Sleep and Orofacial Pain










11
A
pproximately one-third of patients with temporomandibular
disorders (TMDs) or other conditions that manifest orofacial
pain report poor sleep quality or unrefreshed feelings on
awakening. The impact of chronic pain on sleep can be described as
a vicious cycle with mutual deleterious inuences between pain and
disrupted sleep. Several quantitative sleep variables (eg, total sleep
time, slow-wave sleep, sleep stage duration, sleep arousal, pres-
ence of disordered breathing events, and periodic limb movements
during sleep) characterize the pain-related disruption of sleep. The
role of the clinician is to identify patients complaining of poor sleep.
First, it is necessary to exclude the role of concomitant musculo-
skeletal pain, neuropathic pain, or comorbid conditions (eg, com-
plaints related to fatigue, depression, and anxiety). Clinicians should
then refer the patients to a sleep laboratory for further evaluation of
a suspected sleep disorder, such as insomnia (ICD-10 G47.0), sleep
Key Points
The impact of chronic pain on sleep can be described as a
vicious cycle with mutual deleterious inuences causing
an increase in pain and disrupted sleep.
The role of the clinician is to identify orofacial pain patients
complaining of poor sleep and refer them to a sleep labo-
ratory for further evaluation of a suspected concomitant
sleep disorder.
Sleep hygiene advice and cognitive behavioral treatments
or short-term use of medication may help restore sleep
quality.
Management of pain and sleep needs to be customized to
each patient based on his or her psychosocial and medical
history.
Sleep and
Orofacial Pain

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11Approximately one-third of patients with temporomandibular disorders (TMDs) or other conditions that manifest orofacial pain report poor sleep quality or unrefreshed feelings on awakening. The impact of chronic pain on sleep can be described as a vicious cycle with mutual deleterious inuences between pain and disrupted sleep. Several quantitative sleep variables (eg, total sleep time, slow-wave sleep, sleep stage duration, sleep arousal, pres-ence of disordered breathing events, and periodic limb movements during sleep) characterize the pain-related disruption of sleep. The role of the clinician is to identify patients complaining of poor sleep. First, it is necessary to exclude the role of concomitant musculo-skeletal pain, neuropathic pain, or comorbid conditions (eg, com-plaints related to fatigue, depression, and anxiety). Clinicians should then refer the patients to a sleep laboratory for further evaluation of a suspected sleep disorder, such as insomnia (ICD-10 G47.0), sleep Key Points◊ The impact of chronic pain on sleep can be described as a vicious cycle with mutual deleterious inuences causing an increase in pain and disrupted sleep.◊ The role of the clinician is to identify orofacial pain patients complaining of poor sleep and refer them to a sleep labo-ratory for further evaluation of a suspected concomitant sleep disorder.◊ Sleep hygiene advice and cognitive behavioral treatments or short-term use of medication may help restore sleep quality.◊ Management of pain and sleep needs to be customized to each patient based on his or her psychosocial and medical history. Sleep and Orofacial Pain 241Sleep Overviewapnea (ICD-10 G47.3), or periodic limb move-ments (ICD-10 G47.61). The aim of this chap-ter is to provide an overview of the current understanding of pain and sleep interactions and to discuss evidence-based and empirical knowledge to help clinicians recognize, diag-nose, and manage poor sleep in patients with chronic orofacial pain conditions.Sleep OverviewSleep is a natural physiologic activity that is essential for good quality of life and species survival. Most animals totally deprived from sleep become sick from infection or organic dysfunctions within a few weeks. Sleep is vital for recovery from fatigue, memory consolida-tion, heart and muscle tissue repair, and brain function at cellular and network levels. Its du-ration is variable from individual to individual. Most human adults sleep