[Sleepiness among adolescents: etiology and multiple consequences]. / La somnolence chez les adolescents: étiologie et conséquences multiples.

Over the past century a dramatic decline in sleep duration among adolescents, such as more than one hour of sleep loss per night, has been reported. A debt in sleep duration could lead to sleep deprivation, a major risk factor associated with daytime sleepiness. Sleepiness refers to the inability to maintain an adequate level of alertness during the day which may result in more or less being able to control falling asleep at inappropriate times. This literature review updates on sleepiness regarding its characteristics, etiology and consequences on adolescents. Studies revealed that from 25 % to 78 % of adolescents had reported sleepiness. Its manifestations may include heavy lids, yawns, difficulties to concentrate and emotional irritability. In addition, while it is recommended that adolescents under 18 years-old should sleep from eight to ten hours a night, only 63 % of them actually do so. The etiology of sleep deprivation and sleepiness in this population can be explained by various biological and societal factors. First, the sleep-wake cycle of adolescents shows a biological shift from the beginning of pubertal maturation, described as a perfect storm. It refers to a social jetlag by going to sleep and waking up later and accumulating a sleep debt during weekdays which they try to reimburse during weekends. This phenomenon can be explained by physiological changes such as a slower accumulation of sleep pressure. In addition to this perfect storm, environmental and societal factors contribute to the social jetlag and reduce sleep duration in adolescents. Screen exposure before bedtime can delay sleep and wake onset, which is a risk factor for sleeping debt. Substance use such as caffeine, cigarettes or electronic vaporizer, ADHD or freely available medication, alcohol, cannabis use or drug consumption could further disrupt sleep-wake cycle by stimulating, depressing or otherwise disrupting the central nervous system. Early, before 8:30 am, class start times have been associated with chronic sleep deprivation, higher level of sleepiness and delayed melatonin peak secretion. Adolescents working or doing extracurricular occupations for more than 20hours a week are more at risk for reduced sleep duration and sleepiness. Parental supervision about sleep during the weekdays were associated with more appropriate bedtime. Adolescents from low socio-demographic characteristics and from minority ethnic groups have reported displaying a shorter sleep duration. Finally, sleep disorders of a physiological origin such as narcolepsy, sleep apnea or restless legs syndrome, may explain the sleep deprivation and sleepiness. Sleep deprivation and sleepiness in adolescents have consequences on their health. Cognitive functioning, such as problem solving, attention or memory, as well as school performance, can be compromised by sleep deprivation and sleepiness. At the psychological level, adolescents reporting sleepiness are more prone to display mental health problems: associations were found between sleepiness and subjective perception of depression, anxiety, somatic complaints as well as with antisocial behaviors. Finally, 68 % of 16 year-old adolescents reported they drove a car, and the reported sleepiness could lead to road accidents due to reduced attentional functioning, reaction time and decision-making abilities. In the United-States, from 7 % to 16.5 % of deadly accidents were related to driving while drowsy. Highlighting etiology and problems associated with sleep deprivation and sleepiness in adolescents could guide researchers and clinicians towards the development of possible interventions. Public health measures and knowledge transfer programs regarding modifiable psychosocial and societal factors associated with sleep-wake bioregulation could increase awareness in parents as well as in political and societal decision makers.

EEG rhythmic and arrhythmic spectral components and functional connectivity at resting state may predict the development of synucleinopathies in idiopathic REM sleep behavior disorder.

