Sleep bruxism and its associations with insomnia and OSA in the general population of Sao Paulo.

Sleep bruxism (SB) is characterized by recurrent masticatory muscle activity during sleep with occasional tooth grinding. SB can be concomitant with sleep apnea although its association with insomnia is understudied. STUDY OBJECTIVE: Assess the strength of the associations between SB, insomnia and sleep apnea in a general population. METHODS: Data from the 2007 EPISONO general population study (n = 1042; Sao Paulo, Brazil) were reused for the present analyses. The data was collected from polysomnography (PSG) and from a questionnaire. SB could only be assessed as "possible" with self-report questionnaires, but as "definitive" with both self-reports and PSG. Logistic regression and decision tree analyses were performed. RESULTS: Logistic regression analyses revealed that being male, overweight, obese, having an apnea/hypopnea index (AHI) above 30 and insomnia syndrome are among risk factors for SB (prevalence ratio (PR): 1.5-3.3). A high AHI and insomnia syndrome had similar PRs, 2.7 and 2.8, respectively. Decision tree analysis showed that insomnia syndrome contributed to the predictive accuracy of SB self-report (88%). A similar estimate (91%) was observed with SB PSG data. Correspondence analysis illustrated three age profiles in participants: (1) good sleepers aged 20-35 years, (2) females aged 35-50 years with SB and concomitant insomnia syndrome, and (3) participants aged ≥ 50 years with obesity and sleep apnea. CONCLUSIONS: Insomnia is likely a condition associated with SB, especially in middle-age females, while sleep apnea seems age and gender dependent. Such overlap may influence the treatment decision to achieve best outcomes. CLINICAL TRIAL REGISTRATION: EPISONO study; Clinical trials.gov ID # NCT00596713.

Critical Issues in Dental and Medical Management of Obstructive Sleep Apnea.

This critical review focuses on obstructive sleep apnea (OSA) and its management from a dental medicine perspective. OSA is characterized by ≥10-s cessation of breathing (apnea) or reduction in airflow (hypopnea) ≥5 times per hour with a drop in oxygen and/or rise in carbon dioxide. It can be associated with sleepiness and fatigue, impaired mood and cognition, cardiometabolic complications, and risk for transportation and work accidents. Although sleep apnea is diagnosed by a sleep physician, its management is interdisciplinary. The dentist's role includes 1) screening patients for OSA risk factors (e.g., retrognathia, high arched palate, enlarged tonsils or tongue, enlarged tori, high Mallampati score, poor sleep, supine sleep position, obesity, hypertension, morning headache or orofacial pain, bruxism); 2) referring to an appropriate health professional as indicated; and 3) providing oral appliance therapy followed by regular dental and sleep medical follow-up. In addition to the device features and provider expertise, anatomic, behavioral, demographic, and neurophysiologic characteristics can influence oral appliance effectiveness in managing OSA. Therefore, OSA treatment should be tailored to each patient individually. This review highlights some of the putative action mechanisms related to oral appliance effectiveness and proposes future research directions.

International consensus on the assessment of bruxism: Report of a work in progress.

In 2013, consensus was obtained on a definition of bruxism as repetitive masticatory muscle activity characterised by clenching or grinding of the teeth and/or by bracing or thrusting of the mandible and specified as either sleep bruxism or awake bruxism. In addition, a grading system was proposed to determine the likelihood that a certain assessment of bruxism actually yields a valid outcome. This study discusses the need for an updated consensus and has the following aims: (i) to further clarify the 2013 definition and to develop separate definitions for sleep and awake bruxism; (ii) to determine whether bruxism is a disorder rather than a behaviour that can be a risk factor for certain clinical conditions; (iii) to re-examine the 2013 grading system; and (iv) to develop a research agenda. It was concluded that: (i) sleep and awake bruxism are masticatory muscle activities that occur during sleep (characterised as rhythmic or non-rhythmic) and wakefulness (characterised by repetitive or sustained tooth contact and/or by bracing or thrusting of the mandible), respectively; (ii) in otherwise healthy individuals, bruxism should not be considered as a disorder, but rather as a behaviour that can be a risk (and/or protective) factor for certain clinical consequences; (iii) both non-instrumental approaches (notably self-report) and instrumental approaches (notably electromyography) can be employed to assess bruxism; and (iv) standard cut-off points for establishing the presence or absence of bruxism should not be used in otherwise healthy individuals; rather, bruxism-related masticatory muscle activities should be assessed in the behaviour's continuum.

