Chapter 7
Knowledge transfer to patients experiencing pain and poor sleep and sleep disorder

Gilles J. Lavigne^1,2, Alberto Herrero Babiloni^1,3, Beatrice P. De Koninck¹, Marc O. Martel^3,6, Jacqueline Tu Anh Thu Lam^1,4, Cibele Dal Fabbro1, Louis de Beaumont^1,4, & Caroline Arbour^1,5

¹ Center for Advanced Research in Sleep Medicine & Trauma Unit, Research Center, Centre Integre Sante et Services Sociaux du Nord Ile de Montreal (CIUSSS du NIM), Montréal, Québec, Canada

² Faculty of Dental Medicine, Université de Montréal, Québec, Canada

³ Division of Experimental Medicine, McGill University, Montréal, Québec, Canada

⁴ Faculty of Medicine, Université de Montréal, Québec, Canada

⁵ Faculty of Nursing, Université de Montréal, Québec, Canada

⁶ Faculty of Dentistry & Department of Anesthesia, McGill University, Montréal, Québec, Canada

Sleep is a state with partial isolation from vigilance, the dominant state during wake. Despite being apparently obvious, it must be remembered that sleep is not coma nor anesthesia. During sleep, sound, temperature changes, touch and pain can be perceived, thus maintaining the capacity to react to external stimuli (such as a baby’s cry) or to maintain comfort [1].

Approximately 10% of the general population and 50% of individuals with chronic pain complain of poor sleep quality, reporting their sleep to be non‐restorative or unrefreshing. These numbers go as high as 70% in individuals with widespread pain syndrome/fibromyalgia. Many sleep disorders, described in more detail below, may contribute to exacerbate pain and complicate its relief. It has been reported that nearly 44% of people living with chronic pain present sleep disorders with insomnia (72%), sleep apnea and periodic limb movement (32% each) being the most frequent [2]

This narrative practical review will describe the interactions between pain and sleep and how pain is processed during sleep. Furthermore, it will overview the most frequent sleep disorders in chronic pain and it will provide advice for clinicians to guide patients in the management of sleep in the absence or in the presence of sleep disorders. For patients suffering from poor sleep and pain the one size fits all treatment approach has never been a choice as multimodal avenues are the most likely route to be successful as described in this chapter. Thus, it is important for clinicians to gain the expertise and knowledge in providing advice and guide patients toward optimal treatment and, when needed, refer to other health professionals.

Assessment of pain and sleep interactions

Sleep quality can be easily estimated in pain and sleep clinics through patients’ self‐reports, via semi‐structures interviews, which include use of visual analogue scales and screening questionnaires when sleep disorders are suspected. Several sleep disorder screening tools are widely used, but not specifically validated for the sleep and pain interaction. These include the Epworth Sleepiness Scale (ESS), the Pittsburgh Sleep Quality Index (PSQI), the Insomnia Severity Index (ISI) and the STOP‐Bang for sleep apnea, which all are currently available online. The classical self‐reports related to poor sleep, which are not exclusive to people living with chronic pain, are depicted in Figure 7.1.

Polysomnography (PSG) at home or in a sleep laboratory supervised by a physician are both important tools to assess sleep quality and the presence of sleep disorders. Objective testing such as PSG improves diagnosis accuracy from possible (self‐reports on sleep and interview) to probable (screening tools and examination) and definitive, as confirmed for the majority of sleep disorders [3]. Sleep recording is recommended in chronic pain cases: 1) when excessive sleepiness and/or fatigue (a dominant complaint in women) are noted; 2) when sleep comorbidities are suspected; 3) or when there is no clear response to usual treatments. Sleep disorders can be concomitant to chronic pain and have synergic influence on sleep quality and on pain intensity and ability to coping with its burdens. From PSG recordings specifically, several pieces of information can be extracted from people living with chronic pain can be extracted, including: lack of sleep continuity (i.e. frequent sleep stage shifts, periodic limb movement and breathing disruption such as apneas), trouble to initiate or maintaining sleep or long sleep latency, which are frequent characteristics of insomnia. These features can also be monitored at home by using a sleep agenda and/or actigraphy watch (a movement sensor as a proxy to assess quiet period and delay of sleep onset) or home limited number of channel devices recording system. Smart phone applications may increase patient collaboration and motivation according to emerging research.

