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RESEARCH REPORT |
1 Centre d’étude sur le Sommeil et des Rythmes Biologiques, Hôpital du Sacré-Coeur de Montréal;
2 Facultés de médecine et de médecine dentaire, Université de Montréal, CP6128, succursale Centre-ville, Montréal, H3C 3J7, Québec, Canada;
3 Centre de recherche en sciences neurologiques, Université de Montréal;
4 Faculty of Dentistry, McGill University; and
5 Faculty of Dentistry, University of Toronto;
*corresponding author, gilles.lavigne{at}umontreal.ca
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONMATERIALS & METHODSRESULTSDISCUSSIONREFERENCES |
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KEY WORDS: sleep bruxism • rhythmic masticatory muscle activity • sleep micro-arousal • sensory stimuli • arousal reactions
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONMATERIALS & METHODSRESULTSDISCUSSIONREFERENCES |
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Since micro-arousal can be triggered by sensory stimuli without disrupting sleep continuity (Morgan et al., 1996; Monstad and Guilleminault, 1999; Roehr et al., 2000), and based on evidence that tooth-grinding can be triggered by sensory stimulation in SB patients (Satoh and Harada, 1973), we decided to compare responses of SB patients and matched normals to test the following hypotheses: SB patients will (1) have a lower threshold of experimental arousal, (2) show more RMMA during arousal, and (3) have higher resting masticatory EMG levels during sleep.
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MATERIALS & METHODS |
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TOPABSTRACTINTRODUCTIONMATERIALS & METHODSRESULTSDISCUSSIONREFERENCES |
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SB Diagnosis and Study Procedures
Polygraphic recordings were made on three or four nights in a sleep laboratory. The first night was used for acclimatization. The second (baseline) night was used for the diagnosis of SB and to screen for other sleep disorders. A polygraphic diagnosis of SB was based on: (1) more than 4 SB episodes per hour of sleep, (2) more than 25 muscle bursts per hour of sleep, or (3) two or more SB episodes with tooth-grinding noise (Lavigne et al., 1996). No other sleep disorders were found in any of the subjects. The experiment was carried out on a third night, but an additional night was added for one SB patient and two normal subjects because not enough stimuli could be given on the third night. Subjects were instructed to avoid caffeine the day before laboratory recording.
Experimental Set-up
Two types of stimuli were used to induce arousal without triggering complete awakening from sleep (Morgan et al., 1996; Roehr et al., 2000). The first was a combination of vibrotactile and auditory (VT+AD) stimulation at three intensities (vibration—frequencies of 30, 70, and 115 Hz with respective accelerations of ± 0.7, ± 3.1, and ± 12.8 G [Giga]; auditory—39, 42, and 45 dB), produced by an AC motor (diameter, 3 cm; length, 3.5 cm) in contact with the arm of the subject. The second was an auditory stimulus (AD: 39, 42, and 45 dB) produced by the same type of motor at the bedside. Duration was 1 sec.
The following measures were recorded on a computer (sampling rate: 200 Hz) equipped with commercial software (HARMONIE, Stellate, Montréal, PQ, Canada): EEG (C3A2, O2A1), electro-oculogram, electrocardiogram (EKG), chest respiratory movements, and EMG activity from the left masseter, suprahyoid, and tibialis muscles. EMG activity of the right masseter and suprahyoid muscles was recorded simultaneously on a second computer at a sampling rate of 1024 Hz for spectral analysis. Audio-video recording was performed for the identification of oromotor activity (Lavigne et al., 1996; Kato et al., 2001b).
Experimental Procedure
Before the subject went to sleep, resting EMG and EKG activity was recorded with each subject in a supine position with the eyes closed. After sleep onset, the first stimulus was given only after sleep stages 3 and 4 began; otherwise, subjects rarely returned to stable sleep stages 3 and 4. Sleep stages (stages 2, 3, 4, and REM [rapid eye movement]) were identified on a computer screen. Stimuli were delivered at intervals of at least 60 sec to prevent sleep disruption or habituation (Lavigne et al., 2000). Blocks of < 20 stimuli were separated by at least 10 min of undisturbed sleep. When a sleep stage shift occurred, a subject had to remain in the same sleep stage for > 3 min before the next stimulation. In the morning, subjects reported on sleep quality (e.g., whether they slept well or not), and their awareness of stimuli during sleep.