between 6 and 9 hours per night; below or above this range, individuals tend to report more pain.1,2 Adoles-cents tend to have an irregular circadian sleep schedule (ICD-10 G47.23) that may predispose them to some pains. Without enough sleep, humans tend to be less functional and to re-port cognitive problems, mood alterations, im-mune dysfunction, and somatic pain-related complaints within 3 to 4 days.3,4Sleep and wakefulness are under the regu-lation of a circadian process that lasts approxi-mately 24 hours. Typically, sleep and wake cycles are regulated by an oscillatory behavior at the level of the hypothalamus suprachias-matic nucleus in the higher regions of the cen-tral nervous system (CNS). Human sleep and wake rhythms are tuned by the sun and moon (ie, 24-hour light and dark cycle) as well as by external cues like sounds.5,6 It is important to understand circadian rhythms because pain patients may have a cir-cadian phase mismatch that could explain their symptoms. A person who goes to sleep later every night may have a hard time waking up early. This sleep cycle is called circadian phase delayed (ICD-10 G47.21). Conversely, a person who goes to sleep earlier every day may wake up earlier (circadian phase advanced [ICD-10 G47.22]).2,7 Some gene expressions (eg, a tandem-repeat polymorphism in the coding region of the 5-repeat allele of the clock gene PER3 5/5 [period circadian protein homolog 3]) may explain vulnerability to sleep loss as cognitive frontal cortex dysfunction.8,9 The role of circadian rhythm–related genes on cogni-tive function and fatigue is an area of ongoing investigation. The outcomes of this research may also provide better understanding of the interaction between chronic pain and sleep.Sleep is divided into rapid eye movement (REM) and non-REM (NREM) sleep. During a typical night, there are three to ve NREM to REM cycles, termed the ultradian rhythm cycle, in contrast to the 24-hour circadian cycle that is under the sun and moon time sched-ule. NREM sleep is further divided into light sleep (stages N1 and N2) and deep sleep (N3, formerly called stages 3 and 4), which is domi-nated by slow-wave brain activity (Fig 11-1). REM sleep is often called paradoxical sleep because the CNS and the autonomic nervous system are highly active while all skeletal mus-cles are in a hypotonic state, as if the body were paralyzed.5In healthy adults, the majority of body movements (eg, of limbs and jaws) tend to occur in light sleep, more specically in rela-tion to sleep stage shifts, such as from deeper to lighter sleep or from any stage toward REM sleep. The occurrence of movements is peri-odic during sleep and follows a cyclic pattern. Every 20 to 40 seconds, sleep oscillates from quiet periods to more active ones. The active physiologic periods, lasting 3 to 15 seconds, are called arousals; in healthy individuals, these tend to reappear 7 to 15 times per hour of sleep. Such active periods are windows where the sleeping individual can readjust his or her body position, reset body temperature, and, if any harmful event is perceived, become 242Sleep and Orofacial Pain11fully awake (ie, a ght-or-ight reaction could be triggered). About 50% to 80% of sleep bruxism (ICD-10 G47.63) events (ie, repetitive jaw-muscle contractions with or without tooth grinding) are observed during recurrent arousal peri-ods. A method has been developed to monitor such a cyclic alternating pattern (CAP) during sleep. CAP comprises an active phase A that is subdivided into three periods: A1 (dominated by slow-wave brain activity, which preserves sleep), A2 (the transition period between A1 and A3), and A3 (the period dominated by arousal).10 Phase B of a CAP is the quiet pe-riod of sleep. Sleep bruxism seems to occur preferentially in CAP A2 and especially in A3, thereby providing a physiologic window to fa-cilitate the onset of rhythmic movements dur-ing sleep.11 It is important to understand that sleep bruxism tends to occur in association with sleep-stage transitions and when arousal pressure is greater. Patients with chronic pain and more spe-cically bromyalgia (ie, chronic widespread pain) tend to present with 