Pterygoid muscle activity in speech: A preliminary investigation.

BACKGROUND: Speaking depends on refined control of jaw opening and closing movements. The medial pterygoid muscle (MPT), involved in jaw closing, and the lateral pterygoid muscle (LPT), involved in jaw opening, are two key mandibular muscles in mastication and are likely to be recruited for controlled movements in speech. OBJECTIVES: Three hypotheses were investigated, that during speech the MPT and LPT: (1) were both active, (2) but exhibited different patterns of activity, (3) which fluctuated with the vowels and consonants in speech. METHODS: Intramuscular EMG recordings were made from the right inferior head of the LPT and/or the right MPT in five participants during production of 40 target nonsense words (NWs) consisting of three syllables in the form /V1 C1 V2 C2 ə/ (V = vowel; C = consonant; ə = unstressed, reduced vowel), spoken by each participant 10 times per NW; analysis focussed on the target syllable, C1 V2 . RESULTS: Both MPT and LPT exhibited robust increases in EMG activity during utterance of most NWs, relative to rest. Peak LPT activation was time-locked to the final part of the target consonant (C1 ) interval when the jaw begins opening for the target vowel (V2 ), whereas peak MPT activation occurred around the temporal midpoint of V2 , when the jaw begins closing for C2 . EMG amplitude peaks differed in magnitude between "high" vowels, i.e., for which the tongue/jaw are high (e.g., in SEEK), and "low" vowels, i.e., for which the tongue/jaw are low (e.g., in SOCK). CONCLUSIONS: These novel findings suggest a key role for the LPT and MPT in the fine control of speech production. They imply that speech may impose major synergistic demands on the activities of the MPT and the LPT, and thereby provide insights into the possible interactions between speech activities and orofacial activities (e.g. mastication) and conditions (e.g. Temporomandibular Disorders) that involve the masticatory muscles.

Functional properties of single motor units in the human medial pterygoid muscle: Thresholds.

BACKGROUND: Little is known regarding the functional properties of single motor units (SMUs) in the medial pterygoid muscle (MPt) during jaw movements. OBJECTIVES: The aims are (a) to report the thresholds of onset of MPt SMUs during 4 goal-directed jaw movement tasks, and (b) to determine whether the threshold of onset of SMU activation varies with the velocity of jaw movement and the location within the muscle. METHODS: Intra-muscular electrodes were inserted in the right MPt of 18 participants performing ipsilateral (right), contralateral, protrusive and opening-closing jaw movements recorded at 2 velocities. Task phases were as follows: BEFORE, OUT, HOLDING, RETURN and AFTER. SMU onset thresholds were determined from the displacement (mm) of the lower mid-incisor point. Electrode location within 4 arbitrary muscle divisions was determined with computer tomography. Statistical tests: Spearman's correlations, Kruskal-Wallis tests; significance accepted at P < .05. RESULTS: A significant inverse relation occurred between velocity and threshold for the RETURN of the ipsilateral movement (n = 62 SMU thresholds), while a significant positive relation occurred for the OUT of the contralateral movement (n = 208); there were no significant associations for the protrusive (n = 131) and opening-closing (n = 58) tasks. Significant threshold differences occurred across the 4 muscle divisions only during the OUT of the contralateral and protrusive movements. Some evidence was provided for gender differences in MPt SMU properties. CONCLUSIONS: The absence of a significant inverse relation between velocity and SMU threshold for most recorded movements suggests the MPt acts as a stabilizer of the jaw in horizontal and opening-closing jaw movements.

Threshold variations of medial pterygoid single motor units during vertical or horizontal force tasks.

