Bilateral Widespread Mechanical Pain Sensitivity in Women With Myofascial Temporomandibular Disorder: Evidence of Impairment in Central Nociceptive Processing

Our aim was to investigate bilateral, widespread pressure-pain hypersensitivity in nerve, muscle, and joint tissues in women with myofascial temporomandibular disorders (TMD) without concomitant comorbid conditions. Twenty women with myofascial TMD (aged 20 to 28 years old), and 20 healthy matched women (aged 20 to 29 years), were recruited. Pressure-pain thresholds (PPT) were bilaterally assessed over supra-orbital (V1), infra-orbital (V2), mental (V3) nerves, median (C5), radial (C6) and ulnar (C7) nerve trunks, the C5-C6 zygapophyseal joint, the lateral pole of the temporo mandibular joint (TMJ), and the tibialis anterior muscle in a blinded design. The results showed that PPTs were significantly decreased bilaterally over the supra-orbital, infra-orbital, and mental nerves, median, ulnar, and radial nerve trunks, the lateral pole of the TMJ, the C5-C6 zygapophyseal joint, and the tibialis anterior muscle in patients with myofascial TMD as compared to healthy controls (all sites: P < .001). There were no significant differences in the magnitude of PPT decreases between the trigeminal and extratrigeminal test sites. PPT over the mental nerve, the TMJ, C5-C6 zygapophyseal joint and tibialis anterior muscle were negatively correlated to both duration of pain symptoms and TMD pain intensity (P < .05). Our findings revealed bilateral, widespread pressure hypersensitivity in women presenting with myofascial TMD, suggesting that widespread central sensitization is involved in myofascial TMD women.

Perspective

This article reveals the presence of bilateral and widespread pressure-pain hypersensitivity in women with myofascial TMD, suggesting that widespread central sensitization is involved in myofascial TMD. This finding has implications for development of management strategies.     

Glutamate-evoked pain and mechanical allodynia in the human masseter muscle

The present study examined the effect of peripheral administration of the excitatory amino acid (EAA) glutamate on the intensity of perceived pain and pressure pain thresholds (PPTs) in healthy young women (n=17) and men (n=18). Two injections separated by 25 min of 0.2 ml, 1.0M glutamate into the masseter muscle produced significantly higher scores of pain on 0-10 cm visual analogue scales (VAS) in women than in men (analysis of variance, ANOVA: P<0.001). There was no significant difference between the VAS scores for the first and the second injections in either men or women. The PPTs determined in the masseter muscle were significantly reduced following the first injection and further significantly reduced after the second injection (ANOVA: P<0.001). Furthermore, the PPTs were reduced to a similar extent in both women and men (maximum 44-56%), suggesting that gender did not influence the process of sensitization. There were no significant difference in VAS scores or PPTs between women taking oral contraceptives (n=9) and those who did not (n=8) (ANOVAs: P=0.709, P=0.153). It is concluded that the VAS scores produced by intramuscular administration of 1.0M glutamate may reflect a gender-dependent activation of nociceptive pathways which, in part, may be mediated through peripheral EAA receptors. The reduction of PPTs in the masseter muscle following administration of glutamate in a concentration of 1.0M may reflect allodynia to mechanical stimuli. This process of sensitization was not gender-dependent. The present results suggest that injection of 1.0M glutamate into the masseter muscle may provide a useful experimental method to test sensitization and efficacy of peripheral EAA receptor antagonists in human subjects.     

Experimental human muscle pain and muscular hyperalgesia induced by combinations of serotonin and bradykinin.