50% more phase A2 and A3 periods than healthy individuals.10 In contrast, during normal healthy adult sleep, nociception is partially attenuated to preserve sleep continuity. Stages N1 and N2 have higher threshold and lower response rates to nox-ious stimuli than wakefulness, and stage N3 has even higher thresholds, while thresholds vary during REM sleep.1,10,12 Sleep is associ-ated with a partial physiologic deafferentation of sensory (ie, afferent) inputs into the CNS, and there is reduced neuronal activity at the thalamocortical network level with brief and transient reactivation of neural pathways from the brainstem to the cortex during arousal.6,10,12Normal adults usually fall asleep within 20 to 30 minutes of their going to bed. Insomnia may be suspected when sleep onset is longer than 20 to 30 minutes, occurring three to ve times a week, or if spontaneous awakening is present during the night without the ability to resume sleeping.7, 1 3 About 10% of the general population suffers from chronic insomnia, but the prevalence is reported to be around 30% in chronic pain patients.1Pain conditions can alter normal sleep pat-terns. The effect of acute pain on sleep seems to follows a linear model: Pain precedes poor sleep (ie, cause-and-effect sequence), and sleep returns to normal when the acute pain is resolved. However, a circular model seems to predominate in the presence of chronic pain (ie, pain lasting for at least 3 months). In the circular model, a night of poor sleep is followed by a day with complaints of more intense and variable pain, which is then followed by a night of nonrestorative sleep with morning-related complaints of unrefreshing sleep. It is impor-Fig 11-1 Normal hypnogram of a 50-year-old man, showing three complete sleep cycles. Registration began at 20:30 and nished at 8:30. Analysis time (green line) is shown from the time lights were turned off until they were turned back on. M, movement time; W, wake time; R, REM time. (Courtesy of Dr D. M. Laman, Department of Clinical Neurophysiology, Onze Lieve Vrouwe Gasthuis [OLVG], Amsterdam, The Netherlands.)N2 N2N3N2N3 N3StartWakeWake21:00 22:00 23:00 00:00 01:00 02:00 03:00 04:00 05:00 06:00 07:00 08:00REMREM REMMWRN1N2N3Lights onLights offN3N3N2 N2 243Interactions Between Pain and Sleeptant to note that the circular model cannot be generalized to all patients; some may follow a linear model even with chronic pain.1,14Interactions Between Pain and SleepApproximately one- to two-thirds of chronic musculoskeletal pain patients report poor sleep quality.1 Nonrestorative sleep is dened as an unrefreshed feeling on awakening, and it is present in about 10% of the general pop-ulation, with a higher risk as individuals age. Nonrestorative sleep is a frequent complaint found in shift workers who work during the night, in patients who sleep more than 9 hours per night, and in those with insomnia-related symptoms or with fatigue and mood altera-tions.1,3 The presence of restorative sleep (ie, sleep that leaves the individual feeling re-freshed, rested, and reenergized) appears to predict the resolution of chronic widespread pain in some individuals.15 It remains to be demonstrated whether some individuals are genetically protected against the deleterious impact of chronic pain on sleep.1,14The sleep of orofacial pain and TMD pa-tients can often be nonrestorative or of poor quality; such complaints are mostly reported in the morning on awakening.16,17 Approximately 36% of TMD patients experience insomnia, and 28% experience sleep apnea.16 Patients suffering from trigeminal neuralgia or orofacial neuropathic pain also report waking episodes during their sleep.18 About 7% to 10% of adults report frequent pain in the jaw muscles, and TMD patients with muscle pain tend to report their symptoms mostly in the afternoon, simi-lar to delayed-onset muscle soreness.17 Com-mon features or potential risk factors for TMD patients in addition to disturbed sleep include fatigue, depression, somatization, anxiety, and daytime tooth clenching.19–22The frequently assumed association be-tween TMD pain and sleep bruxism was re-cently revisited. In a cohort of