OBJECTIVES: To test the hypotheses that (a) the force thresholds at onset of medial pterygoid muscle single motor unit (SMU) activity do not decrease with an increase in the rate of force generation in standardised vertical or horizontal jaw-force tasks, and (b) there is evidence for functional heterogeneity within the medial pterygoid muscle. METHODS: In 14 healthy participants, electromyographic recordings of the right medial pterygoid muscle were performed with intramuscular fine-wire electrodes during four isometric force tasks: vertical, horizontal contralateral, horizontal protrusion and horizontal ipsilateral, performed at two rates of force development (slow ramp, fast ramp). Computer tomography scans confirmed electrode location within the muscle, which was divided into medial and lateral parts. Force thresholds of onset of discriminated SMUs were compared between rates in each task; significance accepted at p < 0.05. RESULTS: Of 45 SMU force thresholds studied in one or more tasks, there was no significant difference between slow and fast ramp within each force task, except slow ramp thresholds from the lateral part during the vertical force task were significantly higher than fast ramp thresholds. Reversals of recruitment order between tasks provided evidence for functional heterogeneity within the muscle. Force thresholds of the vertical tasks (range: 1-292.6 N) were mostly higher than for the horizontal tasks (range: 0.1-12.5 N). CONCLUSION: The data are consistent with the proposal that the medial pterygoid muscle stabilises the jaw in the vertical plane during isometric force generation in the jaw closing, as well as horizontal directions.

Brainstem Pain-Control Circuitry Connectivity in Chronic Neuropathic Pain.

Preclinical investigations have suggested that altered functioning of brainstem pain-modulation circuits may be crucial for the maintenance of some chronic pain conditions. While some human psychophysical studies show that patients with chronic pain display altered pain-modulation efficacy, it remains unknown whether brainstem pain-modulation circuits are altered in individuals with chronic pain. The aim of the present investigation was to determine whether, in humans, chronic pain following nerve injury is associated with altered ongoing functioning of the brainstem descending modulation systems. Using resting-state functional magnetic resonance imaging, we found that male and female patients with chronic neuropathic orofacial pain show increased functional connectivity between the rostral ventromedial medulla (RVM) and other brainstem pain-modulatory regions, including the ventrolateral periaqueductal gray (vlPAG) and locus ceruleus (LC). We also identified an increase in RVM functional connectivity with the region that receives orofacial nociceptor afferents, the spinal trigeminal nucleus. In addition, the vlPAG and LC displayed increased functional connectivity strengths with higher brain regions, including the hippocampus, nucleus accumbens, and anterior cingulate cortex, in individuals with chronic pain. These data reveal that chronic pain is associated with altered ongoing functioning within the endogenous pain-modulation network. These changes may underlie enhanced descending facilitation of processing at the primary synapse, resulting in increased nociceptive transmission to higher brain centers. Further, our findings show that higher brain regions interact with the brainstem modulation system differently in chronic pain, possibly reflecting top-down engagement of the circuitry alongside altered reward processing in pain conditions.SIGNIFICANCE STATEMENT Experimental animal models and human psychophysical studies suggest that altered functioning of brainstem pain-modulation systems contributes to the maintenance of chronic pain. However, the function of this circuitry has not yet been explored in humans with chronic pain. In this study, we report that individuals with orofacial neuropathic pain show altered functional connectivity between regions within the brainstem pain-modulation network. We suggest that these changes reflect largely central mechanisms that feed back onto the primary nociceptive synapse and enhance the transfer of noxious information to higher brain regions, thus contributing to the constant perception of pain. Identifying the mechanisms responsible for the maintenance of neuropathic pain is imperative for the development of more efficacious therapies.

Single motor units from the medial pterygoid muscle can be active during isometric horizontal and vertical forces.