STUDY OBJECTIVES: Idiopathic/isolated REM-sleep behavior disorder (iRBD) often precedes the onset of synucleinopathies. Here, we investigated whether baseline resting-state EEG advanced spectral power and functional connectivity differ between iRBD patients who converted towards a synucleinopathy at follow-up and those who did not. METHODS: Eighty-one participants with iRBD (66.89±6.91 years) underwent a baseline resting-state EEG recording, a neuropsychological assessment and a neurological examination. We estimated EEG power spectral density using standard analyses and derived spectral estimates of rhythmic and arrhythmic components. Global and pairwise EEG functional connectivity analyses were computed using the weighted phase-lag index (wPLI). Pixel-based permutation tests were used to compare groups. RESULTS: After a mean follow-up of 5.01±2.76 years, 34 patients were diagnosed with a synucleinopathy (67.81±7.34 years) and 47 remained disease-free (65.53±7.09 years). Among patients who converted, 22 were diagnosed with Parkinson's disease and 12 with dementia with Lewy bodies. As compared to patients who did not convert, patients who converted exhibited at baseline higher relative theta standard power, steeper slopes of the arrhythmic component and higher theta rhythmic power mostly in occipital regions. Furthermore, patients who converted showed higher beta global wPLI but lower alpha wPLI between left temporal and occipital regions. CONCLUSION: Analyses of resting-state EEG rhythmic and arrhythmic components and functional connectivity suggest an imbalanced excitatory-to-inhibitory activity within large-scale networks, which is associated with later development of a synucleinopathy in iRBD patients.

How does parkinsonism start? Prodromal parkinsonism motor changes in idiopathic REM sleep behaviour disorder.

Parkinsonism, as a gradually progressive disorder, has a prodromal interval during which neurodegeneration has begun but cardinal manifestations have not fully developed. A systematic direct assessment of this interval has never been performed. Since patients with idiopathic REM sleep behaviour disorder are at very high risk of parkinsonism, they provide a unique opportunity to observe directly the development of parkinsonism. Patients with idiopathic REM sleep behaviour disorder in an ongoing cohort study were evaluated annually with several quantitative motor measures, including the Unified Parkinson's Disease Rating Scale, Purdue Pegboard, alternate-tap test and timed up-and-go. Patients who developed parkinsonism were identified from this cohort and matched according to age to normal controls. Their results on motor testing from the preceding years were plotted, and then assessed with regression analysis, to determine when markers first deviated from normal values. Sensitivity and specificity of quantitative motor markers for diagnosing prodromal parkinsonism were assessed. Of 78 patients, 20 developed parkinsonism. On regression analysis, the Unified Parkinson's Disease Rating Scale first intersected normal values at an estimated 4.5 years before diagnosis. Voice and face akinesia intersected earliest (estimated prodromal interval = 9.8 years), followed by rigidity (4.4 years), gait abnormalities (4.4 years) and limb bradykinesia (4.2 years). Quantitative motor tests intersected normal values at longer prodromal intervals than subjective examination (Purdue Pegboard = 8.6 years, alternate-tap = 8.2, timed up-and-go = 6.3). Using Purdue Pegboard and the alternate-tap test, parkinsonism could be detected with 71-82% sensitivity and specificity 3 years before diagnosis, whereas a Unified Parkinson's Disease Rating Scale score >4 identified prodromal parkinsonism with 88% sensitivity and 94% specificity 2 years before diagnosis. Removal of action tremor scores improved sensitivity to 94% and specificity to 97% at 2 years before diagnosis (cut-off >3). Although distinction between conditions was often difficult, prodromal dementia with Lewy bodies appeared to have a slower progression than Parkinson's disease (prodromal interval = 6.0 versus 3.8 years). Using a cut-off of Unified Parkinson's Disease Rating Scale >3 (excluding action tremor), 25% of patients with 'still-idiopathic' REM sleep behaviour disorder demonstrated evidence of possible prodromal parkinsonism. Therefore, using direct assessment of motor examination before parkinsonism in a REM sleep behaviour disorder, we have estimated a prodromal interval of ∼4.5 years on the Unified Parkinson's Disease Rating Scale; other quantitative markers may detect parkinsonism earlier. Simple quantitative motor measures may be capable of reliably detecting parkinsonism, even before a clinical diagnosis can be made by experienced movement disorders neurologists.

Markers of neurodegeneration in idiopathic rapid eye movement sleep behaviour disorder and Parkinson's disease.