female myo-fascial TMD patients and pain-free controls who agreed to sleep in a laboratory for two consecutive nights, no relationship was found between pain and the number and in-tensity of jaw-muscle contractions related to sleep bruxism.23 However, the TMD patients showed more respiratory effort-related arous-als (RERAs) and higher jaw-muscle tone over the course of the night.24,25 This suggests that TMD patients may have a propensity to keep a type of hyperarousal level during the entire night; in other words, like insomnia patients and contrary to good sleepers, they are not able to wind down.26,27 Further, factors like trait anxiety and an imbalance in the autonomic car-diac activity during sleep may be concomitant associated factors.28,29 Despite these recent insights, the etiology of poor sleep in TMD patients requires further investigation. It is im-portant for the clinician to identify if transient jaw muscle pain in the morning is isolated or if it is secondary to sleep bruxism and/or sleep apnea, because the management strategies will differ.15,17,22,30,31 Most evidence supporting a link between orofacial pain and sleep is de-rived from questionnaire studies; nal trans-lation to clinical application requires further validation from sleep laboratory or home am-bulatory recordings.32,33 ComorbiditiesVarious factors may contribute to the interac-tion between pain and poor sleep: Lifestyle, beliefs, difculties in coping with anxiety, poor physical tness, and chronic fatigue may be risk factors for insomnia, a condition found in 36% of patients with TMD.14,16 In addition, sleep comorbidities like periodic limb move-ments and sleep-disordered breathing (apnea/hypopnea or upper airway resistance) can exacerbate the interaction between pain and poor sleep (Fig 11-2). Periodic limb movements and sleep apnea/hypopnea have been reported in both TMD and chronic widespread pain/ 24411Sleep and Orofacial Painbromyalgia patients with greater frequency than in controls.16,34 A periodic limb movement index over 10 events per hour of sleep (from an electromyogram of the tibialis leg muscle) is the new lower threshold for a polysom-nographic diagnosis for periodic limb move-ments.13 Sleep apnea/hypopnea is diagnosed if there are at least 5 events per hour of sleep in adults or 1 to 2 per hour of sleep in children, while no clear consensus has been reached yet for adolescents.13Compared with adult patients without chronic widespread pain, patients with chronic widespread pain have a higher risk (odds ratio > 3) of reporting comorbid conditions such as fatigue, headache, gastrointestinal problems, and sleep disturbances.35 Orofacial pain pa-tients also report more problems in coping Fig 11-2 Example of a 20-second page of a polysomnographic recording. On top is the hypnogram of the total registration time. The thick black line represents the 20-second epoch shown in the rest of the image. On the left side are the various recording channels: EOG, eye movements (1, left; 2, right); FP2:C4 and C4:O2, long-distance electroencephalogram (EEG) channels from front to back on the right side; EMG, electromyogram of the chin/jaw; ECG, electrocardiogram (electrodes placed near Erb’s point, above the clavicle); snore, channel of the snore sensor; pressure ow, air ow sensor; thorax and abdom, thoracic and abdominal respiratory effort sensors channels; Pos, sleep position (in this case, supine); SPO2, oxygen saturation measured at the ngertip; pulse, pulse rate; PLMr and PLMl, leg movements (right and left). An 8-second event of repetitive jaw-muscle activities is shown in the EMG (chin/jaw) channel (pink area) and in the EEG channels. At the same time or slightly before, the EEG shows signs of arousal (more fast activity), the respiration deepens and becomes more pronounced, the pulse increases, and independently, some repetitive leg movements lasting less than 1 second following the start of the arousal are shown in the PLM channels. (Courtesy of Dr D. M. Laman, Department of Clinical Neurophysiology, Onze Lieve Vrouwe Gasthuis [OLVG], Amsterdam, The Netherlands.) 