OBJECTIVES: To determine (a) whether the medial pterygoid muscle is active in an isometric vertical force task and in isometric horizontal force tasks in the contralateral, protrusion and ipsilateral directions; (b) whether the same single motor units (SMUs) could be active across different directions of isometric force generation; and (c) whether different regions of the medial pterygoid muscle exhibit different patterns of SMU activation during the generation of any one direction of isometric force. METHODS: Intramuscular electromyographic (EMG) recordings were made from the right medial pterygoid muscle in 15 healthy participants during isometric force tasks: vertical and horizontal contralateral, protrusion and ipsilateral. A computed tomography scan divided the EMG recording site into a medial or lateral part in each participant. Single motor units were discriminated in each task. RESULTS: Medial pterygoid SMU activity was recorded in 100% of participants for the vertical biting tasks, 86% of participants for the horizontal contralateral and horizontal protrusion tasks and 57% of the horizontal ipsilateral tasks. Of the 72 SMUs that were discriminated, 36% were active in all tasks; 18% were active only in the vertical tasks and 17% were active in the vertical, horizontal contralateral and horizontal protrusion tasks. The proportion of SMUs that was active in at least 1 horizontal task in the lateral part (33/39) was significantly higher than the proportion (21/33) in the medial part (Chi-Square, P < 0.05). CONCLUSION: The data are consistent with a stabilisation role for the medial pterygoid muscle in isometric jaw forces in the vertical and horizontal planes.

Reorganization of motor unit activity at different sites within the human masseter muscle during experimental masseter pain.

The aims were to test the hypotheses that experimental masseter muscle pain leads to recruitment and/or derecruitment of motor units at different sites within the masseter and that the patterns of change in motor unit activity differ between sites. Single motor unit (SMU) activity was recorded at two sites within the right masseter [superior/anterior, inferior/posterior (IP)] during isometric biting tasks (ramp, step level) on an intraoral force transducer in 17 participants during three experimental blocks comprising no infusion (baseline), 5% hypertonic saline infusion (pain), or isotonic saline infusion (control). A visual analog scale (VAS) was used to score pain intensity. The VAS scores were statistically significantly greater during infusion of hypertonic saline than during infusion of isotonic saline. No significant differences in force levels and rates of force change were found between experimental blocks. In comparison with isotonic saline infusion, SMUs could be recruited and derecruited at both sites during hypertonic saline infusion. The frequency of recruitment or derecruitment, in comparison with no change, was statistically significantly greater at the IP site than at the superior/anterior site. Experimental noxious masseter stimulation results in a reorganization of motor unit activity throughout the muscle, and the pattern of reorganization may be different in different regions of the muscle.

Experimental noxious stimulation of the right masseter muscle does not affect bilateral masseter and temporalis muscle activity and force parameters during standardised isometric biting tasks.

AIM: To determine if the electromyographic (EMG) activity of the left and right masseter and anterior temporalis muscles is altered by experimental right masseter muscle noxious stimulation during goal-directed isometric biting tasks in asymptomatic humans. METHODS: Isometric biting tasks (slow and fast ramp biting tasks, 2-step biting task) were performed on an intraoral force transducer in 18 participants during the following blocks: baseline block, hypertonic saline infusion into the right masseter muscle (painful block) and isotonic saline infusion into the right masseter (control block). Bipolar surface electrodes recorded EMG activity from the bilateral masseter and anterior temporalis muscles. A 100-mm visual analogue scale (VAS) quantified pain intensity, and the McGill Pain Questionnaire (MPQ), the Depression, Anxiety and Stress Scales-21 (DASS-21) and the Pain Catastrophizing Scale (PCS) were completed. Repeated measures ANOVA assessed the effects of pain on the force rates (N/s), force amplitudes (N) and the root mean square (RMS) jaw muscle EMG activity across blocks. Statistical significance accepted at P < 0.05. RESULTS: VAS scores were significantly (P < 0.001) higher during hypertonic than isotonic saline infusion blocks. There was no significant effect of pain on the force rates, or force levels or the RMS EMG activity of each masseter and anterior temporalis muscle. CONCLUSION: The findings suggest that experimentally induced right masseter muscle pain does not modify force or surface jaw muscle EMG activity during isometric biting tasks.

Chronic Neuropathic Pain: It's about the Rhythm.