Idiopathic rapid eye movement sleep behaviour disorder is an important risk factor in the development of Parkinson's disease. Numerous potential predictive markers of Parkinson's disease may present before motor symptoms emerge, but testing of these markers in rapid eye movement sleep behaviour disorder has been performed only in small studies. There has been no comparison of markers between patients with idiopathic rapid eye movement sleep behaviour disorder and Parkinson's disease, and between men and women. We evaluated an array of potential Parkinson's disease predictive markers in 159 patients; including 68 with idiopathic rapid eye movement sleep behaviour disorder, 36 controls, 34 Parkinson's patients with rapid eye movement sleep behaviour disorder and 21 Parkinson's patients without rapid eye movement sleep behaviour disorder. Compared with controls, patients with idiopathic rapid eye movement sleep behaviour disorder demonstrated substantial olfactory loss (P < 0.001). Olfaction was more impaired in Parkinson's disease than idiopathic rapid eye movement sleep behaviour disorder and did not differ between Parkinson's patients with, or without, rapid eye movement sleep behaviour disorder. Numerous measures of motor function including the Unified Parkinson Disease Rating Scale alternate tap, Purdue Peg Board and Timed 'Up and Go' were impaired in idiopathic rapid eye movement sleep behaviour disorder compared with controls (P < 0.01). All of these motor measures were worse with Parkinson's disease than with idiopathic rapid eye movement sleep behaviour disorder, regardless of rapid eye movement sleep behaviour disorder status. Autonomic symptoms and systolic blood pressure drop were impaired in patients with idiopathic rapid eye movement sleep behaviour disorder compared with controls (P = 0.003). Orthostatic abnormalities in Parkinson's disease were found in the group with rapid eye movement sleep behaviour disorder (P < 0.001). However, Parkinson's patients without rapid eye movement sleep behaviour disorder were not different than controls and had less impairment than those with idiopathic rapid eye movement sleep behaviour disorder (P = 0.004) and Parkinson's patients with rapid eye movement sleep behaviour disorder (P < 0.001). Colour vision was impaired in idiopathic rapid eye movement sleep behaviour disorder compared with controls (P < 0.001). However, only Parkinson's patients with rapid eye movement sleep behaviour disorder had abnormalities significantly different than controls (P < 0.001), and there were significant differences between Parkinson's patients with or without rapid eye movement sleep behaviour disorder (P < 0.04). Idiopathic rapid eye movement sleep behaviour disorder patients had slightly increased harm avoidance scores on personality testing (P = 0.04). Other than slightly better performances among women in the Purdue Peg Board, there was no difference in any measure between men and women, suggesting similar pathogenic processes underlying rapid eye movement sleep behaviour disorder. Patients with idiopathic rapid eye movement sleep behaviour disorder demonstrate abnormalities in numerous potential markers of neurodegenerative disease--these markers are heterogeneous, generally correlate with each other and occur equally in men and women. Although these abnormalities are usually intermediate between control values and Parkinson's patients, autonomic dysfunction and colour vision appear to be more linked to rapid eye movement sleep behaviour disorder status than Parkinson's disease, suggesting a unique pathophysiology of these abnormalities.

Identification of a sleep bruxism subgroup with a higher risk of pain.

Sleep bruxism research diagnostic criteria (SB-RDC) have been applied since 1996. This study was performed to validate these criteria and to challenge the hypothesis that pain is associated with lower frequencies of orofacial activities. Polygraphic recordings were made of 100 individuals presenting with a clinical diagnosis of sleep bruxism and 43 control individuals. TwoStep Cluster analyses (SPSS) were performed with sleep bruxism variables to reveal groupings among sleep bruxers and control individuals. Participants completed questionnaires during screening, diagnosis, and recording sessions. Cluster analysis identified three subgroups of sleep bruxers. Interestingly, 45 of the 46 sleep bruxers with values below SB-RDC were classified in the low-frequency cluster. These individuals were more likely to complain of pain and fatigue of masticatory muscles than were the higher-frequency sleep bruxers (odds ratios > 3.9, p < 0.01). Sleep bruxers were distributed among three heterogeneous groups. Sleep bruxers with low frequencies of orofacial activities were more at risk of reporting pain.

