleep was polygraphically recorded to rule out sleep disorders and track multiple sleep parameters.
Pain was induced by applying pressure to the belly of the trapezius muscle, masseter muscle and brachioradialis. The pressure pain threshold was again measured while immersing a hand in ice water (cold pressor task), and the increase in pain threshold was recorded (diffuse noxious inhibitory control or DNIC). An increase in the pressure threshold during cold pressor reflects normal pain-inhibitory processes. In addition to DNIC, the spontaneous occurrence of any potentially painful symptoms was recorded each night.
Subjects were randomly assigned to one of 3 groups: control, forced awakening (FA) or restricted sleep opportunity (RSO). All subjects slept undisturbed for the first 2 nights. Controls slept undisturbed for up to 8 hours on each of the remaining 5 nights. FA subjects were forcibly awakened for either 20 minutes or 60 minutes on each of 3 consecutive nights. This was followed by 36 hours of continuous wakefulness, then by a night of recovery sleep. The night of total sleep deprivation was intended to maximize the possibility of identifying an effect of sleep deprivation on pain inhibition.
The RSO subjects were deprived of sleep by delaying their bedtime while keeping a fixed wake time. The amount of delay was yoked to the amount of sleep achieved by the subjects in the FA group. After partial sleep deprivation, the RSO and FA subjects were deprived of sleep for 36 hours and were then allowed a night of recovery sleep.
FA and RSO subjects demonstrated 50% reductions in total sleep time and increases in nonpainful somatic symptoms during partial sleep deprivation. Sleep deprivation had no effect on pain thresholds. During partial sleep deprivation, however, the FA group showed a significant loss of pain inhibition and an increase in spontaneous pain. Neither of the other 2 groups showed changes in pain inhibition or spontaneous pain during partial sleep deprivation.
Commentary
This is an elaborately designed, well controlled investigation of the effect of two kinds of sleep deprivation on pain perception. Remarkably, simple sleep deprivation, (shortened opportunity for sleep) had no effect on pain perception, but reduction of sleep to the same degree by means of an interspersed nocturnal awakening markedly reduced pain inhibition (DNIC). Why should it matter whether subjects are permitted to sleep a little longer before being awakened for the day (the RSO condition) or, instead, are permitted to sleep for the same total time after a interval of wakefulness (FA condition)? The authors have not shared any speculative explanations for this, their central finding.
If it can be confirmed, the finding may be of great clinical significance. As pointed out by the authors, the impairment of sleep continuity by pain can have a self-reinforcing, perpetuating effect that supports a possible pathophysiologic role of sleep disturbance in chronic pain. If we only knew how to do it (other than by means of analgesic drugs), it follows that insomnia should quickly be remedied in the patient with chronic pain.
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