The neural mechanisms underlying the development and maintenance of chronic neuropathic pain remain unclear. Evidence from human investigations suggests that neuropathic pain is associated with altered thalamic burst firing and thalamocortical dysrhythmia. Additionally, experimental animal investigations show that neuropathic pain is associated with altered infra-slow (<0.1 Hz) frequency oscillations within the dorsal horn and somatosensory thalamus. The aim of this investigation was to determine whether, in humans, neuropathic pain was also associated with altered infra-slow oscillations within the ascending "pain" pathway. Using resting-state functional magnetic resonance imaging, we found that individuals with orofacial neuropathic pain have increased infra-slow oscillatory activity throughout the ascending pain pathway, including within the spinal trigeminal nucleus, somatosensory thalamus, thalamic reticular nucleus, and primary somatosensory cortex. Furthermore, these infra-slow oscillations were temporally coupled across these multiple sites and occurred at frequencies similar to calcium waves in activated astrocytes. The region encompassing the spinal trigeminal nucleus also displayed increased regional homogeneity, consistent with a local spread of neural activity by astrocyte activation. In contrast, no increase in oscillatory behavior within the ascending pain pathway occurred during acute noxious stimuli in healthy individuals. These data reveal increased oscillatory activity within the ascending pain pathway that likely underpins increased thalamocortical oscillatory activity, a self-sustaining thalamocortical dysrhythmia, and the constant perception of pain. Significance statement: Chronic neuropathic pain is associated with altered thalamic firing and thalamocortical dysrhythmia. The mechanisms responsible for these changes remain unknown. In this study, we report in individuals with neuropathic pain increased oscillatory neural activity within the ascending pain pathway with evidence that these changes result from altered neural-astrocyte coupling. We propose a series of neural and glial events after nerve injury that result in the generation of altered thalamocortical activity and a persistent neuropathic pain state. Defining the underlying mechanisms responsible for neuropathic pain is critical if we are to develop more effective treatment regimens.

Effect of a brief episode of experimental muscle pain on jaw movement and jaw-muscle activity during chewing.

The aims of this study were to determine whether: (i) the jaw motor system develops a new pattern of jaw movement and/or jaw-muscle activity after resolution of an acute episode of jaw-muscle pain; and (ii) if jaw-muscle activity and jaw-movement features change progressively with repetition of a chewing sequence. Jaw movement and jaw muscle (masseter, anterior temporalis, and digastric) activity were recorded during free and rate-standardized chewing in eight asymptomatic participants (pain infusion group), before and at three time blocks up to 45 min after a single 0.2-ml bolus infusion of 5% hypertonic saline into the right masseter muscle. The same procedure, without infusion, was performed in another eight participants (control group). There were no significant main effects of group on jaw movement and muscle activity, suggesting that there were no persistent post-pain effects on chewing. Across groups, repetitions of free and unstandardized chewing movements were associated with progressive increases in velocity and amplitude of jaw movement and masseter and temporalis electromyographic (EMG) activity. These findings suggest that factors unrelated to pain, such as practice effects, may be playing a role in the changes in jaw movement and jaw-muscle activity observed after resolution of an acute episode of jaw-muscle pain.

Anatomical changes at the level of the primary synapse in neuropathic pain: evidence from the spinal trigeminal nucleus.

Accumulated evidence from experimental animal models suggests that neuronal loss within the dorsal horn is involved in the development and/or maintenance of peripheral neuropathic pain. However, to date, no study has specifically investigated whether such neuroanatomical changes also occur at this level in humans. Using brain imaging techniques, we sought to determine whether anatomical changes were present in the spinal trigeminal nucleus in subjects with chronic orofacial neuropathic pain. In 22 subjects with painful trigeminal neuropathy and 44 pain-free controls, voxel-based morphometry of T1-weighted anatomical images and diffusion tensor images were used to assess regional gray matter volume and microstructural changes within the brainstem. In addition, deterministic tractography was used to assess the integrity of ascending pain pathways. Orofacial neuropathic pain was associated with significant regional gray matter volume decreases, fractional anisotropy increases, and mean diffusivity decreases within the spinal trigeminal nucleus, specifically the subnucleus oralis. In addition, tractography revealed no significant differences in diffusivity properties in the root entry zone of the trigeminal nerve, the spinal trigeminal tract, or the ventral trigeminothalamic tracts in painful trigeminal neuropathy subjects compared with controls. These data reveal that chronic neuropathic pain in humans is associated with discrete alterations in the anatomy of the primary synapse. These neuroanatomical changes may be critical for the generation and/or maintenance of pathological pain.