245Interactions Between Pain and Sleepwith fatigue, psychologic distress, headaches, and abdominal pains.16,21,36,37 Patients in a fam-ily medical practice who had hypertension, pain syndromes (eg, back pain, arthritis), and depression also had more sleep disturbance–related complaints.38 Several sleep-related problems, such as sleepiness, dozing off dur-ing daily activity, frequent awakenings dur-ing the night, complaints related to restless legs syndrome (ie, the awake symptoms that occur in approximately 80% of periodic limb movement cases), and signs of sleep-related breathing disturbances (eg, loud snoring and cessation of breathing suggestive of apnea) were higher in pain patients.1,7,15 Likewise, a re-cent large-scale US-based case-control study reported a high likelihood of self-reported obstructive sleep apnea being associated with higher odds of chronic TMD (odds ratio > 3).39 While this is an important nding, the absence of polysomnographic conrmation of sleep-disordered breathing calls for a careful interpretation.40 Importantly, clinicians should recog-nize and understand the inuences of the above-described sleep comorbidities on the differential diagnoses and treatment planning for their orofacial pain patients (Box 11-1).Box 11-1 Elements for assessment of orofacial pain and sleep complaints• Identify the nature of the pain and sleep complaints. Ask the patient to keep a 24-hour diary, if possible, to monitor periods of pain exacerbation, time and duration of daily naps, sleep time, and wake time.• Review medication type and dose, time of intake, and use of other treatments for pain or sleep complaints, such as physical therapy or cognitive behavioral therapy.• Identify mood alterations (eg, depression, anxiety).• Identify stressful life events or traumatic events.• Identify poor sleep behavior or hygiene (eg, irregular sleep schedule; disrupted sleep environment; frequent use of caffeine, alcohol, or medications that alter sleep).• Identify the extent of fatigue and/or sleepiness (eg, falling asleep easily during daily activities or while watching TV, driving-related sleepiness) using the Epworth Sleepiness Scale.*• Identify the risk of sleep-disordered breathing using the STOP-Bang or Berlin questionnaire.†• Assess the risk of insomnia (ie, more than 20 to 30 minutes’ delay in falling asleep, depending on nap habits, or difficulty resuming sleep after awakening during the night). • Assess the presence of any periodic limb movements (eg, leg kicks that will increase sleep fragmentation above a cumulative threshold of events per hour of sleep). • Assess if any snoring, alone or with sleep-disordered breathing (RERA upper airway resistance) or apnea/hypopnea (ie, cessation of breathing with reduced oxygenation with concomitant sleepiness), may contribute to increased sleep fragmentation and poor sleep quality complaints.• Identify clinical risk factors associated with sleep-related breathing disorders, such as retrognathia, a deep and narrow palate and narrow arch, a large tongue, and large tonsils and adenoids.*The Epworth Sleepiness Scale is an easy-to-use screening questionnaire to guide the clinician on the extent of daytime sleepiness; scores over 10 to 12 are suggestive of a sleep-related disorder and warrant medical evaluation.41†The STOP-Bang or Berlin sleep questionnaire may help the clinician discern between simple snoring and sleep apnea42,43; see also the recent review on use of sleep questionnaires for TMD patients.40 24611Sleep and Orofacial PainManagement of Orofacial Pain and Related Sleep DisturbancesBox 11-2 outlines how to approach manage-ment of sleep-related disturbances in orofacial pain patients.1,15 Cognitive behavioral therapy (CBT) has been used to aid in the manage-ment of pain conditions as well as sleep dis-turbances. The type of CBT known to improve pain is different than CBT used to manage insomnia or poor sleep behavior. It seems logical that merging both pain and insomnia CBT methods might yield the best results, but to date there have not been enough stud-ies supporting CBT use in patients suffering from both orofacial pain and poor sleep or insomnia.44Manual therapies (ie, physical approaches) are frequently