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Jo Nijs, Olivier Mairesse, Daniel Neu, Laurence Leysen, Lieven Danneels, Barbara Cagnie, Mira Meeus, Maarten Moens, Kelly Ickmans, Dorien Goubert, Sleep Disturbances in Chronic Pain: Neurobiology, Assessment, and Treatment in Physical Therapist Practice, Physical Therapy, Volume 98, Issue 5, May 2018, Pages 325–335, https://doi.org/10.1093/ptj/pzy020
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Abstract
Among people with chronic pain, insomnia is highly prevalent, closely related to the mechanism of central sensitization, characterized by low-grade neuroinflammation, and commonly associated with stress or anxiety; in addition, it often does not respond effectively to drug treatments. This review article applies the current understanding of insomnia to clinical practice, including assessment and conservative treatment of insomnia in people with chronic pain. Cognitive-behavioral therapy for insomnia can be efficacious for improvements in sleep initiation, sleep maintenance, perceived sleep quality, and pain interference with daily functioning in people with chronic pain. A recent systematic review concluded that with additional training, physical therapist–led cognitive-behavioral interventions are efficacious for low back pain, allowing their implementation within the field. Cognitive-behavioral therapy for insomnia, as provided to people with chronic pain, typically includes education, sleep restriction measures, stimulus control instructions, sleep hygiene, and cognitive therapy.
Conservative and pharmacological strategies for chronic pain management offer, at best, modest effect sizes in reducing pain and related disabilities;1–3 thus, there is a need for improved care. A comprehensive approach to chronic pain management should also address pain-associated conditions, such as comorbid insomnia, a topic seldom addressed in the physical therapy literature. Indeed, sleep is increasingly recognized as a plausible therapeutic target for a range of chronic conditions, including chronic pain.4,5 If left untreated, insomnia can represent a barrier for effective chronic pain management.6 Chronic pain is described as debilitating pain with a duration of at least 3 months.
In the absence of other intrinsic sleep disorders and inadequate opportunity or circumstances for sleep (eg, shift work), insomnia in adults is defined as more than 30 minutes of sleep latency and/or minutes awake after sleep onset for more than 3 days per week for more than 3 months.5–7 Insomnia is highly prevalent among people with chronic pain, with 53% to 90% having a clinically significant degree of insomnia.8–11 People with chronic back pain are 18 times more likely to experience clinically defined insomnia than those without chronic back pain.10
Insomnia is closely related to pain severity in people with chronic (low back) pain.10 People with whiplash-associated disorders have insomnia problems such as difficulties initiating sleep and difficulties maintaining sleep, which are related to cognitive disturbances, such as reduced information processing speed.12 Insomnia is usually considered a consequence of chronic pain, but research findings show that sleep disturbances may have a bidirectional relationship with chronic pain.6,9,13
Insomnia may act as both a precipitating factor and a perpetuating factor.5 Population-based longitudinal studies showed that sleep impairments predicted the onset and exacerbation of chronic pain.13 On the basis of the available literature, it was concluded that sleep impairments predict chronic pain more strongly than pain predicts sleep impairments.13 Insomnia is independently associated with the perceived impact of pain on daily functioning and life satisfaction in people with chronic spinal pain.5 Lastly, people with chronic pain spontaneously engage in more physical activity following a better night of sleep14 (Fig. 1). The latter suggests that improving nighttime sleep may be a novel avenue for promoting greater daytime physical activity in people with chronic pain.14
Despite the growing body of scientific literature suggesting a high prevalence of insomnia in individuals with chronic pain, many pain treatment programs propose little other than sedative pain and/or hypnotic neuropharmacological drugs for the treatment of comorbid insomnia.10 These drugs include anticonvulsants, nonbenzodiazepines, benzodiazepines, and tricyclic antidepressants. These drugs are problematic for 2 reasons. First, the efficacy and safety of drug treatment for insomnia in people with chronic pain has not been established. Furthermore, the usage of hypnotic medications is associated with a number of side effects, including sedation, daytime drowsiness, dizziness, lightheadedness, and cognitive and psychomotor impairments.15,16 Pharmacological strategies directed at nociceptive mechanisms do not yield improvements in sleep in people with chronic pain.17–20 Moreover, many trials in people with headaches or musculoskeletal pain found that medication may disturb sleep and even increase pain.21 Finally, reliance on pharmacological treatments for insomnia often opposes patients’ preferences for nonpharmacological alternatives.22
Consequently, there is a need to inform physical therapists about the close interaction between insomnia and the chronic pain experience. Here, we aim to update the reader with the current understanding of the neurobiology behind the interaction between insomnia and chronic pain and suggest a conservative approach to the management of insomnia in people with chronic pain within a physical therapy setting. Henceforth, clinical guidelines for the assessment and treatment of insomnia in people with chronic pain within a physical therapy setting will be provided. These recommendations for assessment and treatment of insomnia are based on the available scientific evidence and the authors’ clinical expertise.
How Sleep Can Influence Chronic Pain: Neuroinflammation, Central Sensitization, and Beyond
Sleep and Central Sensitization: A Bidirectional Interaction
Central sensitization implies increased neuronal response to stimuli in the central nervous system (ie, central hyperexcitability).23–25 Although the concept of central sensitization originates primarily from laboratory, the awareness is growing that it should be part of our clinical reasoning in daily practice.26–28 There is a close interaction between central sensitization and sleep disturbances in people with chronic pain. A single night of total sleep deprivation has been shown to induce generalized hyperalgesia and increase state anxiety in healthy people.29,30 Likewise, sleep curtailment impairs endogenous nociceptive-inhibitory function and increases spontaneous pain in healthy people.31 These findings suggest that sleep disturbances might not only perpetuate central nervous system hyperexcitability in people with chronic pain, but may also serve as an aetiological factor. This may in turn ensue a vicious cycle: poor sleep lowers pain thresholds,6,31 which then contributes to hyperalgesia31 and subsequent increased incidence and/or severity of insomnia.6
The link between central sensitization and insomnia is underscored by various research findings. People with knee osteoarthritis have more central sensitization when they have comorbid insomnia.32 The same study revealed that people with osteoarthritis who have reduced sleep efficiency and higher catastrophizing show more signs of central sensitization.32 Likewise, in a large sample of 961 people with chronic pain, pain-related sleep interference was significantly associated with pain hypersensitivity as measured by quantitative sensory testing, but not with spinal nociceptive hypersensitivity as typically assessed by means of the electromyography response to an electrical stimulus (nociceptive withdrawal reflex).33 Pain hypersensitivity was assessed using pain threshold to electrical stimulation. Moreover, the magnitude of pain-related interference with sleep was associated with increased risk of pain hypersensitivity in people with chronic pain.33 The authors concluded that improving sleep and sleep quality may be important for the management of pain hypersensitivity, potentially leading to pain reduction.33 In people with temporomandibular joint disorder, insomnia is associated with hyperalgesia at a nonorofacial site, suggesting that insomnia may be linked with central sensitization.34
Roles of Dopaminergic, Serotonergic, and Opioidergic Systems in Explaining Insomnia in People With Chronic Pain
The link between insomnia and central sensitization might imply overlapping mechanisms in the central nervous system, for instance mesolimbic dopaminergic pathways playing a cardinal role in both sleep regulation and endogenous analgesia.35 Hence, decreased dopamine availability may explain both sleep disturbances and dysfunctional endogenous analgesia in people with chronic pain. Serotoninergic pathways are also implicated in shared modulatory mechanisms of pain and sleep regulations. Serotonin is critical for top-down orchestration of endogenous analgesia36 as well as of circadian rhythm control.37 Serotoninergic dysfunction can result in altered patterns of circadian behavior or even contribute to a disruption of sleep-wake homeostasis37 along with dysfunctional endogenous analgesia.38 While it is unlikely that either of the 2 mentioned neurotransmitters is the sole factor underlying the links between pain and insomnia, both seem to play major roles in explaining sleep disturbances in people with chronic pain. Essentially, a possible dysfunction in either dopaminergic or serotonergic systems fits within the view that central sensitization is exacerbated or even initiated by sleep disturbances. Preclinical studies support this view by revealing that selective melatonin MT2 receptor partial agonists hold analgesic properties through modulation of “on/off” cells of the brainstem descending antinociceptive systems in neuropathic pain models.39,40
Opioidergic signaling is also implicated in shared modulatory mechanisms of pain and sleep regulations. Opioids are known to influence sleep-wake regulation at least in part mediated by central opioid input to the ventrolateral preoptic nucleus, a key cell group for producing behavioral sleep.41 Morphine decreases the total amount of deep sleep and rapid eye movement sleep in humans through inhibiting the firing rate of sleep-promoting neurons in the ventrolateral preoptic area.42
Poor Sleep Results in Low-Grade Central Nervous System Inflammation
In addition, our current understanding of sleep-related neuro-immunology provides potential links between sleep impairments and pain. While healthy sleep facilitates immune functions, impaired sleep quality or quantity can result in low-grade inflammatory responses.43–45 This low-grade inflammatory response as a consequence of sleep deprivation includes increased levels of interleukin 6, prostaglandin E244,45 and nitric oxide46 possibly mediated by cerebral microglia.46 Allegedly, even low levels of inflammatory cytokines are known to potentially affect brain function.47 These cytokines interfere with central nervous system-mediated fatigue48 and correlate with observations of increased sensitivity to painful stimuli following sleep restriction.30,44,49 Taken together, sleep deprivation conveys a glia-mediated low-grade inflammatory response leading toward increased sensitivity to pain as observable in people with chronic pain.50 The nature of neuro-immunologic links between sleep and pain may be important for the inclusion of pain neuroscience education in people with chronic pain (ie, empower patients to invest time in cognitive-behavioral therapy [CBT] for insomnia [CBT-I]).