Parkinson's Disease Genetic Loci in Rapid Eye Movement Sleep Behavior Disorder.

Rapid eye movement (REM) sleep behavior disorder (RBD) is a prodromal condition for Parkinson's disease (PD) and other synucleinopathies, which often occurs many years before the onset of PD. We analyzed 261 RBD patients and 379 controls for nine PD-associated SNPs and examined their effects, first upon on RBD risk and second, on eventual progression to synucleinopathies in a prospective follow-up in a subset of patients. The SCARB2 rs6812193 (OR = 0.67, 95 % CI = 0.51-0.88, p = 0.004) and the MAPT rs12185268 (OR-0.43, 95 % CI-0.26-0.72, p = 0.001) were associated with RBD in different models. Kaplan-Meier survival analysis in a subset of RBD patients (n = 56), demonstrated that homozygous carriers of the USP25 rs2823357 SNP had progressed to synucleinopathies faster than others (log-rank p = 0.003, Breslow p = 0.005, Tarone-Ware p = 0.004). As a proof-of-concept study, these results suggest that RBD may be associated with at least a subset of PD-associated genes, and demonstrate that combining genetic and prodromal clinical data may help identifying individuals that are either more or less susceptible to develop synucleinopathies. More studies are necessary to replicate these results, and identify more genetic factors affecting progression from RBD to synucleinopathies.

Randomized, double-blind, placebo-controlled crossover trial of modafinil in the treatment of excessive daytime sleepiness in narcolepsy.

Seventy-five patients meeting international diagnostic criteria for narcolepsy enrolled in a 6-week, three-period, randomized, crossover, placebo-controlled trial. Patients received placebo, modafinil 200 mg, or modafinil 400 mg in divided doses (morning and noon). Evaluations occurred at baseline and at the end of each 2-week period. Compared with placebo, modafinil 200 and 400 mg significantly increased the mean sleep latency on the Maintenance of Wakefulness Test by 40% and 54%, with no significant difference between the two doses. Modafinil, 200 and 400 mg, also reduced the combined number of daytime sleep episodes and periods of severe sleepiness noted in sleep logs. The likelihood of falling asleep as measured by the Epworth Sleepiness Scale was equally reduced by both modafinil dose levels. There were no effects on nocturnal sleep initiation, maintenance, or architecture, nor were there any effects on sleep apnea or periodic leg movements. Neither dose interfered with the patients' ability to nap voluntarily during the day nor with their quantity or quality of nocturnal sleep. Modafinil produced no changes in blood pressure or heart rate in either normotensive or hypertensive patients. The only significant adverse effects were seen at the 400-mg dose, which was associated with more nausea and more nervousness than either placebo or the 200-mg dose. As little as a 200-mg daily dose of modafinil is therefore an effective and well-tolerated treatment of excessive daytime somnolence in narcoleptic persons.

Restless legs syndrome and sleep bruxism: prevalence and association among Canadians.

A survey conducted through personal interviews was done in Canada to estimate the prevalence of subjective symptoms related to restless legs syndrome (RLS) and to sleep bruxism. Of the 2,019 respondents, all over 18 years of age, 15% reported leg restlessness at bedtime; 10% reported unpleasant leg muscle sensations associated with awakening during sleep and with the irresistible need to move or walk. Both these complaints are related to RLS. The prevalence of RLS-related symptoms increased linearly with age. Tooth grinding, a symptom related to sleep bruxism, was reported by 8% of the subjects; in contrast to RLS-related symptoms, the prevalence of tooth grinding decreased linearly with age. RLS-related symptoms were reported more frequently in Eastern provinces than in Ontario and Western Canada, and more frequently in Roman Catholic and French-speaking responders. This was not the case for sleep bruxism; between 14.5% and 17.3% of the subjects who reported subjective RLS-related symptoms also reported tooth grinding. Conversely, 9.6-10.9% of the tooth grinders reported RLS-related symptoms. These data suggest that both sleep movement disorders can be concomitant and that socio-geographic and age characteristics influence the prevalence of reports.

Lower number of K-complexes and K-alphas in sleep bruxism: a controlled quantitative study.