suggested to patients for pain and sleep management, but their benefit seems to be variable; indeed, a lack of evi-dence currently prevents the drawing of any conclusion on the benets of manual treat-ment approaches. A recent randomized con-trolled trial failed to demonstrate any benet from progressive muscle relaxation and sleep hygiene measures on sleep bruxism.45 Mild analgesics (most are available over the coun-ter) are commonly used alone or in combina-tion with a muscle relaxant or sleep inducer, but this practice is also not yet based on good evidence for orofacial pain conditions. Due to a heightened risk of respiratory depression, opioid use in the evening is contraindicated for patients with sleep-disordered breathing; such patients need to take advantage of treatment involving a mandibular advancement appliance (MAA), continuous positive airway pressure (CPAP), or bilevel positive airway pressure (BiPAP).1 Duloxetine, a selective serotonin and norepinephrine reuptake inhibitor, reduces Box 11-2 Management of sleep-related disturbances in orofacial pain patients*• Review the patient’s sleep hygiene to provide basic empirical advice on features such as: – Wake-sleep cycle (eg, regular bedtime and awakening schedule) – Sleep environment (eg, dark, cool, quiet bedroom; if the partner snores, use of ear plugs or sleeping in a different room may help) – Lifestyle habits (eg, avoidance of intense exercise, coffee, smoking, alcohol, and intense or troubling discussions 3 to 6 hours before sleep)• Advise the patient on the benefits of regular mild exercise (eg, walking).• Consider the benefits of physical therapy and CBT.• Consider short-term pharmacologic methods: – Analgesics alone or combined with muscle relaxants (eg, methocarbamol) or with sleep aids (eg, diphenhydramine) – Muscle relaxants or sedatives (eg, cyclobenzaprine, temazepam) – Hypnotics or antidepressants (eg, zolpidem, trazodone, amitriptyline, duloxetine) – Other medications (eg, gabapentin, pregabalin)• Consider the possibility of complementary medicine approaches (eg, yoga, meditation, valerian, lavender). • Consider oral appliances for patients with snoring and/or obstructive sleep apnea and sleep bruxism.• If there is any evidence of sleepiness with sleep apnea/hypopnea or other medical conditions, arrange a consultation with a specialist in sleep medicine.*Low on evidence for sleep and TMDs. 247Referencespain in chronic widespread pain/bromyalgia patients with slight improvement in sleep quality. More established medications, such as tricyclic antidepressants (eg, amitriptyline or trazodone), have mild to moderate positive effects on both pain and sleep. Gabapentin, pregabalin, and sodium oxybate also appear to improve pain and sleep quality and continuity. However, it is important to know that none of these medications, with the exception of du-loxetine, have approval from the US Food and Drug Administration for the combination of sleep and pain management. Their use is thus off-label, and clinicians prescribing such medi-cations must take responsibility for such use. Respiratory devices (eg, MAA and CPAP) may help patients with chronic bromyalgia and/or morning headaches.46,47 However, randomized controlled clinical studies on orofacial pain pa-tients are needed before conclusions can be drawn about the benets and safety of such approaches in the general population.Overall, chronic orofacial pain can be associ-ated with disrupted sleep. Clinicians need to identify orofacial pain patients complaining of poor sleep and refer them to a sleep laboratory for further evaluation. Based on the individual patient’s unique psychosocial and medical his-tory, pain and sleep management strategies, including sleep hygiene recommendations, cognitive behavioral treatments, or short-term use of medication, need to be customized.References1. Lavigne GJ, Smith MT, Denis R, Zucconi M. Pain and sleep. In: Kryger HM, Roth T, Dement WC (eds). Princi-ples and Practice of Sleep Medicine. Philadelphia: Elsevier Saunders, 2011:1442–1451.2. Lavigne GJ, Morin CM, Carra MC. The nature of sleep. In: Lavigne GJ, Cistulli PA, Smith MT (eds). Sleep Medi-cine