Pain and Personality: Do Individuals with Different Forms of Chronic Pain Exhibit a Mutual Personality?

The role of personality in the experience of chronic pain is a growing field, with endless debate regarding the existence of a "pain personality". This study aims to compare different chronic pain types and consolidate the existence of a common personality. Thirty-two females with chronic orofacial pain and 37 age-matched healthy females were assessed with the Temperament and Character Inventory-Revised. Chronic pain subjects had either trigeminal neuropathy (neuropathic pain) or temporomandibular disorders (nociceptive pain). This study revealed that individuals with different chronic pain types exhibit a mutual personality profile encompassing significantly higher scores in Harm Avoidance and significantly lower scores in Self-Directedness when compared to healthy subjects. In fact, this combination is associated with Cluster C personality disorders. In conclusion, our study reveals that irrespective of type, chronic pain may be associated with Cluster C personality disorders. Indeed, there has never been empirical evidence in the past to suggest that chronic pain as an overall concept is associated with any particular personality disorders. Therefore, a potential future avenue of chronic pain treatment may lie in targeting particular personality aspects and shift the target of pain-relieving treatments from sensory and psychologically state focused to psychologically trait focused.

Chronic pain: lost inhibition?

Human brain imaging has revealed that acute pain results from activation of a network of brain regions, including the somatosensory, insular, prefrontal, and cingulate cortices. In contrast, many investigations report little or no alteration in brain activity associated with chronic pain, particularly neuropathic pain. It has been hypothesized that neuropathic pain results from misinterpretation of thalamocortical activity, and recent evidence has revealed altered thalamocortical rhythm in individuals with neuropathic pain. Indeed, it was suggested nearly four decades ago that neuropathic pain may be maintained by a discrete central generator, possibly within the thalamus. In this investigation, we used multiple brain imaging techniques to explore central changes in subjects with neuropathic pain of the trigeminal nerve resulting in most cases (20 of 23) from a surgical event. Individuals with chronic neuropathic pain displayed significant somatosensory thalamus volume loss (voxel-based morphometry) which was associated with decreased thalamic reticular nucleus and primary somatosensory cortex activity (quantitative arterial spin labeling). Furthermore, thalamic inhibitory neurotransmitter content was significantly reduced (magnetic resonance spectroscopy), which was significantly correlated to the degree of functional connectivity between the somatosensory thalamus and cortical regions including the primary and secondary somatosensory cortices, anterior insula, and cerebellar cortex. These data suggest that chronic neuropathic pain is associated with altered thalamic anatomy and activity, which may result in disturbed thalamocortical circuits. This disturbed thalamocortical activity may result in the constant perception of pain.

Pain-sensorimotor interactions: New perspectives and a new model.