Schematic illustration of classical self-reports related to poor sleep. — **Figure 7.1** Classical self‐reports related to poor sleep.

In chronic pain (i.e. pain lasting more than 3 months) [4], it is frequent for patients to complain of poor home‐ or work‐related performance due to fatigue. Cognitive impairments such as attention, memory or executive function alterations are either noticed or reported. Furthermore, clinicians have to take into consideration the fact that both pain and sleep have interlaced socio‐psychological impacts [1].

Even in acute pain situations (e.g. after a surgery or a trauma, or in an emergency room), sleep can be disrupted for a few nights [5,6]. In these cases, all of the above socio‐psychological impacts are usually transients. In order to prevent risk of chronicity, it may be wise for clinicians to provide patient guidance as explained in the last section of this chapter.

The circular pain and sleep interactions

In the pain and sleep literature, a simple circular model has been commonly used to investigate and depict the reciprocal impact of sleep and pain disturbances [1]. In the later model, it was proposed that a bad day with pain (regardless of intensity) could be followed by a night with poor sleep, whereas a bad night of sleep could be followed by pain exacerbations on the next day. Nowadays, experiential evidence has made it clearer that a bad day with pain is not the dominant trigger of poor sleep quality; individual vulnerability or comorbidities have to be taken into consideration [1]. However, the impact of a poor sleep night has been shown to exacerbate pain during the first half of the following day [7]. Additionally, women with chronic pain and menopause seem to get longer sleep duration when higher pain is reported, potentially as a means to numb the pain [8]. This recent finding challenges the strength and uniqueness of a circular effect of a day with pain driving a poor sleep quality night or shorter sleep. Furthermore, little evidence is available on the exact contribution of deleterious influences of fatigue and exhaustion, life pressure or task overload. Similarly, although it is clinically reported as a way to cope with fatigue and pain, the benefit of rest and nap on pain symptomatology needs further investigation. Circadian rhythms also shape the pain and sleep interaction, a topic of specific interest for investigators in the field [9]. Therefore, the impact of many independent or synergic risk or protective or palliative factors (e.g., older age, gender/female, life style, sleep hygiene, napping, exercise, substance, or medication misuse or abuse and mood and sleep disorders) need to be identified individually.

Sleep disruption in people living with chronic pain may have different effects between individuals depending on risk factors that have not yet been clearly identified. The search of socio‐psycho‐biological vulnerability (e.g. gender, age, healthy life behavior, inflammatory response) or specific phenotype (circadian rhythm and/or breathing physiology) are paths for future research [9, 10].

Pain processing during sleep and its consequences

The sleeping brain remains reactive to any type of inputs, including potentially painful ones. Experimental pain and sleep studies, using cutaneous heat pain or sub‐cutaneous infusion of hypertonic saline or laser stimulation, have challenged brain reactivity and persistence of placebo analgesia in sleep as described below [11–13].

During sleep, the pre‐alerting reaction (i.e. brief arousal lasting 3–15 seconds without return of consciousness) and the ready to react awakening (i.e. not fully conscious but towards awake state) remain dominant in light sleep (stages 1 and 2: 40–50% response), whereas it is less dominant in deep sleep (stage 3; less than 30%). In REM or paradoxical sleep (i.e. a stage with low responsiveness, muscle paralysis and intense metabolic activity), this reaction is more variable [12, 13].