for Dentists: A Practical Overview. Chicago: Quintessence, 2009:3–10.3. Haack M, Mullington JM. Sustained sleep restriction reduces emotional and physical well-being. Pain 2005; 119:56–64.4. Haack M, Sanchez E, Mullington JM. Elevated inam-matory markers in response to prolonged sleep restric-tion are associated with increased pain experience in healthy volunteers. Sleep 2007;30:1145–1152.5. Amzica F, Lavigne GJ. Sleep neurobiology. In: Lavigne GJ, Cistulli PA, Smith MT (eds). Sleep Medicine for Dentists: A Practical Overview. Chicago: Quintessence, 2009:11–19.6. Krueger JM, Rector DM, Roy S, Van Dongen HP, Belenky G, Panksepp J. Sleep as a fundamental prop-erty of neuronal assemblies. Nat Rev Neurosci 2008; 9:910–919.7. Lavigne GJ, Heinzer RC, Cistulli PA, Smith MT. Classi-cation of sleep disorders. In: Lavigne GJ, Cistulli PA, Smith MT (eds). Sleep Medicine for Dentists: A Practi-cal Overview. Chicago: Quintessence, 2009:21–31.8. Vandewalle G, Archer SN, Wuillaume C, et al. Functional magnetic resonance imaging-assessed brain responses during an executive task depend on interaction of sleep homeostasis, circadian phase, and per3 genotype. J Neurosci 2009;29:7948–79569. Dijk DJ, Archer SN. Period3, circadian phenotypes, and sleep homeostasis. Sleep Med Rev 2010;14:151–160.10. Parrino L, Zucconi M, Terzano GM. Sleep fragmentation and arousal in the pain patient. In: Lavigne GJ, Sessle BJ, Choinière M, Soja PJ (eds). Sleep and Pain. Seattle: IASP, 2007:213–234.11. Carra MC, Macaluso GM, Rompre PH, et al. Clonidine has a paradoxical effect on cyclic arousal and sleep bruxism during NREM sleep. Sleep 2010;33: 1711–1716.12. Peever JH, Sessle BJ. Sensory and motor processing during sleep and wakefulness. In: Kryger HM, Roth T, Dement WC (eds). Principles and Practice of Sleep Medicine, ed 6. Philadelphia: Elsevier Saunders, 2017: 239–249.13. American Academy of Sleep Medicine. International Classication of Sleep Disorders, ed 3. Darrien, IL: American Academy of Sleep Medicine, 2014.14. Davies KA, Macfarlane GJ, Nicholl BI, et al. Restorative sleep predicts the resolution of chronic widespread pain: Results from the EPIFUND study. Rheumatology (Oxford) 2008;47:1809–1813.15. Lavigne GJ, Nashed A, Manzini C, Carra MC. Does sleep differ among patients with common musculoskel-etal pain disorders? Curr Rheumatol Rep 2011;13: 535–542.16. Smith MT, Wickwire EM, Grace EG, et al. Sleep disor-ders and their association with laboratory pain sensi-tivity in temporomandibular joint disorder. Sleep 2009;32:779–790.17. Dao TT, Lund JP, Lavigne GJ. Comparison of pain and quality of life in bruxers and patients with myofascial pain of the masticatory muscles. J Orofac Pain 1994;8:350–356. 2481124811Sleep and Orofacial Pain18. Benoliel R, Eliav E, Sharav Y. Self-reports of pain-related awakenings in persistent orofacial pain patients. J Oro-fac Pain 2009;23:330–338.19. Von Korff M, LeResche L. Epidemiology of pain. In: Merskey H, Loeser JD, Dubner R (eds). The Paths of Pain, 1975–2005. Seattle: IASP, 2005:339–352.20. Velly AM, Gornitsky M, Philippe P. Contributing factors to chronic myofascial pain: A case-control study. Pain 2003;104:491–499.21. de Leeuw R, Studts JL, Carlson CR. Fatigue and fatigue-related symptoms in an orofacial pain popula-tion. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2005;99:168–174.22. Rompré PH, Daigle-Landry D, Guitard F, Montplaisir JY, Lavigne GJ. Identication of a sleep bruxism subgroup with a higher risk of pain. J Dent Res 2007;86: 837–842.23. Raphael KG, Sirois DA, Janal MN, et al. Sleep bruxism and myofascial temporomandibular disorders: A laboratory-based polysomnographic investigation. J Am Dent Assoc 2012;143:1223–1231.24. Dubrovsky B, Raphael KG, Lavigne GJ, et al. Polysom-nographic investigation of sleep and respiratory param-eters in women with temporomandibular pain disor-ders. J Clin Sleep Med 2014;10:195–201.25. Raphael KG, Janal MN, Sirois DA, et al. Masticatory muscle sleep background electromyographic activity is elevated in myofascial temporomandibular disorder pa-tients. J Oral Rehabil 2013;40:883–891.26. Riemann D, Spiegelhalder K, Feige B, et al. The hyper-arousal