Eduardo Castrillon

Effect of conditioning electrical stimuli on temporalis electromyographic activity during sleep.

Inhibitory reflexes during voluntary contractions are well described; however, few studies have attempted to use such reflex-mechanisms to modulate electromyographic (EMG) activity in jaw-closing muscles during sleep. The aim was to apply a new intelligent biofeedback device (Grindcare(R)) using electrical pulses to inhibit EMG activity in the temporalis muscle during sleep. Fourteen volunteers participated who were aware of jaw-clenching activity as indicated by complaints from sleep partner, soreness or pain in the jaw-muscle upon awakening and tooth wear facets. The EMG activity was recorded from the temporalis muscle, online analysed and the frequency content determined using a signal recognition algorithm. Based on specific individual parameters for pattern recognition, an electrical square-wave pulse train, which was adjusted to a clear, but non-painful intensity (range 1-7 mA) was applied through the EMG electrodes, if jaw-clenching activity was detected. All volunteers had baseline EMG recordings for five to seven consecutive nights, followed by 3-weeks EMG recordings with the feedback turned on, 2 weeks without the feedback and finally 3 weeks with the biofeedback on. There were no session effects on the average duration of sleep hours (P = 0.626). The number of EMG episodes/hour sleep was significantly reduced during the two sessions with biofeedback (54 +/- 14%; 55 +/- 17%, P < 0.001) compared with baseline EMG activity and the session without biofeedback. The present study suggests that biofeedback with electrical pulses does not cause major disruption in sleep and is associated with pronounced reduction in temporalis EMG activity during sleep.

Glutamate-evoked jaw muscle pain as a model of persistent myofascial TMD pain?

OBJECTIVE Compare pain-related measures and psychosocial variables between glutamate-evoked jaw muscle pain in healthy subjects (HS) and patients with persistent myofascial temporomandibular disorder (TMD) pain. DESIGN Forty-seven female HS and 10 female patients with persistent myofascial TMD pain participated. The HS received an injection of glutamate into the masseter muscle to model persistent myofascial TMD pain. Participants filled out a coping strategies questionnaire (CSQ), the symptom checklist 90 (SCL-90) and McGill pain questionnaire (MPQ). Pain intensity was assessed on an electronic visual analogue scale (VAS). Pain-drawing areas, numerical rating scale (NRS) scores of unpleasantness, pressure pain thresholds (PPTs) and pressure pain tolerance (PPTOL) were measured. Unpaired t-tests and correlation tests were used for analyses. RESULTS The groups were significantly different when comparing the CSQ scores of control, decrease, diverting attention, increase of behavioural activities and somatization. The peak VAS pain, NRS of unpleasantness and MPQ scores were not significantly different between groups, but PPT and PPTOL were significantly lower in the TMD patients. Significant positive correlations were found in the TMD patients between peak VAS pain and CSQ catastrophizing score and SCL-90 somatization. The scores of PPTs and PPTOLs, in patients showed positive correlations with CSQ reinterpreting pain sensations scores and PPTs correlated with CSQ praying/hoping scores. CONCLUSIONS Glutamate-evoked pain responses in HS and persistent myofascial TMD pain have similar sensory-discriminative and affective-unpleasantness components but differ in psychosocial features. This study suggests that experimental designs based on glutamate injection into muscle can provide an appropriate model for elucidating persistent myofascial pain conditions.