Role of Stress in Explaining Insomnia in People With Chronic Pain
Stress and sleep are consistently interconnected, as evidenced in numerous studies reporting strong associations between anxiety levels and insomnia severity,51,52 such as in people with chronic low back pain.10 Daily life stress (eg, worries about the next morning's workload) can negatively impact sleep.53 Similarly, major stressful life events and/or traumatic events such as natural disasters, combat, or a traffic accident can result in sleep architecture alterations reflecting poor sleep.53 Increased nighttime arousal and decreased sleep efficiency are among the most sensitive sleep variables in response to stressors.53
In addition, health anxiety has also been described as a significant predictor of insomnia severity.10 Health anxiety refers to a specific type of anxiety characterized by excessive concerns about one's health (eg, a preoccupation with fears of having a serious disease, despite medical reassurance). It may contribute to aggravate or even trigger insomnia by inducing hypervigilance and arousal by activation of a cascade of cognitive and behavioral processes such as selective attention to threats and negative appraisal.10 Likewise, depression accounts in part for the variance in sleep quality among people with chronic pain.54,55
The preceding paragraphs have documented how stress can impair sleep, but sleep itself can be a stressor. Individuals with insomnia often show high levels of apprehension about bedtime and performance anxiety in an attempt to control the process of sleep onset; and even engage in catastrophic thinking about potential consequences of poor sleep.56 The latter may in turn result in a marked decrease of coping abilities with every day life's stressors. For these reasons, it comes as no surprise that sleep management is mostly included as a part of stress management programs and vice versa. In a successful trial of CBT-I in people with chronic pain, improvers not only showed a significant increase in perceived sleep efficiency but also a decrease in self-reported levels of distress,57 suggesting that effective coping with stress is a key factor for sleep improvements.
The preceding text has explained how insomnia is of significance to people with chronic pain, with special emphasis on the neurobiology of these interactions. The following text explains how the current understanding of insomnia in people with chronic pain is applied to clinical practice (including assessment and CBT-I).
Applying Science to Practice I: Assessment of Insomnia in People With Chronic Pain in Clinical Practice
Depending on the education received, physical therapists may not be trained to screen for insomnia, and patients are not referred to physical therapists for insomnia either. Yet physical therapists are advised to briefly question people with chronic pain about sleep latency and minutes aware after sleep. This can allow them to estimate whether the patient complies with the definition of insomnia (ie, more than 30 minutes of sleep latency and/or minutes awake after sleep onset for more than 3 days per week for more than 3 months5–7). It is advised to determine from the patient if the insomnia began before or after the pain condition and consider how the pain condition is influencing their insomnia symptoms. In addition, the Insomnia Severity Index generates reliable and valid data to quantify the subjective harshness of insomnia.58 A cutoff level of 14 (ie, range of 0–14 vs 15–28) has been proposed for the clinical significance of chronic insomnia in patients presenting with chronic back pain,10 and greater than 10 was recommended as the cutoff in a community sample.59 In case of suspected insomnia the physical therapists should refer the patient to a sleep physician who can use polysomnography to ascertain whether underlying primary sleep disorders are present.6,60 Such primary sleep disorders include sleep-related breathing or movement disorders, circadian sleep-wake disorders, etc. The polysomnography is not used to diagnose insomnia, but to rule out other sleep disorders.
In case of diagnosed or suspected insomnia disorder, physical therapists should then explore whether insomnia coexists with the chronic pain experience. This is achieved by ascertaining that insomnia is reported by the patient to originate after and/or to be aggravated by the current pain condition. 6 If this is the case and the physical therapist is planning to provide CBT-I, a thorough questioning of the patient's sleep habits and difficulties is required. Such an interview may include the items listed in Table 1. Table 1 comprises not only items for questioning the patient about sleep habits and difficulties, but a guide on how to interpret the obtained information and treatment implications.
Item . | Explanation . | Mode of Assessment . | Sample Questions . | Interpretation . | Treatment Implications . |
---|---|---|---|---|---|
(Non) restorative sleep | Recuperative sleep or not; whether a patient feels refreshed at final awakening. | Questioning/PSQI | Do you feel refreshed when you wake up? | Ideally, good sleep should be refreshing. Nonrestorative sleep can be a symptom of disordered sleep. | If a patient has recurrent sensations of nonrestorative sleep or unrefreshing morning arousals, then further inquiry about sleep is indicated. |
Time in bed80 | Amount of time spent in bed. | Questioning/sleep diary/PSQI/actigraphy | How much time do you spend in bed over the course of 24 h? | Interpretation should take into account time spent in and out of bed as well as time spent awake in bed (ie, sleep efficiency). | Treatment implications rely on the interpretation of various sleep items taken together; the amount of time spent in bed at night alone has no treatment implication per se. |
Time out of bed80 | Amount of time spent (awake or asleep) out of bed at night. | Questioning/sleep diary/actigraphy | How much time do you spend out of bed during the night? | If a patient spends more than half an hour out of bed at night, then further questioning about what he or she does while out of bed is required. In general, this problem may be related to poor sleep quality. | Unless the time spent out of bed is part of stimulus control instructions (Tab. 2), efforts should be made to limit time out of bed at night. Activities during time out of bed at night should be relaxing and not physically or emotionally stimulating and should aim to not further interfere with sleep. |
Sleep latency80 | Time from “lights off” to sleep onset. | Questioning/sleep diary/PSQI/actigraphy | How long does it take for you to fall asleep? | Ideally, sleep latency should not be longer than 30 min. | If sleep latency appears to be recurrently longer than 30 min, then treatment should be aimed at decreasing sleep latency. This goal can be achieved by, eg, delaying bedtime (ie, increasing sleep pressure), improving preparation, reducing the level of stimulating activities or food (energy) intake, or using relaxation techniques in the hour before going to bed. |
Awake after sleep onset80 | Time spent awake in bed after sleep onset. | Questioning/sleep diary/actigraphy | How much time do you spend awake in bed after falling asleep? | If a patient spends more than half an hour awake in bed after sleep onset, then this problem should be addressed. | Time spent awake in bed after sleep onset can be reduced by applying bedtime restriction/sleep compression. A patient who lies awake for more than half an hour should be advised to leave the bedroom and do something relaxing until feeling sleepy again. Motivational interviewing should be applied to promote behavioral change. |
Early–morning awakening80 | Time spent awake prior to planned wake-up time. | Questioning/sleep diary/actigraphy | Do you wake up prior to your planned wake-up time? | Time spent awake in bed prior to getting out of bed should be as short as possible. Ideally, a patient should get out of bed as soon as possible after final arousal. | A patient who stays in bed awake after final arousal should be advised to get out of bed as soon as possible to prevent wake inertia and daytime fatigue. Motivational techniques should be applied to promote behavioral change. |
