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Review Article
Sleep and Pain: A Biopsychosocial Perspective
Matthew W Fiedler1, Amy Coryell2, Ryan Hulla2 and Robert J Gatchel2*
1College of Nursing and Health Innovation, University of Texas at Arlington, Texas, USA
2Department of Psychology, University of Texas at Arlington, Texas, USA
Citation: Fiedler M W., et al. “Sleep and Pain: A Biopsychosocial Perspective”. EC Anaesthesia 4.9 (2018): 362-371.
*Corresponding Author: Robert J Gatchel, Department of Psychology, University of Texas at Arlington, Texas, USA.
Received: August 06, 2018; Published: August 28, 2018
Abstract
a reduction in sleep quantity and quality (Q/Q). Sleep and pain have a bidirectional relationship, meaning individuals with more
severe pain experience worse sleep Q/Q. Disrupted sleep and pain have a cyclic relation with negative physical and mental states.
a decrease in tissue repair. Medications for pain and symptoms associated with pain, have been demonstrated to disrupt the restor-
ative functions of sleep, interrupt normal neurochemistry processes of the brain during sleep, and prevent rapid-eye movement
during sleep. Individuals suffering from sleep disturbances and pain experience a myriad of negative mental states due to pain and
reduced quality of sleep, which can include depression, anxiety, and substance abuse issues. A biopsychosocial approach is crucial
when treating individuals with pain issues, as many medications will hinder their ability to recover from disruption of sleep, whereas
improvement in physical and psychosocial health appear to improve sleep.
Keywords: Sleep; Pain; Hyperalgesia
Introduction
A substantial amount of individuals that experience poor sleep also commonly report undergoing chronic pain [1]. Findings also
suggest that individuals that live with chronic pain and disrupted sleep are more likely to display poor mental health, decreased social
functioning, fatigue, and less involvement with cherished activities [2]. More recent studies concerning the relationship between pain and
sleep hygiene have begun focusing on attention and mood as other facilitating features [1]. The dynamic between pain and sleep were
previously thought to share a bidirectional relationship, commonly seen as pain disrupting sleep, and poor sleep exaggerating the inten-
sity of pain [1]. Pain is often seen as being a predictor of sleep quality, while quality of sleep mediates the association between pain and
fatigue [2]. Individuals experiencing pain concurrently with sleep disturbances might possess greater pain severity and allocate more of
[1]. Disrupted sleep may jeopardize the reparative functions sleep provides, therefore prolonging the healing process and increasing an
individual’s sensitivity to pain [1].
Pain presents a myriad of issues for the patient and provider which can include agitation, decreased life span, and increased risk of sub-
stance abuse [3,4]. A rapidly growing body of research is exploring the bidirectional nature of pain and sleep. In this model, pain, through
a variety of mechanisms, decreases the quality and duration of sleep. Decreased sleep quality and duration then, in turn, increases sen-
363
Sleep and Pain: A Biopsychosocial Perspective
Citation: Fiedler M W., et al. “Sleep and Pain: A Biopsychosocial Perspective”. EC Anaesthesia 4.9 (2018): 362-371.
pain levels based on sleep complaints the night prior [6-10]. Increased understanding of the relationship of pain and sleep presents many
possible advances in the realms of sleep and pain management.
Sleep, Pain, Stress and Inflammation
Sleep has a multitude of restorative functions for the body, accelerating the repair and/or development of virtually every tissue and
hu
markers [11-15]. TNF-alpha promotes osteoclast differentiation (degrading of the bone matrix) and survival, potentially compounding
with other pain sources or enhancing existing musculoskeletal pain via further degradation of skeletal tissue [16,17]. IL-6 is a potent in-
T cell activation. The role of CRP is to reduce lysis of downstream cell membranes [12-15,22,23]. Elevated IL-6 and CRP has been detected
in individuals that suffer from obstructive sleep apnea [24]. Disrupted sleep due to pain, apnea, or other illnesses may indeed be partially
These
a sc
This results in pain virtually every area with a PNS nociceptors. This enhancement, or hyperactivity, of nociceptors increases the release
of neurologically active pain chemicals including Substance P and Glutamate, Brain-Derived Neurotrophic Factor [BDNF], amongst oth-
ers [30-33]. Hyperalgesia (over sensitization) can result, lowering the threshold for painful stimuli, even in completely “normal” tissues
[5,6,8,31-33].