Depressive symptoms account for differences between self-reported versus polysomnographic assessment of sleep quality in women with myofascial TMD.

Patients with temporomandibular disorder (TMD) report poor sleep quality on the Pittsburgh Sleep Quality Index (PSQI). However, polysomnographic (PSG) studies show meagre evidence of sleep disturbance on standard physiological measures. The present aim was to analyse self-reported sleep quality in TMD as a function of myofascial pain, PSG parameters and depressive symptomatology. PSQI scores from 124 women with myofascial TMD and 46 matched controls were hierarchically regressed onto TMD presence, ratings of pain intensity and pain-related disability, in-laboratory PSG variables and depressive symptoms (Symptoms Checklist-90). Relative to controls, TMD cases had higher PSQI scores, representing poorer subjective sleep and more depressive symptoms (both P < 0·001). Higher PSQI scores were strongly predicted by more depressive symptoms (P < 0·001, R2 = 26%). Of 19 PSG variables, two had modest contributions to higher PSQI scores: longer rapid eye movement latency in TMD cases (P = 0·01, R2 = 3%) and more awakenings in all participants (P = 0·03, R2 = 2%). After accounting for these factors, TMD presence and pain ratings were not significantly related to PSQI scores. These results show that reported poor sleep quality in TMD is better explained by depressive symptoms than by PSG-assessed sleep disturbances or myofascial pain. As TMD cases lacked typical PSG features of clinical depression, the results suggest a negative cognitive bias in TMD and caution against interpreting self-report sleep measures as accurate indicators of PSG sleep disturbance. Future investigations should take account of depressive symptomatology when interpreting reports of poor sleep.

The Neurobiology of Orofacial Pain and Sleep and Their Interactions.

This article provides an overview of the neurobiology of orofacial pain as well as the neural processes underlying sleep, with a particular focus on the mechanisms that underlie pain and sleep interactions including sleep disorders. Acute pain is part of a hypervigilance system that alerts the individual to injury or potential injury of tissues. It can also disturb sleep. Disrupted sleep is often associated with chronic pain states, including those that occur in the orofacial region. The article presents many insights that have been gained in the last few decades into the peripheral and central mechanisms involved in orofacial pain and its modulation, as well as the circuits and processes in the central nervous system that underlie sleep. Although it has become clear that sleep is essential to preserve and maintain health, it has also been found that pain, particularly chronic pain, is commonly associated with disturbed sleep. In the presence of chronic pain, a circular relationship may prevail, with mutual deleterious influences causing an increase in pain and a disruption of sleep. This article also reviews findings that indicate that reducing orofacial pain and improving sleep need to be targeted together in the management of acute to chronic orofacial pain states in order to improve an orofacial pain patient's quality of life, to prevent mood alterations or exacerbation of sleep disorder (e.g., insomnia, sleep-disordered breathing) that can negatively affect their pain, and to promote healing and optimize their health.

Could transient hypoxia be associated with rhythmic masticatory muscle activity in sleep bruxism in the absence of sleep-disordered breathing? A preliminary report.