OBJECTIVES: Although patients with sleep bruxism (SB) show a higher incidence of rhythmic masticatory muscle activity (RMMA) during sleep than matched normal controls, they are good sleepers. Sleep macrostructure (e.g. total sleep time, sleep latency, number of awakenings or sleep stage shifts and sleep stage duration) is similar between groups. Differences in sleep microstructure between SB patients and normals have been investigated only in few studies. The aim of the present study was to quantify number of microarousals, K-complexes, K-alphas, EEG spindles, and the density of slow wave activity, in both groups, in order to better understand the pathophysiology of SB. METHODS: Ten normal sleepers were matched for age and gender with 10 patients who exhibited frequent tooth-grinding during sleep. Using quantitative polysomnographic measures, we compared the above-mentioned sleep variables in both groups. Data are presented as indices for total sleep and for consecutive non-rapid eye movement (non-REM) episodes over non-REM to rapid eye movement (REM) cycles and per hour of sleep. RESULTS: SB patients showed 6 times more RMMA episodes per hour of sleep than normals (P<0.001), with a higher frequency in the second and third non-REM to REM cycles. SB patients presented 42.7% fewer K-complexes per hour of stage 2 sleep, but only normals showed a decline from the first to fourth non-REM episode. Only 24% of SB-RMMA episodes were associated with K-complexes in 60 s. The number of K-alphas was 61% lower in SB patients, no change across non-REM episodes was noted. While no difference in electroencephalographic (EEG) spindles or slow wave activity (SWA) was observed between groups, EEG spindles increased and SWA decreased linearly over consecutive non-REM to REM cycles. CONCLUSIONS: According to our observations, good sleep in SB patients is characterized by a low incidence of K-complexes or K-alphas and by the absence of any difference in other sleep microstructure variables or SWA.

Sleep bruxism: validity of clinical research diagnostic criteria in a controlled polysomnographic study.

The clinical validity of diagnostic criteria for sleep orofacial motor activity--more specifically, bruxism--has never been tested. Polysomnographic recordings from 18 bruxers and 18 asymptomatic subjects, selected according to American Sleep Disorders Association criteria, were analyzed (1) to discriminate sleep bruxism from other orofacial motor activities and (2) to calculate sensitivity, specificity, and predictive values of research criteria. Clinical observations and reports revealed that all 18 bruxers reported frequent tooth-grinding during sleep. Tooth wear was noted in 16 out of 18 bruxers and jaw discomfort reported by six of them. These findings were present in none of the controls. The analysis of polysomnographic data showed that the asymptomatic subjects presented a mean of 1.7 +/- 0.3 bruxism episodes per hour of sleep (sustained or repetitive bursting activity in jaw closer muscles), while bruxers had a significantly higher level of activity: 5.4 +/- 0.6. Controls exhibited 4.6 +/- 0.3 bruxism bursts per episode and 6.2 (from 0 to 23) bruxism bursts per hour of sleep, whereas bruxers showed, respectively, 7.0 +/- 0.7 and 36.1 (5.8 to 108). Bruxism-like episodes with at least two grinding sounds were noted in 14 of the 18 bruxers and in one control. The two groups exhibited no difference in any of the sleep parameters. Based on the present findings, the following polysomnographic diagnostic cut-off criteria are suggested: (1) more than 4 bruxism episodes per hour, (2) more than 6 bruxism bursts per episode and/or 25 bruxism bursts per hour of sleep, and (3) at least 2 episodes with grinding sounds. When the polysomnographic bruxism-related variables were combined under logistic regression, the clinical diagnosis was correctly predicted in 81.3% of the controls and 83.3% of the bruxers. The validity of these clinical research criteria needs now to be challenged in a larger population, over time, and in subjects presenting various levels of severity of sleep bruxism.

Striatal D2 receptor binding in sleep bruxism: a controlled study with iodine-123-iodobenzamide and single-photon-emission computed tomography.