Craniofacial Pain and Jaw-muscle Activity during Sleep

This study compared the jaw-muscle electromyographic (EMG) activity during sleep in patients with craniofacial pain (n = 63) or no painful conditions (n = 52) and between patients with tension-type headache (TTH: n = 30) and healthy control individuals (n = 30). All participants used a portable single-channel EMG device (Medotech A/S) for four nights. There was no significant difference in EMG activity between craniofacial pain (24.5 ± 17.9 events/hr) and no painful conditions (19.7 ± 14.5), or between TTH (20.8 ± 15.0) and healthy control individuals (15.2 ± 11.6, p >.050). There were positive correlations between EMG activity and number of painful muscles (r = 0.188; p = 0.044), characteristic pain intensity (r = 0.187; p = 0.046), McGill Pain Questionnaire (r = 0.251; p = 0.008), and depression scores (r = 0.291; p = 0.002). Patients with painful conditions had significantly higher night-to-night variability compared with pain-free individuals (p < 0.050). This short-term observational study suggests that there are no major differences between patients with different craniofacial pain conditions and pain-free individuals in terms of jaw-muscle EMG activity recorded with a single-channel EMG device during sleep. However, some associations may exist between the level of EMG activity and various parameters of craniofacial pain. Longitudinal studies are warranted to further explore the relationship between sleep bruxism and craniofacial pain.

Comparison of glutamate-evoked pain between the temporalis and masseter muscles in men and women

Summary Differences in glutamate‐evoked pain between the temporalis and masseter muscles, and between men and women were shown. There is a possibility that treatment of patients with chronic myofascial temporomandibular disorder with local injections of ketamine at the concentration used in this study may be effective in reducing muscle pain. Abstract Pain in myofascial temporomandibular disorder (TMD) can affect both the masseter and temporalis muscles. Glutamate injection into the masseter muscle evokes pain that is greater in men than in women and this pain is attenuated by co‐injection of the N‐methyl‐d‐aspartate (NMDA) receptor antagonist ketamine (10 mmol/L) in men. Animal studies suggested that pain induced by peripheral NMDA receptor activation could differ between the temporalis and masseter muscles and between men and women. The study aims were to investigate differences in glutamate‐evoked pain between these muscles and the effectiveness of ketamine to attenuate glutamate‐evoked pain in both genders. Pain and mechanical sensitivity were induced in 2 sessions of an experiment in 14 women and 16 men by repeated injections of glutamate (0.5 mol/L) with and without ketamine (20 mmol/L) into the masseter and temporalis muscles. Two injections were applied into the same masseter muscle and 2 injections into the same anterior temporalis muscle at each session. Visual analogue scale (VAS) pain intensities and pain drawing areas were assessed. Glutamate‐evoked pain and pain drawing area were significantly greater from the temporalis muscle than from the masseter muscle (P < .02) in both genders. Women reported significantly greater glutamate‐evoked masseter muscle pain than men (P < .03). Co‐injection of ketamine, at higher dose than previously used, was equally effective in attenuating glutamate‐evoked pain from both muscles in both genders (P < .01). The current findings indicate that the characteristics of pain generated by intramuscular injection of glutamate vary for different masticatory muscles and may be partially generated through activation of peripheral NMDA receptors.

Effect of contingent electrical stimulation on jaw muscle activity during sleep: A pilot study with a randomized controlled trial design

Abstract Objective. To determine the effect of contingent electrical stimulation (CES) on jaw muscle activity during sleep in a double-blinded randomized controlled trial (RCT). Materials and methods. Eleven patients with myofascial TMD (mean age 37 years) and with a clinical diagnosis of bruxism were included. EMG activity (Grindcare®) was recorded from the anterior temporalis muscle during sleep and analyzed online. Jaw muscle activity related to clenching or grinding triggered an electrical square-wave pulse train (450 ms) adjusted to a clear, but non-painful intensity. TMD patients were randomized into two groups: active treatment with CES or no CES (placebo). Number of EMG episodes/hour sleep was the primary outcome parameter. The following variables were assessed as secondary outcome parameters; number of painful muscles, maximum pain-free jaw opening, characteristic pain intensity, depression scores and Oral Health Impact Profile scores. Numerical Rating Scale scores for self-reported pain and muscle tension were registered for at least 4 nights per week during the experiment. Results. The number of EMG episodes/hour sleep was significantly reduced (52 ± 12%) in the CES group during the sessions with CES (ANOVA: p = 0.021) compared to baseline. There were no significant differences in the secondary outcome parameters (ANOVA: p > 0.513) or pain or muscle tension scores between groups (p = 0.645). The average duration of sleep hours during the nights with and without CES was not significantly different (p = 0.646). Conclusions. These results demonstrate a significant inhibitory effect of CES on jaw muscle EMG activity during sleep in a RCT, but with no effects on self-reported pain.