Sleep bruxism (SB) is a repetitive jaw-muscle activity characterised by clenching or grinding of the teeth during sleep. Sleep bruxism activity is characterised by rhythmic masticatory muscle activity (RMMA). Many but not all RMMA episodes are associated with sleep arousal. The aim of this study was to evaluate whether transient oxygen saturation level change can be temporally associated with genesis of RMMA/SB. Sleep laboratory or home recordings data from 22 SB (tooth grinding history in the absence of reported sleep-disordered breathing) and healthy subjects were analysed. A total of 143 RMMA/SB episodes were classified in four categories: (i) no arousal + no body movement; (ii) arousal + no body movement; (iii) no arousal + body movement; (iv) arousal + body movement. Blood oxygen levels (SaO2 ) were assessed from finger oximetry signal at the baseline (before RMMA), and during RMMA. Significant variation in SaO2 over time (P = 0·001) was found after RMMA onset (+7 to +9 s). No difference between categories (P = 0·91) and no interaction between categories and SaO2 variation over time (P = 0·10) were observed. SaO2 of six of 22 subjects (27%) remained equal or slight increase after the RMMA/SB onset (+8 s) compared to baseline; 10 subjects (45%) slightly decreased (drop 0·01-1%) and the remaining (27%) decreased between 1% and 2%. These preliminary findings suggest that a subgroup of SB subjects had (i) a minor transient hypoxia potentially associated with the onset of RMMA episodes, and this (ii) independently of concomitant sleep arousal or body movements.

Validity of self-reported sleep bruxism among myofascial temporomandibular disorder patients and controls.

Sleep bruxism (SB), primarily involving rhythmic grinding of the teeth during sleep, has been advanced as a causal or maintenance factor for a variety of oro-facial problems, including temporomandibular disorders (TMD). As laboratory polysomnographic (PSG) assessment is extremely expensive and time-consuming, most research testing this belief has relied on patient self-report of SB. The current case-control study examined the accuracy of those self-reports relative to laboratory-based PSG assessment of SB in a large sample of women suffering from chronic myofascial TMD (n = 124) and a demographically matched control group without TMD (n = 46). A clinical research coordinator administered a structured questionnaire to assess self-reported SB. Participants then spent two consecutive nights in a sleep laboratory. Audiovisual and electromyographic data from the second night were scored to assess whether participants met criteria for the presence of 2 or more (2+) rhythmic masticatory muscle activity episodes accompanied by grinding sounds, moderate SB, or severe SB, using previously validated research scoring standards. Contingency tables were constructed to assess positive and negative predictive values, sensitivity and specificity, and 95% confidence intervals surrounding the point estimates. Results showed that self-report significantly predicted 2+ grinding sounds during sleep for TMD cases. However, self-reported SB failed to significantly predict the presence or absence of either moderate or severe SB as assessed by PSG, for both cases and controls. These data show that self-report of tooth grinding awareness is highly unlikely to be a valid indicator of true SB. Studies relying on self-report to assess SB must be viewed with extreme caution.

[Placebo analgesia and sleep]. / Analgésie placebo et sommeil.

The placebo response is a psychobiological phenomenon for clinical benefits following the administration of an inert substance whatever its form. This phenomenon can be attributed to a wide range of neurobiological processes, such as expectations of relief, the Pavlovian conditioning and learning, emotional regulation, and reward mechanisms, which are themselves under the influence of processes that take place during sleep. The study of placebo analgesia in healthy from a placebo conditioning associated with analgesic suggestions has highlighted a relationship between sleep, expectations of relief and placebo analgesia: when the induction is persuasive before sleep, expectations of relief modulate placebo response the next morning and paradoxical sleep correlates negatively with both expectations and the placebo response. When the analgesic experience before sleep is less persuasive, expectations of relief are still present but no longer interact with placebo analgesia while paradoxical sleep no longer correlates with the analgesic placebo response. Sleep-processes especially during paradoxical sleep seem to influence the relationship between expectations of relief and placebo analgesia. In this review, we describe the relationship between sleep and placebo analgesia, the mechanisms involved in the placebo response (e.g., conditioning, learning, memory, reward) and their potential link with sleep that could make it a special time for the building placebo response.

Masticatory muscle sleep background electromyographic activity is elevated in myofascial temporomandibular disorder patients.