Number of awakenings80 | Number of conscious arousals experienced per night. | Questioning/sleep diary/actigraphy | Do you wake up during the night and, if so, how many times? | On average, a patient should not consciously wake up more than 2 times during the allotted sleep period. Waking up once per night (eg, for a bathroom visit), however, may not be a clinically relevant issue. | Various parts of CBT-I (Tab. 2) can decrease the number of arousals. If a patient has recurrent awakenings (>2) and/or awakenings lasting more than half an hour in total, then the strategies used for time spent awake in bed after sleep onset should be used. |
Sleep efficiency81 | (Total sleep time/total time in bed) × 100. | Calculation | Ideally, sleep efficiency should be >90%; >85% is acceptable given adequate sleep duration. | If a patient has reduced sleep efficiency, then bedtime restriction (Tab. 2) may be required. The aim is to find a compromise with respect to a realistic estimation of quantitative sleep needs. | |
Sleep hygiene | Recommended behavioral practices intended to promote improved sleep quality. | Questioning | Do you monitor time while being awake in bed? Do you consume stimulant beverages prior to bedtime? Do you intensively exercise close to bedtime? What do you eat before going to bed? | Stimulants (eg, caffeine or nicotine) close to bedtime may impair sleep onset and/or maintenance. A small amount of aerobic exercise could improve sleep quality; however, intense workouts close to bedtime should be avoided. Food that has a high caloric load and/or that affects absorption processes in the digestive tract can cause sleep disruption. | Sleep hygiene (Tab. 2) instructions are needed to explain that clock monitoring in bed, food and beverage consumption, and intense exercise before bedtime may disrupt sleep initiation and maintenance. Motivational interviewing should be applied to promote behavioral change. |
Napping | Whether a patient sleeps or lies down with the intention to sleep, at what time, how long, and how often. | Questioning/sleep diary/actigraphy | Do you sleep during the day or evening and, if so, how long and how often? | In a patient with insomnia, napping generally is not recommended. It may be acceptable if the nap is ≤20 min (ie, “power nap”) and has appropriate timing with respect to circadian rhythms (ie, not later than 15.30 h). Otherwise, a nap can lower sleep pressure or disrupt nighttime sleep. A nap includes falling asleep before bedtime (eg, while watching TV). | Sleep hygiene (Tab. 2) instructions are needed to explain that daytime sleeping may disrupt circadian rhythms or lower sleep pressure at bedtime. A patient should avoid daytime sleeping beyond the duration of a power nap. |
Sleep environment | Physical bedroom characteristics, such as darkness, temperature, noise/quietness, and humidity. | Questioning | Is your bedroom sufficiently dark (ie, even after sunrise)? What is the temperature in your bedroom? Is it sufficiently quiet in your bedroom? | Ambient light may interfere with sleep quality and/or continuity. Ideally, the bedroom temperature should be 16°C–19°C, and the bedroom should be isolated from noise disturbances. | Sleep hygiene (Tab. 2) instructions are needed to explain and improve the sleep environment. |
Perceived sleep quality11 | Subjective sleep quality. | Questioning/sleep diary/PSQI/rating | How well do you sleep? | If a patient perceives sleep quality as satisfying, then further inquiry may not be compulsory. If not, then sleep quality can be used to monitor a therapeutic response. | A lack of improvement in sleep quality over time may indicate that the treatment response to CBT-I is not evolving as intended. |
Beliefs and attitudes with respect to the nature/etiology of the sleep problem | Patient's erroneous causal attributions with respect to insomnia. | Questioning/DBAS | What do you think causes your sleep problem? | Assess whether sleep beliefs are adaptive or prevent behavioral change. | If a patient has maladaptive sleep beliefs, then general sleep education (Tab. 2) is indicated. |
Beliefs and attitudes regarding the evolution of the sleep problem | Whether a patient expects improvement or not. | Questioning/DBAS | Do you think that your sleep can improve? | Assess whether beliefs and attitudes regarding the evolution of insomnia are adaptive or prevent behavioral change. | Maladaptive beliefs and attitudes regarding the evolution of the sleep problem should be addressed with general sleep education (Tab. 2). |
Identification of (life) stressors82 | Whether a patient has experienced life stressors and is currently struggling to cope with certain (daily) stressors. | Questioning | Are you struggling to deal with daily stressors and, if so, which ones? | Interpret the obtained information to assess whether stress is an issue for a patient. If stress is an issue, then assess whether stress influences sleep. | If stress has a negative impact on a patient's sleep, then relaxation training/stress management should be included in the CBT-I treatment (Tab. 2). |
Sleep medication | Whether a patient uses any hypnotic or sedative drug (including any synthetic or herbal treatment). | Questioning/reviewing medical record | Are you using any drug treatments for your sleep? If so, do you consider them useful? Would you like to pursue or discontinue them? | Sole administratration of sleep medication is not recommended for treating chronic insomnia but may provide some temporary benefit or an improved therapeutic response (bimodal therapy). | A patient's perception of sleep medication may interfere with counseling and CBT-I. If a patient wishes to discontine drug treatment, then systematic withdrawal may be initiated. If not, then treatment may be supplemented by CBT-I and withdrawal may be postponed (ie, when the patient is improving, showing increased self-efficacy in regaining sleep efficiency and sleep quality). In any case, therapists may discuss the treatment plan with the prescriber to prevent contradictory messages. |
Substance abuse82 | Past or present substance abuse. | Questioning/reviewing medical record | Are you currently using or have you been using any substances or drugs (including nicotine)? | Substances may have a negative impact on biological functions of sleep. Past or current substance abuse may interfere with adrenergic, cholinergic, and/or dopaminergic pathways. | Motivational interviewing should be applied to promote behavioral change. |
Item . | Explanation . | Mode of Assessment . | Sample Questions . | Interpretation . | Treatment Implications . |
---|---|---|---|---|---|
(Non) restorative sleep | Recuperative sleep or not; whether a patient feels refreshed at final awakening. | Questioning/PSQI | Do you feel refreshed when you wake up? | Ideally, good sleep should be refreshing. Nonrestorative sleep can be a symptom of disordered sleep. | If a patient has recurrent sensations of nonrestorative sleep or unrefreshing morning arousals, then further inquiry about sleep is indicated. |
Time in bed80 | Amount of time spent in bed. | Questioning/sleep diary/PSQI/actigraphy | How much time do you spend in bed over the course of 24 h? | Interpretation should take into account time spent in and out of bed as well as time spent awake in bed (ie, sleep efficiency). | Treatment implications rely on the interpretation of various sleep items taken together; the amount of time spent in bed at night alone has no treatment implication per se. |
Time out of bed80 | Amount of time spent (awake or asleep) out of bed at night. | Questioning/sleep diary/actigraphy | How much time do you spend out of bed during the night? | If a patient spends more than half an hour out of bed at night, then further questioning about what he or she does while out of bed is required. In general, this problem may be related to poor sleep quality. | Unless the time spent out of bed is part of stimulus control instructions (Tab. 2), efforts should be made to limit time out of bed at night. Activities during time out of bed at night should be relaxing and not physically or emotionally stimulating and should aim to not further interfere with sleep. |