Can experimentally evoked pain in the jaw muscles or temporomandibular joint affect anterior bite force in humans

AIMS To test the hypothesis that experimental pain in the masseter muscle or temporomandibular joint (TMJ) will decrease the anterior maximum voluntary bite force (MVBF) and jaw muscle activity in relation to the perceived effort. METHODS Sixteen volunteers participated in two experimental sessions. Participants were injected with 0.2 mL of monosodium glutamate (1.0 M) into either the masseter muscle or TMJ. The MVBF and corresponding electromyographic (EMG) activity of the masseter, anterior temporalis, and digastric muscles were recorded 10 times at an interval of 2 minutes before and after injection. Pain was measured using a visual analog scale and McGill Pain Questionnaire. In addition, participants were asked how they perceived the interference of pain on their biting performance. The data analysis included a two-way analysis of variance model and t test. RESULTS There was no significant difference in peak pain intensity (P = .066) and duration of pain (P = .608) between painful muscle and TMJ injections, but TMJ injection produced a significantly larger area under the curve (P = .005) and a significantly higher pain rating index (P = .030). Pain in the muscle (P = .421) and TMJ (P = .057) did not significantly change the MVBF from baseline levels. The EMG activity also did not differ significantly from baseline levels during muscle pain. However, there was a significant increase (P = .028) in the EMG activity of the anterior temporalis and a significant decrease (P = .010) in the EMG activity of the anterior digastric muscle compared to baseline during TMJ pain. Subject-based reports also revealed that in the majority of cases (62.5%), pain did not interfere with the MVBF task. CONCLUSION Experimental pain from either masseter muscle or TMJ did not affect the MVBF, in accordance with the subject-based reports. Jaw muscle activity, except for EMG activity of the anterior temporalis and anterior digastric muscles during TMJ pain, also remained unaffected by pain. The findings suggest that it is not pain in itself but rather how pain is perceived that may lead to adaptation of motor function, supporting an integrated pain adaptation model.

Experimental myalgia induced by repeated infusion of acidic saline into the human masseter muscle does not cause the release of algesic substances

Animal studies have shown that two repeated intramuscular injections of acidic saline induce mechanical allodynia that lasts for 4 weeks with spread to the contralateral side. In this study, we tested the hypothesis that two repeated intramuscular infusions of acidic saline into the human masseter muscle is associated with pain, mechanical allodynia and release of algesic substances. Eighteen healthy volunteers participated. On day 1, 2.5 mL of acidic saline (pH 3.3) was infused into one of the masseter muscles and isotonic saline (pH 6.0) into the other (randomized and single‐blind). Two days later, intramuscular microdialysis was performed to sample serotonin, glutamate, pyruvate, lactate and glucose, during which the saline infusions were repeated. Pain and pressure pain thresholds (PPTs) were recorded before and after infusions on both days.

Sleep bruxism: an updated review of an old problem

Abstract Objective To provide an update on what is known about bruxism and some of the major clinical highlights derived from new insights into this old problem in dentistry. Materials and methods A selective, non-systematic but critical review of the available scientific literature was performed. Results There are two main different types of bruxism, which are related to different circadian periods (sleep and awake bruxism) that may differ in terms of pathophysiology, but they share some common signs and symptoms. Approximately one out of 10 adult individuals may suffer from bruxism, but not all bruxers may need treatment. Bruxism is complicated to diagnose in the clinic and self-report of bruxism may not necessarily reflect the true presence of jaw muscle activity. Better understanding has been acquired of bruxism relationships with sleep stages, arousal responses and autonomic function with the help of polysomnography and controlled sleep studies. Meanwhile, there is still much more to learn about awake bruxism. With the available scientific knowledge it is possible to systematically assess the effects of bruxism and its potential risk factors for oral and general health. Moreover, we can be aware of the realistic possibilities to manage/treat the patient suffering from bruxism. Conclusion Bruxism is a parafunctional activity involving the masticatory muscles and probably it is as old as human mankind. Different ways have been proposed to define, diagnose, assess the impact and consequences, understand the pathophysiology and treat or manage bruxism. Despite the vast research efforts made in this field, there are still significant gaps in our knowledge.