Off-line Data Analysis
Scoring Sleep Variables and RMMA
Sleep stages and transient arousals were scored according to the standard criteria (Rechtschaffen and Kales, 1968; ASDA, 1992). Experimental arousal was identified as an abrupt shift on either of the two recorded EEG channels with alpha, theta, delta, or frequency over 16 Hz that began < 2 sec after stimulation and lasted between 3 and 15 sec with or without motor events (ASDA, 1992; Roehr et al., 2000). RMMA episodes during experimental arousal were identified, from audio-video recordings and masticatory muscle EMG activity, as either phasic/rhythmic or mixed (phasic and tonic) oromandibular episodes, regardless of grinding sounds (Lavigne et al., 1996 and 2001).
Analysis of Masticatory Muscle Tone and Cardiac Activities in the Absence of RMMA
Masseter and suprahyoid EMG activity was quantified by spectral analysis with Fourier Transformation (cosine window, resolution: 0.25 Hz). Total power (µV2) was calculated from three specific frequency bands (35-55, 75-110, 125-175 Hz) chosen because they are usually free from the vibration frequency range of our device and other electrical artefacts (Gamet et al., 1993). Data were gathered during four consecutive two-second periods before and after stimuli. Using the above software, we calculated instantaneous heart rate from the R-R interval in 10 cycles before and 15 cycles after the stimulus on screen (Kato et al., 2001a). For both variables, we excluded 9% of the experimental arousal responses that occurred with body movement or RMMA. The changes in masticatory muscle tone and heart rate were compared between the groups.
Statistics
For between-group comparisons, we used repeated-measures ANOVAs, a two-sample t test, and the Mann-Whitney test. The rate of experimentally induced RMMA in SB patients was compared between sleep stages by the Friedman test and with a post hoc Wilcoxon test. Significance was assumed at p < 0.05, and data were presented as mean ± SEM or median [range].
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RESULTS |
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TOPABSTRACTINTRODUCTIONMATERIALS & METHODSRESULTSDISCUSSIONREFERENCES |
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). The amount of time spent in sleep stage 2 increased slightly from the baseline to the experimental night (p = 0.024, ANOVA), and decreased in sleep stage 4 (p < 0.001, ANOVA). Seven out of eight SB patients and all normal subjects reported good sleep quality during the experimental night.
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). The number of stimuli that participants remembered during sleep was not different between groups (SB patients, 1.6 ± 0.5%; normals, 2.9 ± 0.5%, p > 0.05; t test).
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). These occurred in all eight SB patients. One normal subject had 5 episodes; the other had none. Evoked RMMA episodes were 7 times more frequent in SB patients (SB patients, 10.9 ± 1.8%; normals, 1.5 ± 1.5%, p = 0.003, Mann-Whitney test, Fig. 1C). Similarly to Satoh and Harada (1973), the mean latency of RMMA after stimulation was 8.0 ± 0.84 sec (range, 2 to 18). In the SB patients, 27 experimentally induced RMMA episodes (87%) occurred during sleep stage 2, 3 episodes (9.7%) in stages 3 and 4, and 2 (6.5%) in REM. In the normal subject, four episodes were in stage 2 and one in REM. In SB patients, the evoked RMMA response rate differed significantly across sleep stages (stage 2, 14.9% [4.8 to 37.5]; stages 3 and 4, 0% [0 to 66.7]; REM, 0% [0 to 7.7], p = 0.025, Friedman test). Post hoc analysis revealed a significant difference between stages 2 and REM (p = 0.012, Wilcoxon test). Audible tooth-grinding occurred during 71% (22/31) of the evoked episodes in the SB patients only (7.5% of overall experimental arousals [22/295]), and most of these (19/22) occurred in sleep stage 2.