model of insomnia: A review of the concept and its evidence. Sleep Med Rev 2010;14:19–31.27. Quartana PJ, Wickwire EM, Klick B, Grace E, Smith MT. Naturalistic changes in insomnia symptoms and pain in temporomandibular joint disorder: A cross-lagged panel analysis. Pain 2010;149:325–331.28. Manfredini D, Fabbri A, Peretta R, Guarda-Nardini L, Lobbezoo F. Inuence of psychological symptoms on home-recorded sleep-time masticatory muscle activity in healthy subjects. J Oral Rehabil 2011;38:902–911.29. Eze-Nliam CM, Quartana PJ, Quain AM, Smith MT. Noc-turnal heart rate variability is lower in temporomandibu-lar disorder patients than in healthy, pain-free individu-als. J Orofac Pain 2011;25:232–239. 30. Lavigne G, Palla S. Transient morning headache: Recog-nizing the role of sleep bruxism and sleep-disordered breathing. J Am Dent Assoc 2010;141:297–299.31. Chen PK, Fuh JL, Lane HY, Chiu PY, Tien HC, Wang SJ. Morning headache in habitual snorers: Frequency, char-acteristics, predictors and impacts. Cephalalgia 2011; 31:829–836.32. Lavigne GJ, Khoury S, Laverdure-Dupont D, Denis R, Rouleau GA. Tools and methodological issues in the in-vestigation of sleep and pain interactions. In: Lavigne GJ, Sessle BJ, Choinière M, Soja P (eds). Sleep and Pain. Seattle: IASP, 2007:235–266.33. Yachida W, Castrillon EE, Baad-Hansen L, et al. Cranio-facial pain and jaw-muscle activity during sleep. J Dent Res 2012;91:562–567.34. Okura K, Lavigne GJ, Huynh N, Manzini C, Fillipini D, Montplaisir JY. Comparison of sleep variables between chronic widespread musculoskeletal pain, insomnia, periodic leg movements syndrome and control subjects in a clinical sleep medicine practice. Sleep Med 2008;9:352–361.35. Rohrbeck J, Jordan K, Croft P. The frequency and char-acteristics of chronic widespread pain in general prac-tice: A case-control study. Br J Gen Pract 2007;57: 92–94.36. Goncalves DA, Camparis CM, Speciali JG, Franco AL, Castanharo SM, Bigal ME. Temporomandibular disor-ders are differentially associated with headache diagno-ses: A controlled study. Clin J Pain 2011;27:611–615.37. Macfarlane TV, Blinkhorn AS, Davies RM, Ryan P, Worthington HV, MacFarlane GJ. Orofacial pain: Just another chronic pain? Results from a population-based survey. Pain 2002;99:453–458.38. Alattar M, Harrington JJ, Mitchell CM, Sloane P. Sleep problems in primary care: A North Carolina family prac-tice research network (NC-FP-RN) study. J Am Board Fam Med 2007;20:365–374.39. Sanders AE, Essick GK, Fillingim R, et al. Sleep apnea symptoms and risk of temporomandibular disorder: OPPERA cohort. J Dent Res 2013;92:70S–77S.40. Sommer I, Lavigne G, Ettlin DA. Review of self-reported instruments that measure sleep dysfunction in patients suffering from temporomandibular disorders and/or orofacial pain. Sleep Med 2015;16:27–38.41. Johns MW. A new method for measuring daytime sleepiness: The Epworth sleepiness scale. Sleep 1991;14:540–545.42. Chung F, Yegneswaran B, Liao P, et al. STOP question-naire: A tool to screen patients for obstructive sleep apnea. Anesthesiology 2008;108:812–821.43. Netzer NC, Stoohs RA, Netzer CM, Clark K, Strohl KP. Using the Berlin Questionnaire to identify patients at risk for the sleep apnea syndrome. Ann Intern Med 1999;131:485–491.44. Tang NK, Lereya ST, Boulton H, Miller MA, Wolke D, Cappuccio FP. Nonpharmacological treatments of in-somnia for long-term painful conditions: A systematic review and meta-analysis of patient-reported outcomes in randomized controlled trials. Sleep 2015;38: 1751–1764.45. Valiente López M, van Selms MK, van der Zaag J, Hamburger HL, Lobbezoo F. Do sleep hygiene mea-sures and progressive muscle relaxation inuence sleep bruxism? Report of a randomised controlled trial. J Oral Rehabil 2015;42:259–265.46. Gold AR, Dipalo F, Gold MS, Broderick J. Inspiratory air-ow dynamics during sleep in women with bromyal-gia. Sleep 2004;27:459–466.47. Franco L, Rompré PH, de Grandmont P, Abe S, Lavigne GJ. A mandibular advancement appliance reduces pain and rhythmic masticatory muscle activity in patients with morning headache. J Orofac Pain 2011;25: 240–249.

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