Sleep latency80 | Time from “lights off” to sleep onset. | Questioning/sleep diary/PSQI/actigraphy | How long does it take for you to fall asleep? | Ideally, sleep latency should not be longer than 30 min. | If sleep latency appears to be recurrently longer than 30 min, then treatment should be aimed at decreasing sleep latency. This goal can be achieved by, eg, delaying bedtime (ie, increasing sleep pressure), improving preparation, reducing the level of stimulating activities or food (energy) intake, or using relaxation techniques in the hour before going to bed. |
Awake after sleep onset80 | Time spent awake in bed after sleep onset. | Questioning/sleep diary/actigraphy | How much time do you spend awake in bed after falling asleep? | If a patient spends more than half an hour awake in bed after sleep onset, then this problem should be addressed. | Time spent awake in bed after sleep onset can be reduced by applying bedtime restriction/sleep compression. A patient who lies awake for more than half an hour should be advised to leave the bedroom and do something relaxing until feeling sleepy again. Motivational interviewing should be applied to promote behavioral change. |
Early–morning awakening80 | Time spent awake prior to planned wake-up time. | Questioning/sleep diary/actigraphy | Do you wake up prior to your planned wake-up time? | Time spent awake in bed prior to getting out of bed should be as short as possible. Ideally, a patient should get out of bed as soon as possible after final arousal. | A patient who stays in bed awake after final arousal should be advised to get out of bed as soon as possible to prevent wake inertia and daytime fatigue. Motivational techniques should be applied to promote behavioral change. |
Number of awakenings80 | Number of conscious arousals experienced per night. | Questioning/sleep diary/actigraphy | Do you wake up during the night and, if so, how many times? | On average, a patient should not consciously wake up more than 2 times during the allotted sleep period. Waking up once per night (eg, for a bathroom visit), however, may not be a clinically relevant issue. | Various parts of CBT-I (Tab. 2) can decrease the number of arousals. If a patient has recurrent awakenings (>2) and/or awakenings lasting more than half an hour in total, then the strategies used for time spent awake in bed after sleep onset should be used. |
Sleep efficiency81 | (Total sleep time/total time in bed) × 100. | Calculation | Ideally, sleep efficiency should be >90%; >85% is acceptable given adequate sleep duration. | If a patient has reduced sleep efficiency, then bedtime restriction (Tab. 2) may be required. The aim is to find a compromise with respect to a realistic estimation of quantitative sleep needs. | |
Sleep hygiene | Recommended behavioral practices intended to promote improved sleep quality. | Questioning | Do you monitor time while being awake in bed? Do you consume stimulant beverages prior to bedtime? Do you intensively exercise close to bedtime? What do you eat before going to bed? | Stimulants (eg, caffeine or nicotine) close to bedtime may impair sleep onset and/or maintenance. A small amount of aerobic exercise could improve sleep quality; however, intense workouts close to bedtime should be avoided. Food that has a high caloric load and/or that affects absorption processes in the digestive tract can cause sleep disruption. | Sleep hygiene (Tab. 2) instructions are needed to explain that clock monitoring in bed, food and beverage consumption, and intense exercise before bedtime may disrupt sleep initiation and maintenance. Motivational interviewing should be applied to promote behavioral change. |
Napping | Whether a patient sleeps or lies down with the intention to sleep, at what time, how long, and how often. | Questioning/sleep diary/actigraphy | Do you sleep during the day or evening and, if so, how long and how often? | In a patient with insomnia, napping generally is not recommended. It may be acceptable if the nap is ≤20 min (ie, “power nap”) and has appropriate timing with respect to circadian rhythms (ie, not later than 15.30 h). Otherwise, a nap can lower sleep pressure or disrupt nighttime sleep. A nap includes falling asleep before bedtime (eg, while watching TV). | Sleep hygiene (Tab. 2) instructions are needed to explain that daytime sleeping may disrupt circadian rhythms or lower sleep pressure at bedtime. A patient should avoid daytime sleeping beyond the duration of a power nap. |
Sleep environment | Physical bedroom characteristics, such as darkness, temperature, noise/quietness, and humidity. | Questioning | Is your bedroom sufficiently dark (ie, even after sunrise)? What is the temperature in your bedroom? Is it sufficiently quiet in your bedroom? | Ambient light may interfere with sleep quality and/or continuity. Ideally, the bedroom temperature should be 16°C–19°C, and the bedroom should be isolated from noise disturbances. | Sleep hygiene (Tab. 2) instructions are needed to explain and improve the sleep environment. |
Perceived sleep quality11 | Subjective sleep quality. | Questioning/sleep diary/PSQI/rating | How well do you sleep? | If a patient perceives sleep quality as satisfying, then further inquiry may not be compulsory. If not, then sleep quality can be used to monitor a therapeutic response. | A lack of improvement in sleep quality over time may indicate that the treatment response to CBT-I is not evolving as intended. |
Beliefs and attitudes with respect to the nature/etiology of the sleep problem | Patient's erroneous causal attributions with respect to insomnia. | Questioning/DBAS | What do you think causes your sleep problem? | Assess whether sleep beliefs are adaptive or prevent behavioral change. | If a patient has maladaptive sleep beliefs, then general sleep education (Tab. 2) is indicated. |
Beliefs and attitudes regarding the evolution of the sleep problem | Whether a patient expects improvement or not. | Questioning/DBAS | Do you think that your sleep can improve? | Assess whether beliefs and attitudes regarding the evolution of insomnia are adaptive or prevent behavioral change. | Maladaptive beliefs and attitudes regarding the evolution of the sleep problem should be addressed with general sleep education (Tab. 2). |
Identification of (life) stressors82 | Whether a patient has experienced life stressors and is currently struggling to cope with certain (daily) stressors. | Questioning | Are you struggling to deal with daily stressors and, if so, which ones? | Interpret the obtained information to assess whether stress is an issue for a patient. If stress is an issue, then assess whether stress influences sleep. | If stress has a negative impact on a patient's sleep, then relaxation training/stress management should be included in the CBT-I treatment (Tab. 2). |
Sleep medication | Whether a patient uses any hypnotic or sedative drug (including any synthetic or herbal treatment). | Questioning/reviewing medical record | Are you using any drug treatments for your sleep? If so, do you consider them useful? Would you like to pursue or discontinue them? | Sole administratration of sleep medication is not recommended for treating chronic insomnia but may provide some temporary benefit or an improved therapeutic response (bimodal therapy). | A patient's perception of sleep medication may interfere with counseling and CBT-I. If a patient wishes to discontine drug treatment, then systematic withdrawal may be initiated. If not, then treatment may be supplemented by CBT-I and withdrawal may be postponed (ie, when the patient is improving, showing increased self-efficacy in regaining sleep efficiency and sleep quality). In any case, therapists may discuss the treatment plan with the prescriber to prevent contradictory messages. |
Substance abuse82 | Past or present substance abuse. | Questioning/reviewing medical record | Are you currently using or have you been using any substances or drugs (including nicotine)? | Substances may have a negative impact on biological functions of sleep. Past or current substance abuse may interfere with adrenergic, cholinergic, and/or dopaminergic pathways. | Motivational interviewing should be applied to promote behavioral change. |
aCBT-I = cognitive-behavioral therapy for insomnia, DBAS = Dysfunctional Beliefs and Attitudes About Sleep, PSQI = Pittsburgh Sleep Quality Index.