Masticatory Muscle Tone and Heart Rate
EMG activity before stimulation decreased significantly from wakefulness to sleep in the masseter and suprahyoid muscles (p < 0.001 for both muscles, ANOVA) and was lowest during REM sleep (p < 0.001), but there was no difference between the groups (Table 2A). Similarly, resting mean heart rate was not different between the two groups during wakefulness and sleep (Table 2B).
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). There were no differences between the two groups in any of the sleep stages. There was also no difference in change in heart rate between the groups for any sleep stage (Fig. 2B).
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DISCUSSION |
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TOPABSTRACTINTRODUCTIONMATERIALS & METHODSRESULTSDISCUSSIONREFERENCES |
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Sleep micro-arousal is usually characterized by a transient change in cortical EEG activity, an increase in heart rate, and, occasionally, in muscle activity, and is thought to be a physiological adjustment to endogenous and environmental influences (ASDA, 1992; Monstad and Guilleminault, 1999; Roehr et al., 2000; Sforza et al., 2000). The frequency of spontaneous sleep micro-arousal is normal in young SB patients (Boselli et al., 1998; Sforza et al., 2000; Kato et al., 2001b; Lavigne et al., 2001, 2002). Our results confirm that sleep in SB patients is normal and lead us to reject the first hypothesis, that SB patients have a lower threshold for sleep arousal to environmental stimuli than do normals.
More importantly, our results showed that RMMA episodes could be induced, following experimental arousal, seven times more frequently in SB patients than in normal subjects. In addition, tooth-grinding was triggered in SB patients only. These results support the suggestion that SB is a consequence of sleep micro-arousal (Satoh and Harada, 1973; Macaluso et al., 1998; Kato et al., 2001a), and confirm the hypothesis that the RMMA follows experimental arousal more frequently in SB patients than in normal subjects.
This study also documented that it was easier to trigger RMMA in sleep stage 2, where 60 to 80% of spontaneous SB episodes occur (Satoh and Harada, 1973; Lavigne et al., 1996; Macaluso et al., 1998). A previous non-controlled study of SB patients showed that visual, tactile, and auditory arousal stimuli induced tooth-grinding in 7.9% of experimental arousals (Satoh and Harada, 1973), which is almost the same value as the 7.5% that we observed. The same authors reported that 65% of evoked tooth-grinding episodes occurred during sleep stage 2 (Satoh and Harada, 1973), which is somewhat less than the 86% seen in our SB population.
The increase in RMMA frequency in SB patients was probably not due to a change in motoneuron excitability during sleep, since the resting masticatory muscle EMG was similar in the two groups. Furthermore, the slow rise in masticatory muscle EMG levels during experimental arousal in trials in which no RMMA occurred was similar in the two groups, as was the change in heart rate. These results allow us to reject the third hypothesis, that SB is associated with higher motor excitability.
Nonetheless, under the influence of experimental arousal, the frequency with which oromotor events are triggered is higher in SB patients. Although the nature of the link between micro-arousal and RMMA is not known, sleep micro-arousal has been suggested to result from the activation of subcortical and reticular systems which control autonomic, thalamo-cortical, and motor activity (Steriade, 1996; Garcia-Rill, 1997; Lund et al., 1998; Lavigne et al., 2003). Recent evidence indicates the importance of neurochemicals (e.g., orexin, monoamine, dopamine) in the arousal-reticular system and in the pathophysiology of sleep-related periodic motor activity (Mignot et al., 2002; Zhang and Luo, 2002). It is therefore possible that SB is associated with a shift in the balance from sleep-maintaining influences toward a transient increase in activity induced by the arousal-reticular system.
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ACKNOWLEDGMENTS |
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Received June 28, 2002; Last revision December 10, 2002; Accepted January 27, 2003
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REFERENCES |
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TOPABSTRACTINTRODUCTIONMATERIALS & METHODSRESULTSDISCUSSIONREFERENCES |
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Boselli M, Parrino L, Smerieri A, Terzano MG (1998). Effect of age on EEG arousals in normal sleep. Sleep 21:351–357.[ISI][Medline]
Gamet D, Duchene J, Garapon-Bar C, Goubel F (1993). Surface electromyogram power spectrum in human quadriceps muscle during incremental exercise. J Appl Physiol 74:2704–2710.
