Effect of sleep restriction on pain perception: Towards greater attention !

The Tiede et al. study [27] in this issue of Pain examines how individuals who suffer from insufficient sleep (partial sleep restriction) in comparison to habitual sleep may process attention related to pain perception differently. All tests were performed the following morning. The authors found that brief heat laser-evoked pain (2ms) after one-night sleep restriction raised pain intensity, confirming many studies showing that sleep restriction (or deprivation) induces hyperalgesia or spontaneous pain in normal subjects [7,12,15,17,19,21,24]. The novelty of Tiede and collaborators’ study is that the amplitude of the P2 cortical evoked potential, used to assess the integrity of sensory pathway function from periphery to cortex, was reduced by over 1/3 after sleep restriction. These results support the view that cognitive processing of noxious inputs following sleep restriction is not independent of attention. 1. Pain and sleep physiology Pain is a physiological and emotional experience that requires consciousness to translate sensory afferent input into pain. The sleeping brain does not discriminate pain from other sensory information but it can react to threatening stimuli [13]. Sleep unconsciousness protects individuals from awakening by irrelevant sensory inputs. Afferent input activates a low-intensity fight-or-flight physiological response, traceable by polygraph as transient increases in autonomic brain activity, called arousals. These arousals are either unconscious (no pain recall) or can be perceived, as in a fully awakened response (motor reaction, vocal reaction). Protective fight-or-flight systems, in turn, can activate a descending system directed toward the limbs or the heart or ascending systems that access the cortex. Main ascending routes include the pedunculopontine tegmental and laterodorsal tegmental nuclei projections to the thalamus; and another parallel network composed of the locus ceruleus to raphe nucleus to lateral hypothalamus and tuberomammilary nucleus and basal forebrain [23]. All inputs may reach the cortex to induce a low- or high-intensity fight-or-flight wake reaction. 2. Methodological issues One-night restriction (first half only) was used by Tiede and colleagues in good and healthy sleepers. Again, caution is essential before extrapolating these observations to patients with chronic pain. Young and healthy subjects do not have the cumulative impact of chronic pain and sleep co-morbidities that may alter quality of life or physiological function. In the presence of chronic pain, patients frequently report persistent lower sleep quality, defined as non-refreshing or non-restorative sleep [26]. Almost 50% of temporomandibular pain and 60% of chronic widespread pain or osteoarthritis patients report poor sleep [5,22,25]. And many chronic pain patients have co-morbidities, such as insomnia (sleep duration restriction) and sleep breathing disorders or periodic limb movements at either low intensity (sub-threshold for treatment but disrupting sleep continuity) or high intensity (reaching treatment cut-off at 10 events per hour of sleep) [18,25]. Non-restorative sleep is frequently assessed by questionnaires (e.g., visual analogue scale or the Pittsburgh Sleep Quality index) [3,8]. Varying methods reduce comparison validity across studies and challenge generalization of findings. Tiede and colleagues use actigraphy to control for sleep restriction. Presence or absence of sleep is based on body movements. Importantly, although actigraphy can be used to assess sleep/pain relationships [20], it should be used with caution in sleep-disordered patients. When there are limb movements or breathing disorders, movement estimates can be imprecise. Thus, when investigating sleep quality/pain interactions in patients with co-morbidities, sleep laboratory or ambulatory recordings with multiple channels are recommended. Sleep quality is then quantified by extracting numbers related to sleep efficiency, sleep arousals, sleep stage shifts, limb movements, respiratory events (apnea–hyponea), and brain activity EEG band powers. 3. Experimental sleep restriction and pain testing protocols Sleep restriction is more applicable than deprivation to pain patients, who normally do not experience complete loss of sleep within a 24-h circadian cycle. Rather, restriction or fragmentation of usual sleep duration induces sleep continuity disruption, because of stage shifts, movement or breathing events, etc., that may prevent refreshing sleep and may exacerbate pain reports the following day [14,24]. Most sleep restriction studies that addressed sleep/pain interactions examined healthy or young subjects. Experimental sleep restriction studies may lack ecological validity (non-clinical settings). Chronic pain patients frequently report long-term sleep loss. Sleep restriction methods vary across studies, including sleep fragmentation, preventing specific sleep stages, partial restriction, and full restriction [7,12,15,17,19,21,24]. In Tiede's study, one-night sleep restriction with morning testing prevented the consequence of cumulative sleep restriction on neurocognitive outcomes, such as attention. For example, major changes in mood, fatigue, or spontaneous somatic pain reports occur after 3–4 nights of sleep restriction in normal healthy young subjects [7]. An alternative is to monitor circadian and cumulative changes in attention-cognitive processing of pain. This could improve the ecological validity and extrapolation of experimental findings to chronic pain patients. Moreover, attention changes related to pain sensory processing after sleep restriction may not be exclusive to nociception. Thus, sleep restriction induces many changes in affect and vigilance [6]. In fact, the auditory P3 evoked cortical potential is sensitive to circadian influences after sleep deprivation. Afternoon tests were associated with longer latency of P3 response [30]. Whether sleep restriction also influences learning and memory abilities are still debated, however, selective sleep stage restriction has paradoxical influences on cognitive functions. Clearly, further investigation is required before one can implicate a direct effect of sleep deprivation [4,28]. The Tiede et al. findings using laser-induced heat pain should be extended to various types of experimental pain testing paradigms, so as to explore the pathophysiology of the chronic pain/poor sleep interaction. In many of the above-cited studies, quantitative sensory testing (QST) was used to assess hyperalgesia (lower pain threshold or tolerance, or rise in pain intensity). Although hyperalgesia is a dominant finding, results varied across studies, because different methods and protocols (brief heat pain to long stimulation, mechanical pressure) were used. With chronic pain (temporomandibular or chronic widespread pain, fibromyalgia), allodynia and central sensitivity (not only peripheral hyperalgesia) may also contribute [24,29]. The new evidence for an impact of sleep restriction and poor sleep quality on pain is an important and exciting finding that allows for the integration of pain and sleep medicine with neuroscience, genetics, and psychology. Tiede and colleagues observations in awake subjects tested in the morning with heat laser P2 evoked cognitive pain perception should be compared to the results of Bastuji et al. [1], who reported that most sleep heat laser P3 evoked potential responses were localized at the frontal cortex. In particular, the somewhat controversial but very interesting findings of gray and white matter loss in the cingulate, medial, and prefrontal cortices in chronic pain patients should be reexamined in the context of changes of attention after sleep loss or in relation to sleep apnea and its management [2,10,16]. Phenotyping patients with cognitive tests and pain QST will also be useful. The generalized hypervigilance hypothesis associated with chronic pain and genetic variation in the HPA axis in pain and sleep disorder patients also merits further attention [8,9]. Thus, individuals are either more resistant or vulnerable to performance alteration following sleep deprivation/restriction. Interestingly, a phenotype called trototype that relates adenosine and other circadian-related genes in subjects with impaired performance after sleep loss was recently described [11]. There is clearly much work to be done. Most importantly, the Tiede et al. findings illustrate a new avenue of research that should help to better understand and characterize how and to what extent the effects of sleep restriction on vigilance and cognition influence attentional and pain processes in chronic pain patients.

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