Item . | Explanation . | Mode of Assessment . | Sample Questions . | Interpretation . | Treatment Implications . |
---|---|---|---|---|---|
(Non) restorative sleep | Recuperative sleep or not; whether a patient feels refreshed at final awakening. | Questioning/PSQI | Do you feel refreshed when you wake up? | Ideally, good sleep should be refreshing. Nonrestorative sleep can be a symptom of disordered sleep. | If a patient has recurrent sensations of nonrestorative sleep or unrefreshing morning arousals, then further inquiry about sleep is indicated. |
Time in bed80 | Amount of time spent in bed. | Questioning/sleep diary/PSQI/actigraphy | How much time do you spend in bed over the course of 24 h? | Interpretation should take into account time spent in and out of bed as well as time spent awake in bed (ie, sleep efficiency). | Treatment implications rely on the interpretation of various sleep items taken together; the amount of time spent in bed at night alone has no treatment implication per se. |
Time out of bed80 | Amount of time spent (awake or asleep) out of bed at night. | Questioning/sleep diary/actigraphy | How much time do you spend out of bed during the night? | If a patient spends more than half an hour out of bed at night, then further questioning about what he or she does while out of bed is required. In general, this problem may be related to poor sleep quality. | Unless the time spent out of bed is part of stimulus control instructions (Tab. 2), efforts should be made to limit time out of bed at night. Activities during time out of bed at night should be relaxing and not physically or emotionally stimulating and should aim to not further interfere with sleep. |
Sleep latency80 | Time from “lights off” to sleep onset. | Questioning/sleep diary/PSQI/actigraphy | How long does it take for you to fall asleep? | Ideally, sleep latency should not be longer than 30 min. | If sleep latency appears to be recurrently longer than 30 min, then treatment should be aimed at decreasing sleep latency. This goal can be achieved by, eg, delaying bedtime (ie, increasing sleep pressure), improving preparation, reducing the level of stimulating activities or food (energy) intake, or using relaxation techniques in the hour before going to bed. |
Awake after sleep onset80 | Time spent awake in bed after sleep onset. | Questioning/sleep diary/actigraphy | How much time do you spend awake in bed after falling asleep? | If a patient spends more than half an hour awake in bed after sleep onset, then this problem should be addressed. | Time spent awake in bed after sleep onset can be reduced by applying bedtime restriction/sleep compression. A patient who lies awake for more than half an hour should be advised to leave the bedroom and do something relaxing until feeling sleepy again. Motivational interviewing should be applied to promote behavioral change. |
Early–morning awakening80 | Time spent awake prior to planned wake-up time. | Questioning/sleep diary/actigraphy | Do you wake up prior to your planned wake-up time? | Time spent awake in bed prior to getting out of bed should be as short as possible. Ideally, a patient should get out of bed as soon as possible after final arousal. | A patient who stays in bed awake after final arousal should be advised to get out of bed as soon as possible to prevent wake inertia and daytime fatigue. Motivational techniques should be applied to promote behavioral change. |
Number of awakenings80 | Number of conscious arousals experienced per night. | Questioning/sleep diary/actigraphy | Do you wake up during the night and, if so, how many times? | On average, a patient should not consciously wake up more than 2 times during the allotted sleep period. Waking up once per night (eg, for a bathroom visit), however, may not be a clinically relevant issue. | Various parts of CBT-I (Tab. 2) can decrease the number of arousals. If a patient has recurrent awakenings (>2) and/or awakenings lasting more than half an hour in total, then the strategies used for time spent awake in bed after sleep onset should be used. |
Sleep efficiency81 | (Total sleep time/total time in bed) × 100. | Calculation | Ideally, sleep efficiency should be >90%; >85% is acceptable given adequate sleep duration. | If a patient has reduced sleep efficiency, then bedtime restriction (Tab. 2) may be required. The aim is to find a compromise with respect to a realistic estimation of quantitative sleep needs. | |
Sleep hygiene | Recommended behavioral practices intended to promote improved sleep quality. | Questioning | Do you monitor time while being awake in bed? Do you consume stimulant beverages prior to bedtime? Do you intensively exercise close to bedtime? What do you eat before going to bed? | Stimulants (eg, caffeine or nicotine) close to bedtime may impair sleep onset and/or maintenance. A small amount of aerobic exercise could improve sleep quality; however, intense workouts close to bedtime should be avoided. Food that has a high caloric load and/or that affects absorption processes in the digestive tract can cause sleep disruption. | Sleep hygiene (Tab. 2) instructions are needed to explain that clock monitoring in bed, food and beverage consumption, and intense exercise before bedtime may disrupt sleep initiation and maintenance. Motivational interviewing should be applied to promote behavioral change. |
Napping | Whether a patient sleeps or lies down with the intention to sleep, at what time, how long, and how often. | Questioning/sleep diary/actigraphy | Do you sleep during the day or evening and, if so, how long and how often? | In a patient with insomnia, napping generally is not recommended. It may be acceptable if the nap is ≤20 min (ie, “power nap”) and has appropriate timing with respect to circadian rhythms (ie, not later than 15.30 h). Otherwise, a nap can lower sleep pressure or disrupt nighttime sleep. A nap includes falling asleep before bedtime (eg, while watching TV). | Sleep hygiene (Tab. 2) instructions are needed to explain that daytime sleeping may disrupt circadian rhythms or lower sleep pressure at bedtime. A patient should avoid daytime sleeping beyond the duration of a power nap. |
Sleep environment | Physical bedroom characteristics, such as darkness, temperature, noise/quietness, and humidity. | Questioning | Is your bedroom sufficiently dark (ie, even after sunrise)? What is the temperature in your bedroom? Is it sufficiently quiet in your bedroom? | Ambient light may interfere with sleep quality and/or continuity. Ideally, the bedroom temperature should be 16°C–19°C, and the bedroom should be isolated from noise disturbances. | Sleep hygiene (Tab. 2) instructions are needed to explain and improve the sleep environment. |
Perceived sleep quality11 | Subjective sleep quality. | Questioning/sleep diary/PSQI/rating | How well do you sleep? | If a patient perceives sleep quality as satisfying, then further inquiry may not be compulsory. If not, then sleep quality can be used to monitor a therapeutic response. | A lack of improvement in sleep quality over time may indicate that the treatment response to CBT-I is not evolving as intended. |
Beliefs and attitudes with respect to the nature/etiology of the sleep problem | Patient's erroneous causal attributions with respect to insomnia. | Questioning/DBAS | What do you think causes your sleep problem? | Assess whether sleep beliefs are adaptive or prevent behavioral change. | If a patient has maladaptive sleep beliefs, then general sleep education (Tab. 2) is indicated. |
Beliefs and attitudes regarding the evolution of the sleep problem | Whether a patient expects improvement or not. | Questioning/DBAS | Do you think that your sleep can improve? | Assess whether beliefs and attitudes regarding the evolution of insomnia are adaptive or prevent behavioral change. | Maladaptive beliefs and attitudes regarding the evolution of the sleep problem should be addressed with general sleep education (Tab. 2). |
Identification of (life) stressors82 | Whether a patient has experienced life stressors and is currently struggling to cope with certain (daily) stressors. | Questioning | Are you struggling to deal with daily stressors and, if so, which ones? | Interpret the obtained information to assess whether stress is an issue for a patient. If stress is an issue, then assess whether stress influences sleep. | If stress has a negative impact on a patient's sleep, then relaxation training/stress management should be included in the CBT-I treatment (Tab. 2). |
Sleep medication | Whether a patient uses any hypnotic or sedative drug (including any synthetic or herbal treatment). | Questioning/reviewing medical record | Are you using any drug treatments for your sleep? If so, do you consider them useful? Would you like to pursue or discontinue them? | Sole administratration of sleep medication is not recommended for treating chronic insomnia but may provide some temporary benefit or an improved therapeutic response (bimodal therapy). | A patient's perception of sleep medication may interfere with counseling and CBT-I. If a patient wishes to discontine drug treatment, then systematic withdrawal may be initiated. If not, then treatment may be supplemented by CBT-I and withdrawal may be postponed (ie, when the patient is improving, showing increased self-efficacy in regaining sleep efficiency and sleep quality). In any case, therapists may discuss the treatment plan with the prescriber to prevent contradictory messages. |
Substance abuse82 | Past or present substance abuse. | Questioning/reviewing medical record | Are you currently using or have you been using any substances or drugs (including nicotine)? | Substances may have a negative impact on biological functions of sleep. Past or current substance abuse may interfere with adrenergic, cholinergic, and/or dopaminergic pathways. | Motivational interviewing should be applied to promote behavioral change. |
Item . | Explanation . | Mode of Assessment . | Sample Questions . | Interpretation . | Treatment Implications . |