Garcia-Rill E (1997). Disorders of the reticular activating system. Med Hypotheses 49:379–387.[ISI][Medline]
Kato T, Rompré P, Montplaisir JY, Sessle BJ, Lavigne GJ (2001a). Sleep bruxism: an oromotor activity secondary to micro-arousal. J Dent Res 80:1940–1944.
Kato T, Thie NM, Montplaisir JY, Lavigne GJ (2001b). Bruxism and orofacial movements during sleep. Dent Clin North Am 45:657–684.[Medline]
Lavigne GJ, Manzini C (2000). Bruxism. In: Principles and practice of sleep medicine. 3rd ed. Kryger M, Roth T, Dement WC, editors. Philadelphia: WB Saunders, pp. 773-785.
Lavigne GJ, Rompré PH, Montplaisir JY (1996). Sleep bruxism: validity of clinical research diagnostic criteria in a controlled polysomnographic study. J Dent Res 75:546–552.
Lavigne G, Zucconi M, Castronovo C, Manzini C, Marchettini P, Smirne S (2000). Sleep arousal response to experimental thermal stimulation during sleep in human subjects free of pain and sleep problems. Pain 84:283–290.[ISI][Medline]
Lavigne GJ, Rompré PH, Poirier G, Huard H, Kato T, Montplaisir JY (2001). Rhythmic masticatory muscle activity during sleep in humans. J Dent Res 80:443–448.
Lavigne GJ, Rompré PH, Guitard F, Sessle BJ, Kato T, Montplaisir JY (2002). Lower number of K-complexes and K-alphas in sleep bruxism: a controlled quantitative study. Clin Neurophysiol 113:686–693.[ISI][Medline]
Lavigne GJ, Kato T, Kolta A, Sessle BJ (2003). Neurobiological mechanisms involved in sleep bruxism. Crit Rev Oral Biol Med 14:30–46.
Lund JP, Kolta A, Westberg KG, Scott G (1998). Brainstem mechanisms underlying feeding behaviors. Curr Opin Neurobiol 8:718–724.[ISI][Medline]
Macaluso GM, Guerra P, Di Giovanni G, Boselli M, Parrino L, Terzano MG (1998). Sleep bruxism is a disorder related to periodic arousals during sleep. J Dent Res 77:565–573.
Mignot E, Taheri S, Nishino S (2002). Sleeping with the hypothalamus: emerging therapeutic targets for sleep disorders. Nat Neurosci 5(Suppl):1071–1075.
Monstad P, Guilleminault C (1999). Cardiovascular changes associated with spontaneous and evoked K-complexes. Neurosci Lett 263:211–213.[ISI][Medline]
Morgan BJ, Crabtree DC, Puleo DS, Badr MS, Toiber F, Skatrud JB (1996). Neurocirculatory consequences of abrupt change in sleep stage in humans. J Appl Physiol 80:1627–1636.
Rechtschaffen A, Kales A (1968). A manual of standardized terminology, techniques and scoring techniques for sleep stages of human subjects. Los Angeles: Brain Information Service, Brain Research Institute.
Roehr T, Carskadon MA, Dement WC, Roth T (2000). Daytime sleepiness and alertness. In: Principles and practice of sleep medicine. 3rd ed. Kryger M, Roth T, Dement WC, editors. Philadelphia: WB Saunders, pp. 43-52.
Satoh T, Harada Y (1973). Electrophysiological study on tooth-grinding during sleep. Electroenceph Clin Neurophysiol 35:267–275.[ISI][Medline]
Sforza E, Jouny C, Ibanez V (2000). Cardiac activation during arousal in humans: further evidence for hierarchy in the arousal response. Clin Neurophysiol 111:1611–1619.[ISI][Medline]
Steriade M (1996). Arousal: revisiting the reticular activating system. Science 272:225–226.[ISI][Medline]
Thorpy MJ (1997). International classification of sleep disorders: diagnostic and coding manual. Rochester, MN: American Sleep Disorders Association.
Zhang J, Luo P (2002). Orexin B immunoreactive fibers and terminals innervate the sensory and motor neurons of jaw-elevator muscles in the rat. Synapse 44:106–110.[ISI][Medline]
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