How pain and sensorimotor behavior interact has been the subject of research and debate for many decades. This article reviews theories bearing on pain-sensorimotor interactions and considers their strengths and limitations in the light of findings from experimental and clinical studies of pain-sensorimotor interactions in the spinal and craniofacial sensorimotor systems. A strength of recent theories is that they have incorporated concepts and features missing from earlier theories to account for the role of the sensory-discriminative, motivational-affective, and cognitive-evaluative dimensions of pain in pain-sensorimotor interactions. Findings acquired since the formulation of these recent theories indicate that additional features need to be considered to provide a more comprehensive conceptualization of pain-sensorimotor interactions. These features include biopsychosocial influences that range from biological factors such as genetics and epigenetics to psychological factors and social factors encompassing environmental and cultural influences. Also needing consideration is a mechanistic framework that includes other biological factors reflecting nociceptive processes and glioplastic and neuroplastic changes in sensorimotor and related brain and spinal cord circuits in acute or chronic pain conditions. The literature reviewed and the limitations of previous theories bearing on pain-sensorimotor interactions have led us to provide new perspectives on these interactions, and this has prompted our development of a new concept, the Theory of Pain-Sensorimotor Interactions (TOPSMI) that we suggest gives a more comprehensive framework to consider the interactions and their complexity. This theory states that pain is associated with plastic changes in the central nervous system (CNS) that lead to an activation pattern of motor units that contributes to the individual's adaptive sensorimotor behavior. This activation pattern takes account of the biological, psychological, and social influences on the musculoskeletal tissues involved in sensorimotor behavior and on the plastic changes and the experience of pain in that individual. The pattern is normally optimized in terms of biomechanical advantage and metabolic cost related to the features of the individual's musculoskeletal tissues and aims to minimize pain and any associated sensorimotor changes, and thereby maintain homeostasis. However, adverse biopsychosocial factors and their interactions may result in plastic CNS changes leading to less optimal, even maladaptive, sensorimotor changes producing motor unit activation patterns associated with the development of further pain. This more comprehensive theory points towards customized treatment strategies, in line with the management approaches to pain proposed in the biopsychosocial model of pain.

Pain and plasticity: is chronic pain always associated with somatosensory cortex activity and reorganization?

The somatosensory cortex remodels in response to sensory deprivation, with regions deprived of input invaded by neighboring representations. The degree of cortical reorganization is correlated with ongoing pain intensity, which has led to the assumption that chronic pain conditions are invariably associated with somatosensory cortex reorganization. Because the presentation and etiology of chronic pain vary, we determined whether cortical changes in human subjects are similar for differing pain types. Using functional and anatomical magnetic resonance imaging, we found that, while human patients with neuropathic pain displayed cortical reorganization and changes in somatosensory cortex activity, patients with non-neuropathic chronic pain did not. Furthermore, cortical reorganization in neuropathic pain patients was associated with changes in regional anatomy. These data, by showing that pain per se is not associated with cortical plasticity, suggest that treatments aimed at reversing cortical reorganization should only be considered for use in patients with certain types of chronic pain.

Association between resting jaw muscle electromyographic activity and mandibular advancement splint outcome in patients with obstructive sleep apnea.

INTRODUCTION: The muscles of mastication are important in positioning the mandible and can therefore affect the patency of the upper airway. The aim of this study was to determine whether resting masticatory muscle activity influences the response to mandibular advancement splint treatment in patients with obstructive sleep apnea. METHODS: Thirty-eight adult patients with obstructive sleep apnea were recruited for the study. Baseline electromyographic activities of the right anterior and posterior temporalis, masseter, and submandibular muscles were recorded with surface electrodes while the patients were awake, in the upright and supine positions, with the jaw in the postural position, and with and without a mandibular advancement splint. Muscle activity of the patients with obstructive sleep apnea was compared between responders (apnea-hypopnea index change ≥50%, and <10 events per hour) and nonresponders (apnea-hypopnea index change <50%) to mandibular advancement splint treatment. RESULTS: There were 18 responders and 20 nonresponders to mandibular advancement splint treatment. The responders had a trend for increased muscle activity in all muscle groups and scenarios. The resting muscle activity of the submandibular and masseter muscles while lying at rest and of the submandibular and posterior temporalis muscles while lying with the mandibular advancement splint in place were significantly greater (P <0.05) in the responders than in the nonresponders. CONCLUSIONS: Inherent baseline differences in muscle activity between responders and nonresponders to mandibular advancement splint treatment in adults with obstructive sleep apnea were observed. This preliminary study suggests that there might be a correlation between responsiveness with mandibular advancement splint treatment and baseline muscle activity.

Different pain, different brain: thalamic anatomy in neuropathic and non-neuropathic chronic pain syndromes.