The neurochemical mechanisms underlying sleep bruxism are little understood at present. However, recent pharmacologic evidence suggests that the central dopaminergic system may be involved in the pathophysiology of sleep bruxism. This possibility was further assessed by means of functional neuroimaging of dopamine D2 receptors with single-photon-emission computed tomography (SPECT). Ten controls and ten patients with polysomnographically confirmed sleep bruxism were injected intravenously with 185 MBq (5 mCi) iodine-123-iodobenzamide, a specific D2 receptor antagonist radioligand, and data acquisition was performed 90 min post-injection. Following image reconstruction, it was found that striatal D2 receptor binding potential (basal ganglia/background ratio) did not differ significantly between bruxism patients and controls. However, side-to-side differences between unilateral values of the striatal D2 binding potential ("highest side" values minus "lowest side" values) were significantly larger for the bruxism patients (p < 0.001, by two-independent-samples t test with pooled variances). It was concluded that an abnormal side imbalance in striatal D2 receptor expression can be associated with sleep bruxism. This reinforces the possibility that the central dopaminergic system plays a role in the pathophysiology of this disorder.

Evidence that experimentally induced sleep bruxism is a consequence of transient arousal.

Spontaneous rhythmic masticatory muscle activity (RMMA) during sleep occurs more frequently following spontaneous transient micro-arousal in patients with sleep bruxism (SB) and normal controls. Here, we tested the hypothesis that an experimental arousal would be followed by an increase in RMMA. We identified RMMA on polygraphic recordings taken before and after sensory stimulation to induce experimental arousal in eight SB patients and eight matched normal subjects. The rate of experimental arousal and the level of resting electromyographic activity in masseter and suprahyoid muscles during sleep did not differ between the groups. In both, muscle tone and heart rate increased during the experimental arousal. Although post-arousal RMMA occurred in all SB patients, it was seen in only one normal subject. Moreover, tooth-grinding occurred during 71% of the evoked RMMA in SB patients. These results support the hypothesis that SB is an exaggerated form of oromotor activity associated with sleep micro-arousal.

Sleep bruxism: an oromotor activity secondary to micro-arousal.

Spontaneous rhythmic masticatory muscle activity (RMMA) during sleep occurs in relation to transient activation in the cerebral and autonomic nervous systems of normal subjects and in patients with sleep bruxism (SB). In this study, we made a quantitative assessment of the sequential changes in cortical electroencephalographic (EEG) and autonomic-cardiac activities associated with micro-arousals preceding RMMA episodes. We matched 10 SB patients with 10 normal subjects. The onset of RMMA episodes was defined in terms of the onset of activation in the suprahyoid muscles. In SB patients, an increase in cortical EEG activity was observed 4 seconds before the onset of suprahyoid activity in 79% of episodes. A significant acceleration in heart rate was initiated one cardiac cycle before RMMA onset. A clear sequence of cortical to autonomic-cardiac activation precedes jaw motor activity in SB patients. This suggests that SB is a powerful oromotor manifestation secondary to micro-arousal.

Rhythmic masticatory muscle activity during sleep in humans.

Rhythmic Masticatory Muscle Activity (RMMA) is frequently observed during sleep in normal subjects and sleep bruxers. We hypothesized that some normal subjects exhibit RMMA at a lower frequency than sleep bruxers. Polysomnographic data from 82 normal subjects were compared with data from 33 sleep bruxers. RMMA episodes were defined as three or more consecutive bursts of masseter EMG activity, with or without tooth-grinding. Such episodes were observed in nearly 60% of normal subjects. A lower frequency of episodes was noted in normal subjects than in bruxers. Sleep organization was similar between groups. Bruxers had twice as many masseter muscle bursts per episode and episodes of higher amplitude compared with controls with RMMA. The high prevalence of RMMA observed in normal subjects suggests that this activity is related to certain sleep-related physiological functions, including autonomic activation.

Effects of the D2 receptor agonist bromocriptine on sleep bruxism: report of two single-patient clinical trials.