Stress is a global response to a stressor enveloping essentially all systems and organs. An early evolutionary tool, modern humans
experience stress from non-life-threatening events such as job loss or relationships. Pain initiates and maintains a global stress response
which is, for the most part, a negative feedback response. Prolonged pain can begin to disrupt the negative feedback response, leaving the
body in a prolonged, global state of stress [34-36]. Worry or anxiety over the pain itself is a common phenomenon in prolonged pain pa-
tients, and can create additional stress independent of stress from the “real” pain [1,6,37]. A slew of hormones are responsible for global
stress response, but one hormone in particular is cortisol [35,38]. This stressed state results in an increase in serum energy abilities (glu-
cose, glucagon, fatty acids, free ATP), increased blood pressure, increased blood/brain oxygen, and overall increased alertness [39,40].
creating pain through tissue damage. This results in global pain, hyperalgesia, and potential worry/anxiety. Neuroendocrine responses
to pain create a stress response, resulting in an increased state of alertness. This mental state makes falling and staying in sleep more dif-
Sleep involves a decrease in serum energy abilities, decreased blood pressure, normal blood/brain oxygen, and a lack of conscious alert-
ness. Patients suffering from insomnia tend to have heightened measurements of the above criteria [40,41]. Studies have demonstrated
clinically-diagnosed insomniacs chronically experience reduced sleep Q/Q, abnormal and/or irregular sleep wake cycles, amongst many
other comorbidities such as pain [42,43]. A study by Savard and Morin [44] found 30-50% of patients experiencing chronic pain condi-
has also been associated with reduced sleep time and suicidal ideation, similar to symptoms of major depressive disorder [45].
Citation: Fiedler M W., et al. “Sleep and Pain: A Biopsychosocial Perspective”. EC Anaesthesia 4.9 (2018): 362-371.
Sleep and Pain: A Biopsychosocial Perspective
364
Since pain negatively impacts sleep Q/Q, an obvious improvement should be the removal (or, more realistically, reduction) of day and
nig
reduction in pain [46,47].
Non-Steroidal Anti-Inflammatory Drugs (NSAIDs)
NSAIDs relieve pain by inhibiting cyclooxygenase [COX-1 (common) or COX-2 (rare)], reducing prostaglandin [48-50]. PGs, particularly
PG-D2 and PG-E2 are involved in the sleep and wake response, respectively. Short-term NSAID usage in healthy, young individuals resulted
NSAIDs on body temperature and salivary melatonin. When taken at night before sleep, NSAIDs hindered the body’s ability to decrease
body temperature and produce melatonin [54]. Importantly to sleep’s restorative properties and the sleep-pain cycle, melatonin is an
Steroidal Anti-Inflammatory Drugs (SAIDs)
-
tio
typical sleep Q/Q by disrupting homeostasis of brain mineralocorticoid and glucocorticoid, resulting in a stimulatory effect [59,60]. The
effect appears to be dose dependent, with more sleep Q/Q reduction as dosing increases [61]. Fortunately, most SAIDs have relatively
short half-lives, and a single morning dose can reduce sleep Q/Q in most adults [62,63]. More severely, SAIDs can induce a rare disorder
known as steroid psychosis (SP), an extreme and potentially chronic disruption of normal behaviors and cognitive functions. SP can be
present during treatment or during weaning/withdrawal phase of coming off SAIDs. Symptoms include insomnia, anxiety and even clini-
cal psychosis in rare occasions [57,64-66].
Paracetamol (APAP)
There is currently little research on the effect of paracetamol (also known as acetaminophen or APAP) on sleep. A study of 210 os-
teoarthritis patients found that patients report better sleep with extended release APAP over standard APAP at a 2:1 ratio [67]. Another
from sleep diaries [68].
Opioids and Substance Abuse
Disrupted sleep is also common among patients of substance use including alcohol, nicotine, marijuana, and heroin [69]. Sleep distur-
bances often acts as a salient trigger for relapse, and a reliable predictor of treatment outcome. Unfortunately, sleep related issues found
among substance use patients have been seen to persist for weeks, months, or even years, upon termination of substance use. More im-
portantly, individuals will often use alcohol to self-medicate symptoms of insomnia resulting in considerably higher rates of relapse [69].
When treating chronic pain, both pharmacological and psychological interventions should be utilized to enhance physical and cogni-
tive restoration [1]. Regrettably, certain pain relieving compounds have been found to cause sleep fragmentation, and often times pro-
mote symptoms of insomnia [1]. The use of prescription opioids (PO) are commonly found among individuals experiencing chronic
pain; although it is not uncommon for individuals to report using PO for alternative reasons, for example to improve sleep [68]. Opioids
notably have a wide range of side effects on sleep, pain, immunology, and essentially every other system. Many of these side effects are
antagonistic. For example, opioids relieve pain and have sedative effects, but can also cause hyperalgesia and decrease sleep Q/Q [6,8,70].
Opioids have been demonstrated to interfere with many aspects of sleep including sleep respiration (potentially fatal), duration, sleep
pattern transition, and waking fatigue [6,71-74]. Hartwell and colleagues [68] concluded roughly 80% of PO dependent individuals also
delayed onset of sleep, and total time awake.
Citation: Fiedler M W., et al. “Sleep and Pain: A Biopsychosocial Perspective”. EC Anaesthesia 4.9 (2018): 362-371.