Trigeminal neuropathic pain (TNP) and temporomandibular disorders (TMD) are thought to have fundamentally different etiologies. It has been proposed that TNP arises through damage to, or pressure on, somatosensory afferents in the trigeminal nerve, whereas TMD results primarily from peripheral nociceptor activation. Because some reports suggest that neuropathic pain is associated with changes in brain anatomy, it is possible that TNP is maintained by changes in higher brain structures, whereas TMD is not. The aim of this investigation is to determine whether changes in regional brain anatomy and biochemistry occur in both conditions. Twenty-one TNP subjects, 20 TMD subjects, and 36 healthy controls were recruited. Voxel-based morphometry of T1-weighted anatomical images revealed no significant regional gray matter volume change in TMD patients. In contrast, gray matter volume of TNP patients was reduced in the primary somatosensory cortex, anterior insula, putamen, nucleus accumbens, and the thalamus, whereas gray matter volume was increased in the posterior insula. The thalamic volume decrease was only seen in the TNP patients classified as having trigeminal neuropathy but not those with trigeminal neuralgia. Furthermore, in trigeminal neuropathy patients, magnetic resonance spectroscopy revealed a significant reduction in the N-acetylaspartate/creatine ratio, a biochemical marker of neural viability, in the region of thalamic volume loss. The data suggest that the pathogenesis underlying neuropathic and non-neuropathic pain conditions are fundamentally different and that neuropathic pain conditions that result from peripheral injuries may be generated and/or maintained by structural changes in regions such as the thalamus.

The effects of capsaicin-induced intraoral mucosal pain on jaw movements in humans.

AIMS: To determine whether mucosal pain, evoked through a novel topical capsaicin model, has an effect on jaw movement and whether psychologic factors have an association with any pain-induced movement effects. METHODS: Mandibular movement was recorded from 26 asymptomatic subjects during free opening and closing, resistant opening jaw movements, and free and standardized chewing, at baseline and in test sessions while the subjects were wearing a custom maxillary mouthguard coated with either capsaicin cream (pain group, 13 subjects) or placebo cream (control group, an additional 13 subjects). All subjects completed the Depression Anxiety Stress Scales (DASS) and the Pain Catastrophizing Scale (PCS). Statistical analyses were made with independent t tests and bivariate correlation analyses. RESULTS: Capsaicin induced moderate pain in the pain group, but there were no significant differences between the two groups in the change of kinematic variables from baseline except for a significantly greater increase from baseline in the number of chewing cycles per second (chewing rate) for free (t = 2.74, P = .011) and standardized chewing (t = 2.10, P = .047) in the pain group compared with the control group. In the pain group, the DASS anxiety score was negatively correlated (r = -.70, P = .007), with the change of mean opening velocity from the baseline to the test session in the free opening task, and the DASS depression score was negatively correlated to the increase of chewing rate in the free chewing task from the baseline to the test session (r = -.56, P = .046). CONCLUSION: Capsaicin-induced mucosal pain resulted in a significant increase in chewing rate but had no effect on amplitude or velocity in opening/closing jaw movements and chewing. Anxiety and depression scores correlated negatively with velocity in free opening jaw movement and chewing rate, respectively.

Development and validation of a screening checklist for temporomandibular disorders.

AIMS: To develop and validate a short screening tool for temporomandibular disorders (TMD) from the comprehensive Research Diagnostic Criteria for TMD (RDC/TMD) assessment. METHODS: Complete RDC/TMD assessments of four subject groups (96 TMD; 102 dental pain; 68 headache; 115 no-pain patients) were compared. Classification tree and multiple logistic regression analyses were utilized to develop the tool. To test external validity, a further 54 TMD and 51 non-TMD subjects whose diagnoses had been established by RDC/TMD assessment were reassessed with the new screening tool. The sensitivity, specificity, positive predictive value (PPV), negative predictive value (NPV), and likelihood ratios (LRs) were calculated for the screening tool in the validation set of subjects. RESULTS: A short TMD checklist was developed. This screening instrument had sensitivity of 94.4% (95% confidence intervals [CI], 84.9% to 98.1%), specificity of 94.1% (95% CI, 84.1% to 98%), PPV of 94.4% (95% CI, 84.9% to 98.1%), NPV of 94.1% (95% CI, 84.1% to 98%), and positive and negative LRs of 16.056 (95% CI, 5.346 to 48.219) and 0.059 (95% CI, 0.02 to 0.178) in an independent validation set. CONCLUSION: A short TMD screening checklist with high validity has been developed. This checklist may have good utility in general practice as a primary screening tool for TMD.