An altered dopamine receptor status has been associated with sleep bruxism. Evidence from a functional neuro-imaging study has implicated an abnormal side imbalance in striatal D2 receptor expression in its pathophysiology. To assess the significance of this finding, we studied the effects of short-term administration of the preferential dopamine D2 receptor agonist bromocriptine on sleep bruxism in a double-blind, placebo-controlled polysomnographic and neuro-imaging study with a single crossover design. Six otherwise healthy and drug-free patients with sleep bruxism were entered into the trial. One of the patients dropped out due to an intercurrent illness, while three others were discontinued from the study due to severe adverse reactions to bromocriptine. Because of the high frequency and intensity of the side-effects, the trial was interrupted. Two patients, however, completed the trial without any adverse reactions. Their outcome measures are presented as single-patient clinical trials. Following a two-week administration of bromocriptine, both patients showed a decrease in the number of bruxism episodes per hour of sleep of about 20% to 30% with respect to the placebo. WHile no significant differences between both conditions (i.e., placebo and bromocriptine) were found for the number of bruxism bursts per episode, significantly lower root-mean-squared EMG levels per bruxism burst occurred during bromocriptine use. In association with this polysomnographically established attenuation of sleep bruxism, bromocriptine afforded a decreased normal side distribution of striatal D2 receptor binding, as was evidenced by single-photon-emission computed tomography using the radioactive D2 receptor antagonist iodine-123-iodobenzamide. This study supports previous suggestions that the central dopaminergic system may be involved in the modulation of sleep bruxism. To see if the present findings apply across a population, investigators should use a peripheral D-2 antagonist to prevent side-effects.

Double-blind, crossover, placebo-controlled trial of bromocriptine in patients with sleep bruxism.

This study was designed to assess the effects of bromocriptine, a dopamine D2 receptor agonist, on sleep bruxism. Seven otherwise healthy patients with severe and frequent sleep bruxism participated in this randomized, double-blind, placebo-controlled study. The study used a crossover design that included 2 weeks of active treatment or placebo with a washout period of 1 week. To further evaluate whether bromocriptine influences striatal D2 receptor binding, we used iodine-123-iodobenzamide single photon emission computed tomography (SPECT) under both placebo and bromocriptine regimens. Bromocriptine did not reduce the frequency of episodes of bruxism during sleep (mean +/- SEM, 9.0 +/- 1.0 and 9.6 +/- 1.5 bruxism episodes per hour for placebo and bromocriptine, respectively) or the amplitude of masseter muscle contractions (root mean square values, 48.2 +/- 15.5 microV and 46.9 +/- 12.7 microV for placebo and bromocriptine, respectively). SPECT also failed to reveal that either treatment had any influence on striatal D2 binding (values for total binding in counts/pixel, 1.80 [1.72-1.93] and 1.79 [1.56-1.87] for placebo and bromocriptine, respectively). This study shows that a nightly dose of bromocriptine does not exacerbate or reduce sleep bruxism motor activity.

Relationship between sleep, neck muscle activity, and pain in cervical dystonia.

OBJECTIVE: The interactions between sleep, neck muscle activity, and cervical spinal pain were examined in a controlled study with nine patients suffering from idiopathic cervical dystonia (ICD; also referred to as spasmodic torticollis), and nine gender- and age-matched controls. METHODS: From each participant, two all-night polysomnograms with additional electromyographic recordings from the sternocleidomastoid and upper trapezius muscles were obtained. The first night was for habituation to the laboratory environment; the second night for experimental data collection. Visual analogue scales were used to collect intensity and unpleasantness ratings of cervical spinal pain before and after the second sleep recording. RESULTS: None of the standard sleep variables showed statistically significant differences between average values of both groups of participants. However, a significantly larger variance in sleep latency was obtained for the ICD patients. In general, abnormal cervical muscle activity decreased immediately when lying down without the intention to go to sleep. Subsequently, abnormal muscle contractions were gradually abolished in all ICD patients during the transition from relaxed wakefulness to light NREM sleep. Following this transition phase, no more abnormal EMG activity was found in any of our patients. Finally, cervical spinal pain intensity and unpleasantness were reduced by about 50% overnight. CONCLUSIONS: Both supine position and sleep can be associated with an improvement of symptoms of ICD, and this disorder does not induce any sleep perturbations.