Sleep and Pain: A Biopsychosocial Perspective
365
Depression, Anxiety and Antidepressants
-
stance abuse and suicide ideation/intention [75,76]. Research indicates that symptoms of insomnia often precede depressive symptoms,
therefore identifying insomnia as not only a symptom of depression, but also a potential predictor of depressive symptoms [76,77]. De-
-
crease the prospect of depressive symptoms [2]. A decline in daytime activities might lead individuals to alienate themselves from others,
this isolation might induce dysfunctional ruminative cognitions concerning their pain and uncontrollability of sleep, resulting in feelings
of helplessness and hopelessness [1,78].
It is believed that insomnia is maintained through negative cognitive activity, including rumination and dysfunctional beliefs in terms
of sleep [79]. On the other hand, anxiety is comprised of two components: worrying (cognitive component) and somatic anxious arousal
-
tioning and wellbeing [79]. Symptoms of anxiety often work in parallel with depressive symptoms, with negative cognitive activity being
abundant within both mood disorders. The relation between sleep disturbances, mood disorders, and negative cognitive activity often
perpetuate symptoms of insomnia [79,80]. Similarly, social anxiety has been found to be associated with an increase of insomnia symp-
toms as well as noticeability of a sleep problem to others and distress regarding sleep disturbances [81]. Social anxiety negatively impacts
numerous areas of daily life: education, employment, and interpersonal relationships. Compared to healthy sleepers, individuals suffering
insomnia are more likely to ruminate over social situations and possible negative outcomes while preparing to fall asleep [82]. Avoiding
social engagements due to disrupted sleep and rumination might result in a reduction of involvement in daily activities. This lack of activ-
assist better-quality sleep outcomes, resulting in a general reduction in social anxiety [81].
Different types of antidepressants such as tricyclic antidepressants (TCAs), selective serotonin reuptake inhibitors (SSRIs), and mono-
amine oxidase inhibitors (MAOIs) have been used in the treatment of depression, anxiety, and chronic pain. Exactly how these drugs
reduce pain is unknown, though two popular theories suggest serotonin and norepinephrine reuptake inhibition and/or sodium channel
inhibition as a possible responsible mechanism [83,84]. These drugs severely limit, or even eliminate (in the case of MAOIs), rapid-eye
movement (REM) sleep. While this used to be believed as their mechanism of action as an antidepressant, it is now understood that this is
a major side effect of antidepressant drugs along with sleep architecture modulation [85-87]. Evidence suggests that severely limiting or
eliminating REM sleep, and taking TCAs (except amitriptyline), SSRIs, and MAOIs appear to have little to no cognitive or memory effects
does not affect cognitive or memory function [86,88,90]. Individual’s measures of sleep quality also do not seem change between placebo
or single-dose SSRI [90]. There is also evidence to the contrary, where antidepressants negatively affected objective and subjective sleep
quality (which includes nocturnal awakenings), but still no impact on cognitive or memory function [88,91]. The area of antidepressant
Emotional dysfunction
Growing evidence suggests that sleep deprivation also drastically impacts empathy and emotional functioning of an individual. Sleep
loss increases physiological reactivity when confronted with emotional stressors, reduces the ability to cope with stress, and is associated
with poor frustration tolerance, as well as a skewed perception of the intentions of others. Furthermore, sleep disturbances are related
to a substantial decline in understanding another individual’s emotional response, resulting in inadequate interpersonal skills, empathy,
stress management capabilities, and increased impulsivity [92]. Sleep deprivation has also been correlated with diminished responsive-
ness to faces displaying fear and sadness [93]. With this said, being able to properly process emotional stimuli is crucial to empathizing
with another individual’s emotions, feelings, and thoughts, all of which are obligatory skills in sustaining strong social connections [93].
Sleep quality in general has been cited as a predictor of empathic abilities, regardless of the intensity of the stimuli being presented [93].
Citation: Fiedler M W., et al. “Sleep and Pain: A Biopsychosocial Perspective”. EC Anaesthesia 4.9 (2018): 362-371.
Sleep and Pain: A Biopsychosocial Perspective
366
Conclusion
Therefore, when considering the treatment of chronic pain including intervention options that encompass the co-occurring factors
and
sleep Q/Q [1]. Cognitive behavioral therapy (CBT) has been effective in relieving sleep disturbances, thus alleviating pain-associated dis-
ability, and enhancing mood [1]. For example, improving the quality of sleep could indirectly improve the severity of pain among patients
imagery interventions actively improve fatigue and sleep disturbances among individuals with chronic pain [94]. Bruck and colleagues
[95] found unrealistic beliefs regarding sleep as commonplace, with healthy sleep being mistakenly seen as unbroken throughout the
night. Simply educating individuals about healthy sleep might show preventative health implications and reduce sleep anxieties. Lastly,
research suggests that staying active, engaging in physical exercise, and living a satisfying social life functions as protective factors against
insomnia symptoms and other sleep related disturbances, and should be recommended in patients undergoing treatment for sleep dis-
turbances [81,96,97].
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