Despite theoretical speculation and strong clinical belief, recent research using laboratory polysomnographic (PSG) recording has provided new evidence that frequency of sleep bruxism (SB) masseter muscle events, including grinding or clenching of the teeth during sleep, is not increased for women with chronic myofascial temporomandibular disorder (TMD). The current case-control study compares a large sample of women suffering from chronic myofascial TMD (n = 124) with a demographically matched control group without TMD (n = 46) on sleep background electromyography (EMG) during a laboratory PSG study. Background EMG activity was measured as EMG root mean square (RMS) from the right masseter muscle after lights out. Sleep background EMG activity was defined as EMG RMS remaining after activity attributable to SB, other orofacial activity, other oromotor activity and movement artefacts were removed. Results indicated that median background EMG during these non-SB event periods was significantly higher (P < 0·01) for women with myofascial TMD (median = 3·31 µV and mean = 4·98 µV) than for control women (median = 2·83 µV and mean = 3·88 µV) with median activity in 72% of cases exceeding control activity. Moreover, for TMD cases, background EMG was positively associated and SB event-related EMG was negatively associated with pain intensity ratings (0-10 numerical scale) on post-sleep waking. These data provide the foundation for a new focus on small, but persistent, elevations in sleep EMG activity over the course of the night as a mechanism of pain induction or maintenance.

The effect of surgically assisted rapid maxillary expansion on sleep architecture: an exploratory risk study in healthy young adults.

Maxillary transverse deficiencies (MTD) cause malocclusions. Rapid maxillary expansion treatment is commonly used treatment for correcting such deficiencies and has been found to be effective in improving respiration and sleep architecture in children with obstructive sleep apnoea (OSA). However, thus far, the effect of surgically assisted rapid maxillary expansion (SARME) treatment on sleep architecture and breathing of normal subjects has not been assessed. We hypothesised that sleep quality will improve after maxillary expansion treatment. The objective of this study is to access the effect of maxillary expansion treatment on sleep structure and respiratory functions in healthy young adults with severe MTD. This is a prospective and exploratory clinical study. Twenty-eight consecutive young adult patients (15 males and 13 females, mean age 20·6 ± 5·8 years) presenting with severe MTD at the orthodontic examination were recruited into the study. All the participants underwent a standardised SARME procedure (mean expansion 6·5 ± 1·8 and 8·2 ± 1·8 mm, intercanine and intermolar distance, respectively) to correct malocclusion caused by MTD. An overnight in-laboratory polysomnography, before and after the treatment, was performed. The mean follow-up time was 9 months. The main outcome parameters were the changes in sleep architecture, including sleep stages, arousals, slow-wave activity (SWA) and respiratory variables. Before surgery, young adult patients with MTD presented no evidence of sleep breathing problems. At baseline sleep recording, 7 of 28 (25%) had apnoea-hypopnoea index (AHI) ≥ 5 events per hour. No negative effect of the SARME was observed in questionnaires or sleep laboratory parameters. In the patients with a higher baseline AHI (AHI ≥ 5 h of sleep), we observed a reduction in AHI after surgical treatment (P = 0·028). SARME did not have a negative effect on any sleep or respiration parameters in healthy young individuals with MTD. It normalised the breathing index in the patients with a mild AHI index.

Bruxism defined and graded: an international consensus.

To date, there is no consensus about the definition and diagnostic grading of bruxism. A written consensus discussion was held among an international group of bruxism experts as to formulate a definition of bruxism and to suggest a grading system for its operationalisation. The expert group defined bruxism as a repetitive jaw-muscle activity characterised by clenching or grinding of the teeth and/or by bracing or thrusting of the mandible. Bruxism has two distinct circadian manifestations: it can occur during sleep (indicated as sleep bruxism) or during wakefulness (indicated as awake bruxism). For the operationalisation of this definition, the expert group proposes a diagnostic grading system of 'possible', 'probable' and 'definite' sleep or awake bruxism. The proposed definition and grading system are suggested for clinical and research purposes in all relevant dental and medical domains.

Comparison of ambulatory and polysomnographic recording of jaw muscle activity during sleep in normal subjects.