A piece of the puzzle came from studies on placebo analgesia paradigm applied to sleep studies. The brain can still process pain related information during sleep following induction of conditioned analgesia. In placebo studies, there are non‐responders and responders. Indeed, placebo responders are individuals who typically had a prior positive experience with a therapeutic modality [14]. The latter is among variables that seem to moderate hypoalgesia or pain relief expectation. In experimental protocols, 50–60% of healthy individuals can be identified as placebo responders. For several reasons, some individuals can be responders in a specific context, in a given time, but not in others. In relation to sleep, experimental investigations from Dr. Lavigne’s laboratory have shown that the placebo effect remains active during sleep as individuals who had a higher pain relief expectation while awake before sleep experienced more placebo analgesia following a night of sleep. Indeed, individuals with high analgesia expectation prior to sleep had shorter REM sleep, experienced less pain, reported better sleep and were less anxious [11]. The role of REM sleep in potentiating the placebo analgesia via expectation was further documented with use of clonidine, a medication that suppresses REM sleep [11].

Retention of placebo analgesia during sleep may also be associated to learning processes; considerable evidence supports the conclusion that learning is consolidated during sleep [11]. The ‘sleep on it’ idiom illustrates that sleep is an active process also involved in memory consolidation and learning [15]. The neuropsychological process associated with these functions may contribute to explain some of the discrepancies between experimental studies performed on healthy subjects vs. chronic pain subjects [16, 17]. Indeed, in individuals with chronic pain, working memory and episodic memory performance are altered, which seems to be independent of age but related to the more specific ‘pain attention deficit state’ [17]. Moreover, sleep and sensory/pain processing are sleep stage dependent and inter‐related [12, 13]. Noxious and sensory inputs activate mid and prefrontal cortex, the insula and the opercular cortex up to sensory motor cortex in order to prepare for movements; this is a normal gradation in preparing a response to a threatening event such as pain [18].

Ideally, sleep duration should be between 7 to 9 hours per day for most individuals. Duration of sleep of less than 6 or more than 9 hours influences pain perception and report the next day [19]. In fact, mood, social reactivity and pain are exacerbated by short sleep duration (4 instead of 7‐8 hours) as tested experimentally by inducing a few days up to 3 weeks of sleep deprivation [20]. Experimental short‐term sleep deprivation alters endogenous ‘relief’ mechanisms and exacerbates pain in heathy individuals [21]. Recent brain imaging studies have shown that cortical pain sensory motor processing, including periaqueductal gray matter and accumbens adenosinergic activities, are enhanced, whereas thalamic, insula and striatum plus accumbens dopaminergic activities are blunted following acute sleep deprivation [22, 23]. Likewise, activities in structures associated to pain modulation and to deficient pain‐reward reactivity are exacerbated by lack of sleep [1].

Sleep Disorders in Patients With Pain

Insomnia and its management related to pain

Insomnia can be acute, transient or chronic and can be comorbid [24]. It is characterized by complaint or dissatisfaction about sleep quantity or quality, related to a series of criteria. As examples:

Difficulty to initiate sleep, usually taking more than 20 minutes in a child and or young adult and up to 30 minutes in adult (but it can be longer if the individual nap during late afternoon);
Difficulty to resume sleep if the individual awakes at night to go to the bathroom or other reasons, or;
The ‘petit matin’ or early morning insomnia that is described by complains of awaking too early with expectations to get longer sleep to prevent fatigue and improve performance.

Insomnia is classified as Chronic Insomnia Disorder if complaints occur at least 3 times per week for at least 3 months and as Short‐term Insomnia Disorder if insomnia symptoms are present for less than 3 months in an irregular pattern. Both need to be reported as a problem by the individual[24]. Some individuals have atypical sleep patterns and cope well with it. Insomnia is frequently associated with mood alterations, hypervigilance, fatigue, chronic pain, brain trauma and sometimes addiction²⁵.