Lack of associations between occlusal and cephalometric measures, side imbalance in striatal D2 receptor binding, and sleep-related oromotor activities.

AIMS: First, to evaluate possible orofacial morphologic differences between sleep bruxers and non-bruxers, and second, to determine possible correlations between morphologic factors and striatal D2 receptor expression in persons with sleep-related oromotor activities. METHODS: Twenty subjects were included in this study; half of them had polysomnographically confirmed oromotor values above the cutoff points for sleep bruxism. For all participants, 26 standard occlusal measures were recorded clinically and from dental study casts. In addition, 25 standard angular and linear measures were taken from standardized cephalometric films, and variables were derived to evaluate dental and skeletal relationships. Fourteen of the 20 participants had also participated in a previous study that included iodine-123-iodobenzamide (I-123-IBZM) and single-photon emission-computed tomography (SPECT). For them, the side-to-side difference in striatal D2 receptor binding was determined as the neurochemical outcome measure. RESULTS: Following the classical Bonferroni adjustment for multiple testing, no morphologic differences were found between the sleep bruxers and the non-bruxers. In addition, none of the morphologic variables were significantly associated with the neuroimaging data. CONCLUSION: Taking into account the low power of this retrospective, exploratory study, the results suggest that the orofacial morphology of sleep bruxers does not differ from that of non-bruxers. In addition, morphologic factors are probably not involved in the asymmetry in striatal D2 receptor distribution that was previously observed in association with sleep bruxism.

Bruxism and orofacial movements during sleep.

Several issues remain to be clarified in the future research and management of SB. It is important to differentiate SB from other normal sleep orofacial activities and concomitant sleep disorders. Other orofacial activities may obscure the diagnosis of SB and may give an ambiguous clinical picture when evaluating treatment efficacy. Laboratory recordings provide a more specific diagnosis. Most of the clinical signs (e.g., tooth wear, masseter hypertrophy) are not exclusive to SB but could be concomitant with other habits or activities during wakefulness. No pathologic features in the central nervous system, such as a dysfunction of the dopaminergic system, have been observed in SB patients. Recent neurophysiologic studies have suggested that SB is a powerful microarousal event associated with central and autonomic nervous system activity during sleep. The additive contribution of psychosocial stress cannot be overlooked. There have been no recent major breakthroughs in SB management. Cognitive and behavioral managements, which include stress management, lifestyle changes, or improved coping mechanisms, may be beneficial. Oral splint appliances are useful to protect teeth from damage. A few medications (e.g., benzodiazepines, muscle relaxants) may be helpful for a short-term period, particularly when there is secondary pain, but controlled studies are needed to assess their efficacy, safety, and patient acceptance and tolerance.

Bruxism: A factor associated with temporomandibular disorders and orofacial pain.

Rhythmic masticatory muscle activities are probably part of normal jaw motor behavior. Certain factors, like disease, stress, personality, alcohol, and medication, may turn this normal activity into a condition that might include abnormal tooth wear, myofascial pain, and temporomandibular joint problems. This condition then corresponds with bruxism. Bruxism and masticatory muscle pain may reciprocally influence one another: although not a compulsory finding, bruxism may be associated with the predisposition, initiation, and perpetuation of temporomandibular disorders and orofacial pain. On the other hand, the presence of jaw muscle pain may reduce bruxism motor activity. Research on the integrity and nature of the relationship between bruxism and pain is hampered by controversies that exist regarding definition, diagnostic criteria, and measurement techniques. Moreover, the pathophysiology of bruxism and its association with other sleep-related and movement disorders are still unclear. Consequently, there is no real cure for bruxism, although several treatments may be used to control its adverse effects. However, there is very limited research to support the efficacy of behavioral, physical, dental, pharmacological, and orthopedic treatments. Probably the best current treatment modality for bruxism is the occlusal stabilization splint. Although such an orthopedic device may not actually prevent bruxism, it may help to reduce its symptoms.