Clinicians and investigators need a simple and reliable recording device to diagnose or monitor sleep bruxism (SB). The aim of this study was to compare recordings made with an ambulatory electromyographic telemetry recorder (TEL-EMG) with those made with standard sleep laboratory polysomnography with synchronised audio-visual recording (PSG-AV). Eight volunteer subjects without current history of tooth grinding spent one night in a sleep laboratory. Simultaneous bilateral masseter EMG recordings were made with a TEL-EMG and standard PSG. All types of oromotor activity and rhythmic masseter muscle activity (RMMA), typical of SB, were independently scored by two individuals. Correlation and intra-class coefficient (ICC) were estimated for scores on each system. The TEL-EMG was highly sensitive to detect RMMA (0·988), but with low positive predictive value (0·231) because of a high rate of oromotor activity detection (e.g. swallowing and scratching). Almost 72% of false-positive oromotor activity scored with the TEL-EMG occurred during the transient wake period of sleep. A non-significant correlation between recording systems was found (r = 0·49). Because of the high frequency of wake periods during sleep, ICC was low (0·47), and the removal of the influence of wake periods improved the detection reliability of the TEL-EMG (ICC = 0·88). The TEL-EMG is sensitive to detect RMMA in normal subjects. However, it obtained a high rate of false-positive detections because of the presence of frequent oromotor activities and transient wake periods of sleep. New algorithms are needed to improve the validity of TEL-EMG recordings.

Sleep bruxism and sleep arousal: an experimental challenge to assess the role of cyclic alternating pattern.

Rhythmic masticatory muscle activity (RMMA) is the characteristic electromyographic pattern of sleep bruxism (SB), a sleep-related motor disorder associated with sleep arousal. Sleep arousals are generally organised in a clustered mode known as the cyclic alternating pattern (CAP). CAP is the expression of sleep instability between sleep maintaining processes (phase A1) and stronger arousal processes (phases A2 and A3). This study aimed to investigate the role of sleep instability on RMMA/SB occurrence by analysing CAP and electroencephalographic (EEG) activities. The analysis was performed on the sleep recordings of 8 SB subjects and 8 controls who received sensory stimulations during sleep. Baseline and experimental nights were compared for sleep variables, CAP, and EEG spectral analyses using repeated measure ANOVAs. Overall, no differences in sleep variables and EEG spectra were found between SB subjects and controls. However, SB subjects had higher sleep instability (more phase A3) than controls (P= 0·05). The frequency of phase A3 was higher in the pre-REM sleep periods (P < 0·001), where peaks in RMMA/SB activity were also observed (P = 0·05). When sleep instability was experimentally increased by sensory stimuli, both groups showed an enhancement in EEG theta and alpha power (P = 0·04 and 0·02, respectively) and significant increases in sleep arousal and all CAP variables. No change in RMMA/SB index was found within either groups (RMMA/SB occurred in all SB subjects and only one control during the experimental night). These findings suggest that CAP phase A3 may act as a permissive window rather than a generator of RMMA/SB activity in predisposed individuals.

Oro-facial activities in sleep bruxism patients and in normal subjects: a controlled polygraphic and audio-video study.

To our knowledge, the large spectrum of sleep motor activities (SMA) present in the head and neck region has not yet been systematically estimated in normal and sleep bruxism (SB) subjects. We hypothesized that in the absence of audio-video signal recordings, normal and SB subjects would present a high level of SMA that might confound the scoring specificity of SB. A retrospective analysis of several SMA, including oro-facial activities (OFA) and rhythmic masticatory muscle activities (RMMA), was made from polygraphic and audio-video recordings of 21 normal subjects and 25 SB patients. Sleep motor activities were scored, blind to subject status, from the second night of sleep recordings. Discrimination of OFA included the following types of activities: lip sucking, head movements, chewing-like movements, swallowing, head rubbing and scratching, eye opening and blinking. These were differentiated from RMMA and tooth grinding. The frequency of SMA per hour of sleep was lower in normal subjects in comparison with SB patients (P < 0.001). Up to 85% of all SMA in normal subjects were related to OFA while 30% of SMA in SB patients were related to OFA scoring (P < 0.001). The frequency of RMMA was seven times higher in SB patients than in normal subjects (P < 0.001). Several SMA can be observed in normal and SB subjects. In the absence of audio-video signal recordings, the discrimination of various types of OFA is difficult to achieve and may lead to erroneous estimation of SB-related activities.

Bruxism physiology and pathology: an overview for clinicians.