---|---|---|---|---|---|
(Non) restorative sleep | Recuperative sleep or not; whether a patient feels refreshed at final awakening. | Questioning/PSQI | Do you feel refreshed when you wake up? | Ideally, good sleep should be refreshing. Nonrestorative sleep can be a symptom of disordered sleep. | If a patient has recurrent sensations of nonrestorative sleep or unrefreshing morning arousals, then further inquiry about sleep is indicated. |
Time in bed80 | Amount of time spent in bed. | Questioning/sleep diary/PSQI/actigraphy | How much time do you spend in bed over the course of 24 h? | Interpretation should take into account time spent in and out of bed as well as time spent awake in bed (ie, sleep efficiency). | Treatment implications rely on the interpretation of various sleep items taken together; the amount of time spent in bed at night alone has no treatment implication per se. |
Time out of bed80 | Amount of time spent (awake or asleep) out of bed at night. | Questioning/sleep diary/actigraphy | How much time do you spend out of bed during the night? | If a patient spends more than half an hour out of bed at night, then further questioning about what he or she does while out of bed is required. In general, this problem may be related to poor sleep quality. | Unless the time spent out of bed is part of stimulus control instructions (Tab. 2), efforts should be made to limit time out of bed at night. Activities during time out of bed at night should be relaxing and not physically or emotionally stimulating and should aim to not further interfere with sleep. |
Sleep latency80 | Time from “lights off” to sleep onset. | Questioning/sleep diary/PSQI/actigraphy | How long does it take for you to fall asleep? | Ideally, sleep latency should not be longer than 30 min. | If sleep latency appears to be recurrently longer than 30 min, then treatment should be aimed at decreasing sleep latency. This goal can be achieved by, eg, delaying bedtime (ie, increasing sleep pressure), improving preparation, reducing the level of stimulating activities or food (energy) intake, or using relaxation techniques in the hour before going to bed. |
Awake after sleep onset80 | Time spent awake in bed after sleep onset. | Questioning/sleep diary/actigraphy | How much time do you spend awake in bed after falling asleep? | If a patient spends more than half an hour awake in bed after sleep onset, then this problem should be addressed. | Time spent awake in bed after sleep onset can be reduced by applying bedtime restriction/sleep compression. A patient who lies awake for more than half an hour should be advised to leave the bedroom and do something relaxing until feeling sleepy again. Motivational interviewing should be applied to promote behavioral change. |
Early–morning awakening80 | Time spent awake prior to planned wake-up time. | Questioning/sleep diary/actigraphy | Do you wake up prior to your planned wake-up time? | Time spent awake in bed prior to getting out of bed should be as short as possible. Ideally, a patient should get out of bed as soon as possible after final arousal. | A patient who stays in bed awake after final arousal should be advised to get out of bed as soon as possible to prevent wake inertia and daytime fatigue. Motivational techniques should be applied to promote behavioral change. |
Number of awakenings80 | Number of conscious arousals experienced per night. | Questioning/sleep diary/actigraphy | Do you wake up during the night and, if so, how many times? | On average, a patient should not consciously wake up more than 2 times during the allotted sleep period. Waking up once per night (eg, for a bathroom visit), however, may not be a clinically relevant issue. | Various parts of CBT-I (Tab. 2) can decrease the number of arousals. If a patient has recurrent awakenings (>2) and/or awakenings lasting more than half an hour in total, then the strategies used for time spent awake in bed after sleep onset should be used. |
Sleep efficiency81 | (Total sleep time/total time in bed) × 100. | Calculation | Ideally, sleep efficiency should be >90%; >85% is acceptable given adequate sleep duration. | If a patient has reduced sleep efficiency, then bedtime restriction (Tab. 2) may be required. The aim is to find a compromise with respect to a realistic estimation of quantitative sleep needs. | |
Sleep hygiene | Recommended behavioral practices intended to promote improved sleep quality. | Questioning | Do you monitor time while being awake in bed? Do you consume stimulant beverages prior to bedtime? Do you intensively exercise close to bedtime? What do you eat before going to bed? | Stimulants (eg, caffeine or nicotine) close to bedtime may impair sleep onset and/or maintenance. A small amount of aerobic exercise could improve sleep quality; however, intense workouts close to bedtime should be avoided. Food that has a high caloric load and/or that affects absorption processes in the digestive tract can cause sleep disruption. | Sleep hygiene (Tab. 2) instructions are needed to explain that clock monitoring in bed, food and beverage consumption, and intense exercise before bedtime may disrupt sleep initiation and maintenance. Motivational interviewing should be applied to promote behavioral change. |
Napping | Whether a patient sleeps or lies down with the intention to sleep, at what time, how long, and how often. | Questioning/sleep diary/actigraphy | Do you sleep during the day or evening and, if so, how long and how often? | In a patient with insomnia, napping generally is not recommended. It may be acceptable if the nap is ≤20 min (ie, “power nap”) and has appropriate timing with respect to circadian rhythms (ie, not later than 15.30 h). Otherwise, a nap can lower sleep pressure or disrupt nighttime sleep. A nap includes falling asleep before bedtime (eg, while watching TV). | Sleep hygiene (Tab. 2) instructions are needed to explain that daytime sleeping may disrupt circadian rhythms or lower sleep pressure at bedtime. A patient should avoid daytime sleeping beyond the duration of a power nap. |
Sleep environment | Physical bedroom characteristics, such as darkness, temperature, noise/quietness, and humidity. | Questioning | Is your bedroom sufficiently dark (ie, even after sunrise)? What is the temperature in your bedroom? Is it sufficiently quiet in your bedroom? | Ambient light may interfere with sleep quality and/or continuity. Ideally, the bedroom temperature should be 16°C–19°C, and the bedroom should be isolated from noise disturbances. | Sleep hygiene (Tab. 2) instructions are needed to explain and improve the sleep environment. |
Perceived sleep quality11 | Subjective sleep quality. | Questioning/sleep diary/PSQI/rating | How well do you sleep? | If a patient perceives sleep quality as satisfying, then further inquiry may not be compulsory. If not, then sleep quality can be used to monitor a therapeutic response. | A lack of improvement in sleep quality over time may indicate that the treatment response to CBT-I is not evolving as intended. |
Beliefs and attitudes with respect to the nature/etiology of the sleep problem | Patient's erroneous causal attributions with respect to insomnia. | Questioning/DBAS | What do you think causes your sleep problem? | Assess whether sleep beliefs are adaptive or prevent behavioral change. | If a patient has maladaptive sleep beliefs, then general sleep education (Tab. 2) is indicated. |
Beliefs and attitudes regarding the evolution of the sleep problem | Whether a patient expects improvement or not. | Questioning/DBAS | Do you think that your sleep can improve? | Assess whether beliefs and attitudes regarding the evolution of insomnia are adaptive or prevent behavioral change. | Maladaptive beliefs and attitudes regarding the evolution of the sleep problem should be addressed with general sleep education (Tab. 2). |
Identification of (life) stressors82 | Whether a patient has experienced life stressors and is currently struggling to cope with certain (daily) stressors. | Questioning | Are you struggling to deal with daily stressors and, if so, which ones? | Interpret the obtained information to assess whether stress is an issue for a patient. If stress is an issue, then assess whether stress influences sleep. | If stress has a negative impact on a patient's sleep, then relaxation training/stress management should be included in the CBT-I treatment (Tab. 2). |
Sleep medication | Whether a patient uses any hypnotic or sedative drug (including any synthetic or herbal treatment). | Questioning/reviewing medical record | Are you using any drug treatments for your sleep? If so, do you consider them useful? Would you like to pursue or discontinue them? | Sole administratration of sleep medication is not recommended for treating chronic insomnia but may provide some temporary benefit or an improved therapeutic response (bimodal therapy). | A patient's perception of sleep medication may interfere with counseling and CBT-I. If a patient wishes to discontine drug treatment, then systematic withdrawal may be initiated. If not, then treatment may be supplemented by CBT-I and withdrawal may be postponed (ie, when the patient is improving, showing increased self-efficacy in regaining sleep efficiency and sleep quality). In any case, therapists may discuss the treatment plan with the prescriber to prevent contradictory messages. |
Substance abuse82 | Past or present substance abuse. | Questioning/reviewing medical record | Are you currently using or have you been using any substances or drugs (including nicotine)? | Substances may have a negative impact on biological functions of sleep. Past or current substance abuse may interfere with adrenergic, cholinergic, and/or dopaminergic pathways. | Motivational interviewing should be applied to promote behavioral change. |
aCBT-I = cognitive-behavioral therapy for insomnia, DBAS = Dysfunctional Beliefs and Attitudes About Sleep, PSQI = Pittsburgh Sleep Quality Index.