In the present study, we assessed the muscle pain and possible development of muscular hyperalgesia to mechanical stimuli after two subsequent intramuscular infusions of serotonin (5-HT) and bradykinin (BKN). The pain intensity after the infusions was continuously scored on a visual analogue scale (VAS). The subjects drew the distribution of the pain areas on a map. Pressure pain thresholds (PPTs) and suprapressure pain thresholds (SPPTs) stimulations as 150% of the pre-infusion PPTs were assessed with a pressure algometer at the injection site (10 cm below the patella), at the ankle, and at the contralateral leg and ankle. Skin sensibility was assessed with a Von Frey hair at the same sites. This was done before and after an infusion into the tibialis anterior (TA) muscle on the right leg in ten volunteers. The first infusion in each combination was either serotonin (20 nmol) or isotonic saline (NaCl 0.9%). The second infusion was bradykinin (5 or 10 nmol) or isotonic saline. The two infusions were given over 20 s and separated by 3 min. The isotonic saline followed by BKN did not induce muscle pain or muscular hyperalgesia. However, the combination of 5-HT and BKN (10 nmol) produced: (1) significantly higher VAS scores (P < 0.05) compared with all other combinations; (2) significantly longer pain offset (P < 0.05) compared with the combinations of isotonic saline and BKN; (3) significantly lower PPTs at 5, 20, and 40 min post-infusion (P < 0.05) compared with baseline PPT and PPTs after all other combinations. Cutaneous sensibility to mechanical stimuli and SPPTs were not affected by any of the combinations. The combinations of serotonin and bradykinin produce experimental muscle pain and muscular hyperalgesia to mechanical stimuli. Pre-treatment with serotonin may enhance the effect of bradykinin in the generation of muscle pain and muscular hyperalgesia in humans.     

Diffuse noxious inhibitory control evoked by tonic craniofacial pain in humans

Tonic pain in one body segment can inhibit the perception of pain in another body segment. This phenomenon is mediated by diffuse noxious inhibitory controls (DNIC), and its efficacy in craniofacial regions is investigated in this study. A compressive device that evoked a tonic, moderate/severe, headache‐like, conditioning pain (～8/10 on a visual analogue scale) was applied for 15 min. Eleven males participated in the study. Pressure pain threshold (PPT) and pressure pain tolerance (PPTol) at multiple heterosegmental body sites (right masseter, splenius capitis, second intermediate phalange, brachioradialis and tibialis anterior) were measured before, during and at multiple time points (5, 20 and 35 min) after the termination of the conditioning pain. PPTs and PPTols were compared within participants across two experimental sessions; one that included painful conditioning stimulation, and a separate control session on a different day. Painful conditioning increased PPT significantly during pain over the masseter (p <0.05) and over the tibialis anterior (p <0.01). PPTol was unchanged. In the period after the painful conditioning stimulation PPT was depressed compared to control. This study shows that pain evoked from the craniofacial region evokes DNIC‐like mechanisms on segmental as well as heterosegmental sites.     

Effect of muscle relaxants on experimental jaw-muscle pain and jaw-stretch reflexes: a double-blind and placebo-controlled trial.

A randomised, double-blind, placebo-controlled three-way cross-over study was performed to investigate the effect of two muscle relaxants (tolperisone hydrochloride and pridinol mesilate) on experimental jaw-muscle pain and jaw-stretch reflexes. Fifteen healthy men participated in three randomised sessions separated by at least 1 week. In each session 300 mg tolperisone, 8 mg pridinol mesilate or placebo was administered orally as a single dose. One hour after drug administration 0.3 ml hypertonic saline (5.8%) was injected into the right masseter to produce muscle pain. Subjects continuously rated their perceived pain intensity on an electronic 10-cm visual analogue scale (VAS). The pressure pain threshold (PPT) was measured and short-latency reflex responses were evoked in the pre-contracted (15% maximal voluntary contraction) masseter and temporalis muscles by a standardised stretch device (1 mm displacement, 10 ms ramp time) before (baseline), 1 h after medication (post-drug), during ongoing experimental muscle pain (pain-post-drug), and 15 min after pain had vanished (post-pain). Analysis of variance demonstrated significantly lower VAS peak pain scores (5.9 +/- 0.4 cm) after administration of tolperisone hydrochloride compared with pridinol mesilate (6.8 +/- 0.4 cm) and placebo (6.6 +/- 0.4 cm) (P=0.020). Administration of pridinol mesilate was associated with a significant decrease in PPTs compared with tolperisone hydrochloride and placebo (P=0.002) after medication, but not after experimental jaw-muscle pain. The normalised peak-to-peak amplitude of the stretch reflexes were not significantly influenced by the test medication (P=0.762), but were in all sessions significantly facilitated during ongoing experimental jaw-muscle pain (P=0.034). In conclusion, tolperisone hydrochloride provides a small, albeit significant reduction in the perceived intensity of experimental jaw-muscle pain whereas the present dose had no effect on the short-latency jaw-stretch reflex.     