Awake bruxism is defined as the awareness of jaw clenching. Its prevalence is reported to be 20% among the adult population. Awake bruxism is mainly associated with nervous tic and reactions to stress. The physiology and pathology of awake bruxism is unknown, although stress and anxiety are considered to be risk factors. During sleep, awareness of tooth grinding (as noted by sleep partner or family members) is reported by 8% of the population. Sleep bruxism is a behaviour that was recently classified as a 'sleep-related movement disorder'. There is limited evidence to support the role of occlusal factors in the aetiology of sleep bruxism. Recent publications suggest that sleep bruxism is secondary to sleep-related micro-arousals (defined by a rise in autonomic cardiac and respiratory activity that tends to be repeated 8-14 times per hour of sleep). The putative roles of hereditary (genetic) factors and of upper airway resistance in the genesis of rhythmic masticatory muscle activity and of sleep bruxism are under investigation. Moreover, rhythmic masticatory muscle activity in sleep bruxism peaks in the minutes before rapid eye movement sleep, which suggests that some mechanism related to sleep stage transitions exerts an influence on the motor neurons that facilitate the onset of sleep bruxism. Finally, it remains to be clarified when bruxism, as a behaviour found in an otherwise healthy population, becomes a disorder, i.e. associated with consequences (e.g. tooth damage, pain and social/marital conflict) requires intervention by a clinician.

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.

Sleep bruxism is associated to micro-arousals and an increase in cardiac sympathetic activity.

Sleep bruxism (SB) subjects show a higher incidence of rhythmic masticatory muscle activity (RMMA) than control subjects. RMMA is associated with sleep micro-arousals. This study aims to: (i) assess RMMA/SB episodes in relation to sleep cycles; (ii) establish if RMMA/SB and micro-arousals occur in relation to the slow wave activity (SWA) dynamics; (iii) analyze the association between RMMA/SB and autonomic cardiac activity across sleep cycles. Two nights of polygraphic recordings were made in three study groups (20 subjects each): moderate to high SB, low SB and control. RMMA episodes were considered to occur in clusters when several groups of RMMA or non-specific oromotor episodes were separated by less than 100 s. Correlations between sleep, RMMA/SB index and heart rate variability variables were assessed for the first four sleep cycles of each study group. Statistical analyses were done with SYSTAT and SPSS. It was observed that 75.8% of all RMMA/SB episodes occurred in clusters. Micro-arousal and SB indexes were highest during sleep cycles 2 and 3 (P < 0.001). Within each cycle, micro-arousal and RMMA/SB indexes showed an increase before each REM sleep (P

Experimentally induced arousals during sleep: a cross-modality matching paradigm.

Micro-arousals occur spontaneously or in response to exogenous and endogenous sensory input during sleep. The function of micro-arousals remains unclear, for example, whether it reflects a disturbance or a preparatory response to environmental changes. The goal of this study was to assess arousal responsiveness when two types of sensory stimulations were used: auditory (AD) alone and the addition of a vibrotactile (VT) sensation. Ten normal sleepers participated in three nights of polygraphic recordings. The first night was for habituation and to rule out sleep disorders, and the second to collect baseline sleep data. During the third night, AD and VT + AD stimuli, with three levels of intensities for auditory and vibratory signals, were randomly given to induce arousal responses in sleep stages 2, 3 and 4 and rapid eye movement (REM). The frequency of the arousal responses increased with stimulus intensity for all sleep stages and was lowest in stages 3 and 4. In non-REM (NREM) sleep, combined VT + AD stimulation induced more frequent and more intense arousal responses than AD alone. In REM sleep, more frequent micro-arousals rather than awakenings were triggered by combined stimulations. In stage 2, the response rate of total induced K-complexes did not differ between both types of stimulations while more K-complexes followed by arousals were evoked by the combined VT + AD stimulation than by the AD alone. The induced arousals were associated with an increase in heart rate in all sleep stages. An increase in suprahyoid muscle tone was observed in NREM sleep only, REM being not associated with a rise in muscle tone following experimental stimulation. Most leg and body movements occurred in response to induced awakenings. These results suggest that the cross-modality sensory stimuli triggered more arousal responses in comparison with single-modality stimuli. In an attempt to wake a sleeping subject, the addition of a tactile stimulation, such as shaking the shoulder, is an effective strategy that increases the arousal probability.