Whether the patient has been or is currently a substance abuser is not only important because of its potentially negative impact on biological functions of sleep, but also because past or current substance abusers’ dopaminergic circuits may be altered as a consequence of repeated activations associated with consumption.35 In addition to sleep history taking, therapists may consider using self-reported tools for the assessment of sleep parameters. Such self-reported tools include sleep diaries, questionnaires like the Insomnia Severity Index, the Pittsburgh Sleep Quality Index and/or the Epworth sleepiness scale.61,62
Applying Science to Practice II: Conservative Treatment of Insomnia in People With Chronic Pain
CBT is effective for the treatment of chronic pain.2,63–65 CBT is a psychosocial intervention that aims at changing unhelpful thoughts, beliefs, and attitudes in order to improve their coping skills, self-regulation, and healthy behavior. CBT is widely used for the treatment of chronic pain and depression. A systematic review concluded with high-quality evidence that with additional training, physical therapist-led cognitive-behavioral interventions are effective for low back pain.66 CBT-I is a specific form of CBT for a specific condition, one that is a candidate to be considered for psychologically informed practice delivered by physical therapists.67
Available Evidence for Conservative Sleep Treatment in People With Chronic Pain
A meta-analysis of available studies examining the effects of nonpharmacological treatments of insomnia for cancer and non–cancer-related chronic pain conditions showed that addressing sleep resulted in large immediate improvements in sleep quality, relatively small reductions in pain and fatigue and moderate decrease of depression symptoms.4 The improvements in sleep quality and fatigue were maintained after a 1-year follow-up.4
CBT-I is the recommended evidence-based treatment for chronic primary insomnia.60 The advantage over sedative drugs or classical hypnotics mainly lies in the sustainability of treatment effects and a lower risk for side effects.60 Based on the available treatment studies in people with chronic pain, a similar picture arises. The first report of a treatment trials targeted at sleep for people with chronic pain dates back to 2010.5,68 CBT-I results in improvements in various sleep parameters (eg, self-reported sleep onset latency, time spent awake after sleep onset, sleep efficiency, and sleep quality), sleep and pain interference with daily functioning in people with chronic pain.5,68,69 Improvements were maintained at the 3-month follow-up.68 The clinical relevance of the treatment effects was emphasized by the large difference between group responders (78% in the CBT-I-group vs 22% in the control group) and nonresponders (42% vs 11%).5 The effect sizes varied from moderate to large for sleep parameters and pain interference, but were small for pain intensity.5
Should CBT only target sleep, or should it target both pain and sleep? The results from 2 smaller pilot studies are in support of the latter: combining CBT for pain with CBT-I was feasible and produced significant improvements in sleep, disability from pain, pain interference, depression, and fatigue.6,70 Importantly, the combined intervention appeared to have a strong advantage over CBT for pain alone and modest advantage over CBT-I alone in reducing insomnia severity in people with chronic pain.6 The gains in insomnia severity and pain interference were maintained at 1- and 6-months follow-up.70
Taken together, recently accumulated knowledge in the field has progressed and contributed to increase our understanding about the interplay between sleep and pain. It has been shown that CBT-I is efficacious for the improvement of sleep duration, maintenance of sleep, perceived sleep quality,60 and pain interference with daily functioning5 in people with chronic pain. Additionally, there is relatively little available evidence about the optimal care-path for sleep related problems in the context of chronic pain.11 There is a need for an improved reporting of procedural information allowing clinicians to replicate study findings in daily routine.66 To these extents, the subsequent question is: what should be the exact content of such a CBT-I in people with chronic pain?
Introduction to CBT-I for People With Chronic Pain and Insomnia
CBT-I includes sleep and bedtime restrictions, stimulus control instructions, education for sleep and promoting good sleep habits (or sleep hygiene), teaching relaxation skills, and cognitive therapy.5,68,71 Each of these main tenets of CBT-I are introduced and described in Table 2 (to be used together with Tab. 1 to allow individually tailored CBT-I). For more details and a comprehensive guide for clinicians, readers are referred to an available manual.72 Clinicians who wish to provide CBT-I can benefit from additional training and are advised to attend an educational course.
Component . | Description/Content . |
---|---|
General sleep education83 | Explaining the importance of sleep and the behavioral neuroscience behind sleep, including the role of melatonin in initiating/sustaining deep sleep, the role of daylight, and the influence of regular sleeping hours. |
Sleep (or bedtime) restriction therapy84 | Manipulation of homeostatic sleep drive to consolidate sleep via sleep restriction60: initially limiting the amount of time spent in bed to an amount equal to the average sleep time for 1 wk.85 Once sleep becomes more efficient, total sleep time is incrementally increased on a week-to-week basis, and the sleep window is adjusted in time.85 |
In a broader sense, sleep restriction therapy also includes the alteration of circadian regularity and alignment,60 ie, imposing a regular wake-up time in an attempt to synchronize “strong” (fairly unresponsive to light) and “weak” (depending on exposure to bright light) endogenous clocks by modulating behavior. | |
Stimulus control instructions84 | Application of operant and classical conditioning principles via stimulus control instructions,60 including restricting bedroom behaviors to sleep and sex,85 limiting the amount of time spent awake in bed or in the bedroom,85 and promoting counterconditioning by ensuring that the bed and the bedroom environment are tightly coupled with sleepiness and sleep.85 |
Sleep hygiene instructions86 | Replacement of sleep-interfering behaviors with sleep-promoting behaviors through sleep hygiene education and behavior change counseling.60 |
(Sleep-specific) cognitive therapy84 | Modification of maladaptive sleep-related cognition.60 |
Relaxation training/stress management83 | Teaching patients to cope better with stress, including relaxation skills training (eg, deep breathing60 or guided imagery60). |
Patient's self-monitoring of daily sleeping patterns60 | Daily self-monitoring of time in bed, sleep onset latency, time spent awake after sleep onset, and total sleep time.60 |
Component . | Description/Content . |
---|---|
General sleep education83 | Explaining the importance of sleep and the behavioral neuroscience behind sleep, including the role of melatonin in initiating/sustaining deep sleep, the role of daylight, and the influence of regular sleeping hours. |
Sleep (or bedtime) restriction therapy84 | Manipulation of homeostatic sleep drive to consolidate sleep via sleep restriction60: initially limiting the amount of time spent in bed to an amount equal to the average sleep time for 1 wk.85 Once sleep becomes more efficient, total sleep time is incrementally increased on a week-to-week basis, and the sleep window is adjusted in time.85 |
In a broader sense, sleep restriction therapy also includes the alteration of circadian regularity and alignment,60 ie, imposing a regular wake-up time in an attempt to synchronize “strong” (fairly unresponsive to light) and “weak” (depending on exposure to bright light) endogenous clocks by modulating behavior. | |
Stimulus control instructions84 | Application of operant and classical conditioning principles via stimulus control instructions,60 including restricting bedroom behaviors to sleep and sex,85 limiting the amount of time spent awake in bed or in the bedroom,85 and promoting counterconditioning by ensuring that the bed and the bedroom environment are tightly coupled with sleepiness and sleep.85 |
Sleep hygiene instructions86 | Replacement of sleep-interfering behaviors with sleep-promoting behaviors through sleep hygiene education and behavior change counseling.60 |
(Sleep-specific) cognitive therapy84 | Modification of maladaptive sleep-related cognition.60 |
Relaxation training/stress management83 | Teaching patients to cope better with stress, including relaxation skills training (eg, deep breathing60 or guided imagery60). |
Patient's self-monitoring of daily sleeping patterns60 | Daily self-monitoring of time in bed, sleep onset latency, time spent awake after sleep onset, and total sleep time.60 |
Component . | Description/Content . |
---|---|
General sleep education83 | Explaining the importance of sleep and the behavioral neuroscience behind sleep, including the role of melatonin in initiating/sustaining deep sleep, the role of daylight, and the influence of regular sleeping hours. |
Sleep (or bedtime) restriction therapy84 | Manipulation of homeostatic sleep drive to consolidate sleep via sleep restriction60: initially limiting the amount of time spent in bed to an amount equal to the average sleep time for 1 wk.85 Once sleep becomes more efficient, total sleep time is incrementally increased on a week-to-week basis, and the sleep window is adjusted in time.85 |