Bilateral Mechanical-Pain Sensitivity Over the Trigeminal Region in Patients With Chronic Mechanical Neck Pain

The aim of this study was to investigate bilateral pressure-pain sensitivity over the trigeminal region, the cervical spine, and the tibialis anterior muscle in patients with mechanical chronic neck pain. Twenty-three patients with neck pain (56% women), aged 20 to 37 years old, and 23 matched controls (aged 20 to 38 years) were included. Pressure pain thresholds (PPTs) were bilaterally assessed over masseter, temporalis, and upper trapezius muscles, the C5-C6 zygapophyseal joint, and the tibialis anterior muscle in a blinded design. The results showed that PPT levels were significantly decreased bilaterally over the masseter, temporalis, and upper trapezius muscles, and also the C5-C6 zygapophyseal joint (P < .001), but not over the tibialis anterior muscle (P = .4) in patients with mechanical chronic neck pain when compared to controls. The magnitude of PPT decreases was greater in the cervical region as compared to the trigeminal region (P < .01). PPTs over the masseter muscles were negatively correlated to both duration of pain symptoms and neck-pain intensity (P < .001). Our findings revealed pressure-pain hyperalgesia in the trigeminal region in patients with mechanical chronic neck pain, suggesting spreading of sensitization to the trigeminal region in this patient population.PerspectiveThis article reveals the presence of bilateral pressure-pain hypersensitivity in the trigeminal region in patients with idiopathic neck pain, suggesting a sensitization process of the trigemino-cervical nucleus caudalis in this population. This finding has implications for development of management strategies.     

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

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.     

Temporal summation of pain evoked by mechanical stimulation in deep and superficial tissue.

Temporal summation of deep tissue pain has been suggested to be facilitated in chronic musculoskeletal pain syndromes. This study aimed to test whether temporal summation of mechanical induced pressure pain is (1) more pronounced at short (1 second) interstimulus intervals (ISIs) compared with long ISI (30 seconds), (2) more potent than summation elicited by pure skin stimulation, and (3) attenuated in women compared with men. Twelve age-matched men and 12 women were included. A computer-controlled pressure stimulator with a probe surface of 1 cm2 was used to give 10 stimulations to the tibialis anterior, tibia periosteum, and the first web of the hand. Sequential stimulation at pressure pain threshold intensity was applied with different ISIs (1, 3, 5, 10, and 30 seconds). The pain intensity was assessed on a visual analog scale (VAS) after each individual stimulus. The VAS scores after the 10th stimulation with 1-second ISI were increased (P < .05) by 418% +/- 77%, 378% +/- 89%, and 234% +/- 66% compared with the first stimulation for tibia, tibialis anterior, and web, respectively. Temporal summation of pain was observed for all ISIs in tibialis anterior and tibia, eg, 30-second ISI evoked a VAS increase of 192% +/- 71 % (tibia) and 117% +/- 42% (tibialis anterior) compared with the first stimulation. The VAS score after the 10th web stimulation was smaller (P < .05) than that of the 10th tibialis anterior or tibia stimulation. A regression analysis between stimulation number and VAS score showed that the pain intensity increased progressively (1) more for 1-second ISIs compared with longer ISIs (P < .01) and (2) faster in deep tissue compared with skin (P < .01). No gender difference was observed. The temporal summation might be related to both central and peripheral mechanisms. PERSPECTIVE: Pain originating in deep tissue influences central pain processing systems more than superficial tissue. This might be of importance in patients with musculoskeletal pain.     

Involvement of ATP and its receptors on nociception in rat model of masseter muscle pain