Chewing in temporomandibular disorder patients: an exploratory study of an association with some psychological variables.

AIMS: To compare kinematic parameters (ie, amplitude, velocity, cycle frequency) of chewing and pain characteristics in a group of female myofascial temporomandibular disorder (TMD) patients with an age-matched control female group, and to study correlations between psychological variables and kinematic variables of chewing. METHODS: Twenty-nine female participants were recruited. All participants were categorized according to the Research Diagnostic Criteria for TMD (RDC/TMD) into control (n = 14, mean age 28.9 years, SD 5.0 years) or TMD (n = 15, mean age 31.3 years, SD 10.7) groups. Jaw movements were recorded during free gum chewing and chewing standardized for timing. Patients completed the Depression, Anxiety, and Stress Scales (DASS-42), the Pain Catastrophizing Scale (PCS), the Fear of Pain Questionnaire-III (FPQ-III), and the Pain Self-Efficacy Questionnaire (PSEQ). Statistical analyses involved evaluation for group differences, and correlations between kinematic variables and psychological questionnaire scores (eg, depression, anxiety, stress) and pain intensity ratings. RESULTS: Velocity and amplitude of standardized (but not free) chewing were significantly greater (P < .05) in the TMD group than the control group. There were significant (P < .05) positive correlations between pain intensity ratings and velocity and amplitude of standardized chewing but not free chewing. There were significant (P < .05) positive correlations between depression and jaw amplitude and stress and jaw velocity for standardized but not free chewing. CONCLUSION: This exploratory study has provided data suggesting that psychological factors, manifesting in depression and stress, play a role in influencing the association between pain and motor activity.

Altered Brainstem Pain Modulating Circuitry Functional Connectivity in Chronic Painful Temporomandibular Disorder.

There is evidence from preclinical models of chronic pain and human psychophysical investigations to suggest that alterations in endogenous brainstem pain-modulation circuit functioning are critical for the initiation and/or maintenance of pain. Whilst preclinical models have begun to explore the functioning of this circuitry in chronic pain, little is known about such functioning in humans with chronic pain. The aim of this investigation was to determine whether individuals with chronic non-neuropathic pain, painful temporomandibular disorders (TMD), display alterations in brainstem pain-modulating circuits. Using resting-state functional magnetic resonance imaging, we performed static and dynamic functional connectivity (FC) analyses to assess ongoing circuit function in 16 TMD and 45 control subjects. We calculated static FC as the correlation of functional magnetic resonance imaging signals between regions over the entire scan and dynamic FC as the correlation of signals in short (50s) windows. Compared with controls, TMD subjects showed significantly greater (static) FC between the rostral ventromedial medulla and both the subnucleus reticularis dorsalis and the region that receives orofacial nociceptive afferents, the spinal trigeminal nucleus. No differences were found in other brainstem pain-modulating regions such as the midbrain periaqueductal gray matter and locus coeruleus. We also identified that TMD subjects experience greater variability in the dynamic functional connections between the rostral ventromedial medulla and both the subnucleus reticularis dorsalis and spinal trigeminal nucleus. These changes may underlie enhanced descending pain-facilitating actions over the region that receives nociceptive afferents, ultimately leading to enhanced nociceptive transmission to higher brain regions and thus contributing to the ongoing perception of pain. PERSPECTIVE: Psychophysical studies suggest that brainstem pain-modulation circuits contribute to the maintenance of chronic pain. We report that individuals with painful TMD display altered static and dynamic FC within the brainstem pain-modulation network. Modifying this circuitry may alter an individual's ongoing pain.