According to the DSM‐IV and ICSD‐3 criteria, the prevalence of insomnia in the general population is 6‐10% and is age related [26]. However, in a Canadian survey, 29.9% of the general population self‐reported insomnia symptoms, with 9.5% of complaints consistent with insomnia syndrome [27]. In the EPISONO general population sample (Brazil), the estimated self‐reported insomnia prevalence was 32%, for symptoms and only about 15% meet the DSM‐IV criteria for insomnia syndrome [28]. Interestingly, the prevalence of insomnia seems to have increased over recent decades. A Finish survey reported a 4.5% rise from 2008 to 2013 in occasional insomnia symptoms, with no change for chronic insomnia [29]/ Similarly, a comparative 10‐year study (1999/2000–2009/2010) in Norway found that insomnia cases increased from 11.9% to 15.5% using the DSM‐IV criteria [30].

Changes in sleep quality and risk of emerging insomnia, may concur to predict chronic pain, and chronic insomnia is a dominant comorbidity in people living with chronic pain of various origins [2, 31]. Many studies suggest that insomnia, lack of sleep quantity or quality and mood disorders are important risk factors or mediators for chronic pain [25, 32]. This is illustrated by one study, carried out over 6 years in a large sample of the Netherlands population, that revealed that both insomnia and short sleep had hazard ratios of 1.6 and 1.5, respectively, for onset of new chronic multisite musculoskeletal pain [32]. Importantly, suicidal risk needs to be considered when chronic pain and insomnia overlap [33].

Sleep disorders breathing

Sleep disorders breathing (SDB) includes snoring to respiratory effort related arousal (RERA), obstructive sleep apnea (OSA) and central sleep apnea (CSA) [24].

Snoring is a frequent precursor sign of a sleep breathing problem, whereas OSA is the dominant sleep breathing disorder in the population. RERA is a respiratory event in which there is a sequence of breath lasting > 10 seconds, characterized by increasing respiratory effort or by fattening of the inspiration waveform leading to arousal [24 34]. OSA is observed on sleep recoding by a combination of partial reductions (hypopneas) and complete pauses (apneas) in breathing that last at least 10 seconds or more with oxygen desaturation (3% or 4%). CSA occurs due to a lack of input form the brain respiratory network to motor centers of breathing.

Opioids, benzodiazepines and gabapentin (an anticonvulsant frequently used to manage chronic pain) may contribute to CSA in a subgroup of vulnerable individuals not yet well characterized [35, 36]. Thereby, phenotyping or disease characterization based on individual traits is an active domain of research in sleep breathing disorders [37[.

In this context, many anatomical risk factors are associated to OSA, including narrow upper airway due to small oral development (retrognathia) or large tissue (macroglossia, large tonsil and pharyngeal pillar, which is fat accumulation at the base of the tongue). Obesity also concurs to exacerbate that risk and being a male or a post‐menopausal woman is also part of the equation. Identified non‐anatomical risk factors are: 1) low muscle tone or responsiveness that prevent airway patency to be optimal; 2) low arousal threshold that contribute to interrupt sleep continuity; and 3) high loop‐gain, that is an excessive breathing activity or “overshoot”, when the oxygen level is too low causing irregular breathing and poor sleep maintenance [37].

OSA prevalence with a mild apnea‐hypopnea index (AHI ≥ 5 and <15) ranges from 9% to 38% and moderate (IAH ≥15 and <30) to severe (IAH ≥ 30) range from 6% to 17%; OSA prevalence is higher in male and increase with age [38]. OSA is associated with headache (a marker of therapy success is when it disappears), cognitive alterations (memory, executive function), sexual dysfunction and sleepiness in men, fatigue (dominant in woman), increased risk of transportation or work accidents and increased risk of cardiovascular disease, diabetes and depression in both sexes [39]. Overall mortality and cancer is higher in OSA [40].

SDB, mainly OSA, is present in 30 to 90% of people living with chronic pain with a higher incidence in opioid users seen in sleep clinics [2, 41, 42

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