In a broader sense, sleep restriction therapy also includes the alteration of circadian regularity and alignment,60 ie, imposing a regular wake-up time in an attempt to synchronize “strong” (fairly unresponsive to light) and “weak” (depending on exposure to bright light) endogenous clocks by modulating behavior. | |
Stimulus control instructions84 | Application of operant and classical conditioning principles via stimulus control instructions,60 including restricting bedroom behaviors to sleep and sex,85 limiting the amount of time spent awake in bed or in the bedroom,85 and promoting counterconditioning by ensuring that the bed and the bedroom environment are tightly coupled with sleepiness and sleep.85 |
Sleep hygiene instructions86 | Replacement of sleep-interfering behaviors with sleep-promoting behaviors through sleep hygiene education and behavior change counseling.60 |
(Sleep-specific) cognitive therapy84 | Modification of maladaptive sleep-related cognition.60 |
Relaxation training/stress management83 | Teaching patients to cope better with stress, including relaxation skills training (eg, deep breathing60 or guided imagery60). |
Patient's self-monitoring of daily sleeping patterns60 | Daily self-monitoring of time in bed, sleep onset latency, time spent awake after sleep onset, and total sleep time.60 |
Component . | Description/Content . |
---|---|
General sleep education83 | Explaining the importance of sleep and the behavioral neuroscience behind sleep, including the role of melatonin in initiating/sustaining deep sleep, the role of daylight, and the influence of regular sleeping hours. |
Sleep (or bedtime) restriction therapy84 | Manipulation of homeostatic sleep drive to consolidate sleep via sleep restriction60: initially limiting the amount of time spent in bed to an amount equal to the average sleep time for 1 wk.85 Once sleep becomes more efficient, total sleep time is incrementally increased on a week-to-week basis, and the sleep window is adjusted in time.85 |
In a broader sense, sleep restriction therapy also includes the alteration of circadian regularity and alignment,60 ie, imposing a regular wake-up time in an attempt to synchronize “strong” (fairly unresponsive to light) and “weak” (depending on exposure to bright light) endogenous clocks by modulating behavior. | |
Stimulus control instructions84 | Application of operant and classical conditioning principles via stimulus control instructions,60 including restricting bedroom behaviors to sleep and sex,85 limiting the amount of time spent awake in bed or in the bedroom,85 and promoting counterconditioning by ensuring that the bed and the bedroom environment are tightly coupled with sleepiness and sleep.85 |
Sleep hygiene instructions86 | Replacement of sleep-interfering behaviors with sleep-promoting behaviors through sleep hygiene education and behavior change counseling.60 |
(Sleep-specific) cognitive therapy84 | Modification of maladaptive sleep-related cognition.60 |
Relaxation training/stress management83 | Teaching patients to cope better with stress, including relaxation skills training (eg, deep breathing60 or guided imagery60). |
Patient's self-monitoring of daily sleeping patterns60 | Daily self-monitoring of time in bed, sleep onset latency, time spent awake after sleep onset, and total sleep time.60 |
Addressing poor sleep routine by scheduling a new sleep pattern11 and poor sleep efficiency (eg, 8 hours in bed and only 4 hours of sleep)11 can be done by providing classical bedtime restriction approaches.5,11 In case of impaired sleep efficiency and inappropriate sleep routines, this includes sticking to the same getting up time (or advancing the latter) as usual, but getting into bed at a later time when sufficiently sleepy, in order to reduce the amount of time spent in bed and increase homeostatic sleep pressure, or sleep drive, at sleep onset. If sleep efficiency increases to 85% or more, then the upward titration is initiated by adding 15 minutes to the prescribed time in bed.5 While people with insomnia knowingly often have lower levels of sleep pressure (ie, sleep onset) and increased levels of wake drives (ie, maintenance difficulties and hypervigilance),73 interventions involving sleep and bedtime restrictions are aimed at improving sleep homeostasis, which occurs with the expansion of sleep opportunity, not only in response to sleep loss but also as a means of managing pain.5
Sleep hygiene should be improved alongside with improved stimulus control in order to reestablish an enhanced and optimal associations between bedroom and sleep, allowing for sleep to solely occur in association with the bedroom and related controlled parameters (eg, complete darkness, stable and sufficiently low room temperature, and lowest levels of sensory stimuli).5 Cognitive therapy entails changing negative thoughts about sleep. It includes “decatastrophization” to address the perception of dire consequences of sleep loss.5 It is essential for clinicians to acknowledge that the barriers for achieving adequate sleep can present with substantial interindividual variabilities.11 Such interventions are not limited to a specific discipline but available for any caregiver willing to learn more about the role of sleep and how to improve it. Regarding administration modalities, conservative sleep treatment are effective when delivered face-to-face4,5 or through the Internet.74,75
Other interventions not directly targeting sleep may have a positive effect on sleep quality and quantity. For instance, stress management76 and exercise therapy76–79 improve sleep in patients with cancer and noncancer pain.
Role of the Funding Source
This work was funded by the Applied Biomedical Research Program, Research Foundation Flanders (Fonds voor Wetenschappelijk Onderzoek Vlaanderen), Belgium (FWO-TBM project no. T001117N entitled “Cognitive behavioural therapy for insomnia in people with chronic spinal pain: a multi-center randomized controlled trial”). The funder played no role in the conduct of this study.
Conclusion
Insomnia among individuals with chronic pain is highly prevalent and closely related to mechanisms of central sensitization. It is characterized by low-grade neuroinflammation, associated with stress/anxiety, and does not respond effectively to pharmacological treatment. CBT-I is effective for improvements of sleep initiation, efficiency and maintenance, perceived sleep quality and pain interference with daily activities in people with chronic pain. In addition, there is relatively little evidence about optimal administration procedures (timing, simultaneous priming, or hierarchy) for the treatment of sleep disorders in contexts of chronic pain. A recent systematic review concluded with high quality evidence that with additional training, physical therapist-led cognitive-behavioral interventions are effective for low back pain, allowing implementation within the field. CBT-I typically includes sleep (or bedtime) restriction recommendations, stimulus control instructions, psychoeducation regarding sleep and sleep hygiene, and cognitive therapy. CBT-I may not be a stand-alone treatment for people with chronic pain and comorbid insomnia, but may preferentially be combined with other effective treatment interventions, such as exercise therapy and CBT for pain.
Author Contributions
Concept/idea/research design: J. Nijs, O. Mairesse, D. Neu, L. Danneels, B. Cagnie, K. Ickmans, D. Goubert
Writing: J. Nijs, O. Mairesse, D. Neu, L. Danneels, B. Cagnie, M. Meeus, M. Moens, K. Ickmans
Project management: J. Nijs, L. Danneels
Providing institutional liaisons: D. Neu, M. Meeus
Consultation (including review of manuscript before submitting): O. Mairesse, D. Neu, L. Leysen, B. Cagnie, M. Meeus, M. Moens, K. Ickmans, D. Goubert
Funding
This work was funded by the Applied Biomedical Research Program, Research Foundation Flanders (Fonds voor Wetenschappelijk Onderzoek Vlaanderen), Belgium (FWO-TBM project no. T001117N, “Cognitive behavioural therapy for insomnia in people with chronic spinal pain: a multi-center randomized controlled trial”). K. Ickmans is a postdoctoral researcher funded by the Applied Biomedical Research Program, Institute for the Agency for Innovation by Science and Technology, Belgium (IWT-TBM project no. 150,180). D. Goubert is a postdoctoral researcher funded by the Applied Biomedical Research Program, Institute for the Agency for Innovation by Science and Technology, Belgium (IWT-TBM project no. IWT-TBM 130,246).
Disclosures
The authors completed the ICMJE Form for Disclosure of Potential Conflicts of Interest. M. Moens reported an independent research grant paid to his institution from Medtronic, Nevro, and money paid to him as a consulting fee or honorarium from Medtronic and Pfizer. D. Goubert reported a grant paid to her institution from the Applied Biomedical Research Program, Research Foundation Flanders (Fonds voor Wetenschappelijk Onderzoek Vlaanderen), Belgium (grant no. 130,246). There are no other conflict-of-interest disclosures from the authors.
J. Nijs is holder of the Chair “Exercise immunology and chronic fatigue in health and disease,” funded by the Berekuyl Academy/European College for Decongestive Lymphatic Therapy, the Netherlands. M. Moens received the Lyrica Independent Investigator Research Award (LIIRA).
References
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