The exact mechanism of the masseter muscle pain recognized as a prominent symptom in temporomandibular disorders remains unclear, although it is clinically known that excessive muscular contraction causes tenderness in masseter muscles. It has been demonstrated that P2X3 receptors (P2X3Rs) in sensory neurons play a role in pain signaling from the periphery. We determined the role of P2X(3)R on pressure pain and mechanical hyperalgesia in a newly developed rat model of masseter muscle pain. The pain in the masseter muscle was assessed by the pressure pain threshold (PPT), which was defined as the amount of pressure required to induce head flinching. In naive animals, systemic treatment with morphine was associated with increase of PPTs. Changes in PPTs were examined after administration of P2XR agonists or antagonists into the masseter muscle. The masseter muscle injection of alpha,beta-meATP (P2X(1,3,2/3)R-specific agonist) induced a significantly greater behavioral response than its vehicle. This enhanced response was completely blocked by the co-application of alpha,beta-meATP with PPADS (P2X(1,2,3,5,1/5,2/3)R-specific antagonist). Excessive contraction in masseter muscle was produced by electrical stimulation. The exerted masseter muscles showed a significant reduction in PPTs indicating the induction of mechanical hyperalgesia of the muscle. Moreover, administration of PPADS to the exerted masseter muscles produced a complete recovery of reducing PPT. Immunohistochemically, the number of P2X3R-positive neurons innervating the masseter muscles increased in the excessively contracted condition in trigeminal ganglia. Our results suggested that P2X3R plays an important role in pressure pain and mechanical hyperalgesia in masseter muscle caused by excessive muscular contraction.     

Thermographic evaluation of occlusal splint and low level laser therapy in myofascial pain syndrome

ObjectiveThe purpose of this study was to compare and evaluate the effects of occlusal splint and low dose laser treatments clinically and thermographically in patients with myofascial pain syndrome.MethodsTwenty patients aged 18–45 with myofascial pain syndrome were involved into this study. Patients were examined by clinically and Research Diagnostic Criteria for Temporomandibular Disorders (RDC/TMD) was used for the diagnosis of TMD. Patients divided into two groups. First group treated with stabilisation splint, while the other one with low level laser therapy (LLLT). Pre- and post-treatment pain intensity, muscle sensitivity and the superficial skin temperature differences over the masseter and anterior temporal muscle were assessed, and comparison was made within and between the groups pre- and post-operatively.ResultsIn both groups, there was a significant decrease in temperature values, especially in the masseter region (p < 0.05) and post-treatment pain intensity and muscle sensitivity values were lower than the pre-treatment values (p < 0.05). In addition, the heat values in certain regions of the masseter were lower in the LLLT group than in the splint group and there was a statistical difference in these regions between two groups (p < 0.05). However, there was no statistical difference in the pain intensity and muscle sensitivity between both groups (p > 0.05).ConclusionIt was concluded that both occlusal splint therapy and low level laser therapy were effective in the treatment of MPS, and when thermographic data were taken into account, LLLT treatments could provide more advantageous results in these patients.     

Acidic buffer induced muscle pain evokes referred pain and mechanical hyperalgesia in humans

While tissue acidosis causes local deep-tissue pain, its effect on referred pain and mechanical muscle hyperalgesia is unknown. The aim of this study was to investigate a human experimental acidic muscle pain model using a randomized, controlled, single-blinded study design. Seventy-two subjects (36 female) participated in three visits, each involving one 15 min intramuscular infusion into the anterior tibialis muscle: acidic phosphate buffer (pH 5.2) at 40 ml/h (N=69) or 20 ml/h (N=54), normal phosphate buffer (pH 7.3) at 40 ml/h (N=70), or isotonic saline at 40 ml/h (N=19). Pain ratings and pressure sensitivity of superficial and deep tissues were assessed before, during, and 20 min after infusion. Acidic buffer produced light to moderate, rate-dependent, muscle pain (not sex-dependent) compared to the control infusions, that referred pain to the ankle in 80% of women and 40% of men. Pain did not vary across self-reported menstrual phases. Pressure pain thresholds (PPTs) were reduced over the infused muscle with acidic infusion, defined as primary mechanical hyperalgesia. PPTs decreased at the ankle in those with referred pain in response to acidic buffer, i.e. referred mechanical hyperalgesia, but not at the foot. No pain or changes in PPTs occurred in the contralateral leg. These results demonstrate muscle acidosis can lead to local and referred pain and hyperalgesia, with significant sex differences in development of referred pain.     