Biofeedback for treatment of awake and sleep bruxism in adults: systematic review protocol

BackgroundBruxism is a disorder of jaw-muscle activity characterised by repetitive clenching or grinding of the teeth which results in discomfort and damage to dentition. The two clinical manifestations of the condition (sleep and awake bruxism) are thought to have unrelated aetiologies but are palliated using similar techniques. The lack of a definitive treatment has prompted renewed interest in biofeedback, a behaviour change method that uses electronic detection to provide a stimulus whenever bruxism occurs. This systematic review aims to provide a comprehensive overview of the state of research into biofeedback for bruxism; to assess the efficacy and acceptability of biofeedback therapy in management of awake bruxism and, separately, sleep bruxism in adults; and to compare findings between the two variants.MethodsA systematic review of published literature examining biofeedback as an intervention directed at controlling primary bruxism in adults. We will search electronic databases and the grey literature using a predefined search strategy to identify randomised and non-randomised studies, technical reports and patents. Searches will not be restricted by language or date and will be expanded through contact with authors and experts, and by following up reference lists and citations. Two authors, working independently, will conduct screening of search results, study selection, data extraction and quality assessment and a third will resolve any disagreements. The primary outcomes of acceptability and effectiveness will be assessed using only randomised studies, segregated by bruxism subtype. A meta-analysis of these data will be conducted only if pre-defined conditions for quality and heterogeneity are met, otherwise the data will be summarized in narrative form. Data from non-randomised studies will be used to augment a narrative synthesis of the state of technical developments and any safety-related issues. PROSPERO registration number: CRD42013006880.DiscussionBiofeedback is not new, but its place in the clinical management of bruxism remains unclear. New research, and the availability of miniaturized consumer-grade devices, makes a systematic review timely to guide treatment decisions and inform future research.

Diagnostic validity of self-reported measures of sleep bruxism using an ambulatory single-channel EMG device

PURPOSE Self-reported measures have been widely used to indicate the presence of possible and probable sleep bruxism (SB) in both research and clinical situations. However, few studies have attempted to assess the diagnostic validity of this approach. The aim of this study was to estimate the diagnostic validity of self-reported measures of SB using an ambulatory single-channel electromyographic (EMG) device. METHODS A total of 115 participants were enrolled and examined by standardized Research Diagnostic Criteria for Temporomandibular Disorders (RDC/TMD) including two questions related to SB: self-reported SB and morning-jaw symptoms. An ambulatory single-channel EMG device (GrindCare3™, Medotech A/S) was used for measuring jaw-muscle EMG activity during sleep for seven consecutive nights. Cut-off values for different measures of EMG activity (average, maximum and minimum) and the coefficient of variation (CV) were selected to divide participants into two groups, with higher or lower EMG activity or CV values. The sensitivity and specificity for each question and combination of them were calculated. RESULTS Self-reported SB had the highest sensitivity (compared with morning-jaw symptoms) for all measures of EMG activity and CV, although the values were low to modest (average: 76.0%, maximum: 76.9%, minimum: 77.3%, CV: 61.0%). The specificity was low for both the questions related to the different measures of EMG activity and CV (35.1-52.4%). CONCLUSIONS This study indicated that the diagnostic validity of self-reported measures of SB was low to modest using an ambulatory EMG device assessment as a reference. Using only self-reported measures for the assessment of SB may not have a high validity, which should be taken into consideration in the clinical evaluation of patients.