Characteristics of referred muscle pain to the head from active trigger points in women with myofascial temporomandibular pain and fibromyalgia syndrome

Our aim was to compare the differences in the prevalence and the anatomical localization of referred pain areas of active trigger points (TrPs) between women with myofascial temporomandibular disorder (TMD) or fibromyalgia (FMS). Twenty women (age 46 ± 8 years) with TMD and 20 (age 48 ± 6 years) with FMS were recruited from specialized clinic. Bilateral temporalis, masseter, sternocleidomastoid, upper trapezius, and suboccipital muscles were examined for TrPs. TrPs were identified by palpation and considered active when the pain reproduced familiar pain symptom experienced by the patient. The referred pain areas were drawn on anatomical maps, digitalized and also measured. A new analysis technique based on a center of gravity (COG) method was used to quantitative estimate of the localization of the TrP referred pain areas. Women with FMS exhibited larger areas of usual pain symptoms than women with myofascial TMD (P < 0.001). The COG coordinates of the usual pain on the frontal and posterior pain maps were located more superior in TMD than in FMS. The number of active TrPs was significantly higher in TMD (mean ± SD 6 ± 1) than in FMS (4 ± 1) (P = 0.002). Women with TMD exhibited more active TrPs in the temporalis and masseter muscles than FMS (P < 0.01). Women with FMS had larger referred pain areas than those with TMD for sternocleidomastoid and suboccipital muscles (P < 0.001). Significant differences within COG coordinates of TrP referred pain areas were found in TMD, the referred pain was more pronounced in the orofacial region, whereas the referred pain in FMS was more pronounced in the cervical spine. This study showed that the referred pain elicited from active TrPs shared similar patterns as usual pain symptoms in women with TMD or FMS, but that distinct differences in TrP prevalence and location of the referred pain areas could be observed. Differences in location of referred pain areas may help clinicians to determine the most relevant TrPs for each pain syndrome in spite of overlaps in pain areas.     

Increased muscle pain sensitivity in patients with tension-type headache

Nociceptive mechanisms in tension-type headache are poorly understood. The aim was to investigate the pain sensitivity of pericranial muscles and a limb muscle in patients with tension-type headache. Experimental muscle pain was induced by standardized infusions of 0.5 ml of 1 M hypertonic saline into two craniofacial muscles (anterior temporalis (TPA) and masseter (MAS)) and a limb muscle (anterior tibial (TA)) in 24 frequent episodic tension-type headache patients (FETTH), 22 chronic tension-type headache patients (CTTH) and 26 age and gender matched healthy subjects. Headache patients were examined twice, both on days with and on days without headache. The pressure pain thresholds (PPTs) were determined before and after infusions. The subjects continuously reported intensity of saline-induced pain on an electronic visual analogue scale (VAS) and the perceived area of pain was drawn on anatomical maps. Headache patients demonstrated significantly lower PPTs, higher saline-evoked VAS pain scores and greater pain areas than healthy subjects at all the tested muscle sites (P<0.05). There was a significant gender difference for the PPTs in all three groups of participants (P<0.05) and for VAS pain scores in the CTTH patients (P<0.05). There was no difference in pain sensitivity between FETTH and CTTH or between patients with or without headache. In conclusion, the present study demonstrates the presence of generalized pain hypersensitivity both in FETTH and CTTH compared to controls which is unrelated to actual headache status and extends to include responses to longer-lasting stimuli which are clinically highly relevant. Gender differences in deep pain sensitivity seem to be a consistent finding both in healthy controls and patients with tension-type headache.     

Expression of 5-HT3 receptors and TTX resistant sodium channels (NaV1.8) on muscle nerve fibers in pain-free humans and patients with chronic myofascial temporomandibular disorders

Background

Previous studies have shown that 5-HT₃-antagonists reduce muscle pain, but there are no studies that have investigated the expression of 5-HT₃-receptors in human muscles. Also, tetrodotoxin resistant voltage gated sodium-channels (Na_V) are involved in peripheral sensitization and found in trigeminal ganglion neurons innervating the rat masseter muscle. This study aimed to investigate the frequency of nerve fibers that express 5-HT_3A-receptors alone and in combination with Na_V1.8 sodium-channels in human muscles and to compare it between healthy pain-free men and women, the pain-free masseter and tibialis anterior muscles, and patients with myofascial temporomandibular disorders (TMD) and pain-free controls.

Methods

Three microbiopsies were obtained from the most bulky part of the tibialis and masseter muscles of seven and six healthy men and seven and six age-matched healthy women, respectively, while traditional open biopsies were obtained from the most painful spot of the masseter of five female patients and from a similar region of the masseter muscle of five healthy, age-matched women. The biopsies were processed by routine immunohistochemical methods. The biopsy sections were incubated with monoclonal antibodies against the specific axonal marker PGP 9.5, and polyclonal antibodies against the 5-HT_3A-receptors and Na_V1.8 sodium-channels.

Results

A similar percentage of nerve fibers in the healthy masseter (85.2%) and tibialis (88.7%) muscles expressed 5-HT_3A-receptors. The expression of Na_V1.8 by 5-HT_3A positive nerve fibers associated with connective tissue was significantly higher than nerve fibers associated with myocytes (P < .001). In the patients, significantly more fibers per section were found with an average of 3.8 ± 3 fibers per section in the masseter muscle compared to 2.7 ± 0.2 in the healthy controls (P = .024). Further, the frequency of nerve fibers that co-expressed Na_V1.8 and 5-HT_3A receptors was significantly higher in patients (42.6%) compared to healthy controls (12.0%) (P < .001).

Conclusions

This study showed that the 5-HT_3A-receptor is highly expressed in human masseter and tibialis muscles and that there are more nerve fibers that express 5-HT_3A-receptors in the masseter of women with myofascial TMD compared to healthy women. These findings indicate that 5-HT₃-receptors might be up-regulated in myofascial TMD and could serve as potential biomarkers of chronic muscle pain.     

Widespread sensory hypersensitivity is a feature of chronic whiplash-associated disorder but not chronic idiopathic neck pain

OBJECTIVES: To investigate sensory changes present in patients with chronic whiplash-associated disorders and chronic idiopathic neck pain using a variety of quantitative sensory tests to better understand the pain processing mechanisms underlying persistent symptoms. METHODS: A case control study was used with 29 subjects with chronic whiplash-associated disorders, 20 subjects with chronic idiopathic neck pain, and 20 pain-free volunteers. Pressure pain thresholds were measured over the articular pillars of C2-C3, C5-C6, the median, radial, and ulnar nerve trunks in the arm and over a remote site, the muscle belly of tibialis anterior. Heat pain thresholds, cold pain thresholds, and von Frey hair sensibility were measured over the cervical spine, tibialis anterior, and deltoid insertion. Anxiety was measured with the Short-Form of the Spielberger State Anxiety Inventory. RESULTS: Pressure pain thresholds were decreased over cervical spine sites in both subject groups when compared with controls (P < 0.05). In the chronic whiplash-associated disorders group, pressure pain thresholds were also decreased over the tibialis anterior, median, and radial nerve trunks (P < 0.001). Heat pain thresholds were decreased and cold pain thresholds increased at all sites (P < 0.03). No differences in heat pain thresholds or cold pain thresholds were evident in the idiopathic neck pain group at any site compared with the control group (P > 0.27). No abnormalities in von Frey hair sensibility were evident in either neck pain group (P > 0.28). DISCUSSION: Both chronic whiplash-associated disorders and idiopathic neck pain groups were characterized by mechanical hyperalgesia over the cervical spine. Whiplash subjects showed additional widespread hypersensitivity to mechanical pressure and thermal stimuli, which was independent of state anxiety and may represent changes in central pain processing mechanisms. This may have implications for future treatment approaches.     

Local vibrotactile and pain sensitivities are negatively related in temporomandibular disorders.

Earlier research has shown that cutaneous experimental pain can elevate the vibrotactile threshold at the same skin locus. The purpose of this study was to determine whether vibrotactile and pain thresholds in a clinical (temporomandibular disorders [TMD]) population are consistent with the hypothesis that chronic pain causes a similar elevation. Specifically, we predicted that TMD subjects with soreness (low palpation-pain threshold) at a given skin site would have relatively high vibrotactile thresholds at the same location. Measurements on the skin overlying the masseter in 18 individuals with TMD showed that pain sensitivity was negatively correlated with sensitivity to 20-Hz vibration (presumed to activate a rapidly adapting mechanoreceptive channel), but not with sensitivity to 200-Hz vibration (thought to activate primarily a slowly adapting channel, because the Pacinian channel is lacking in the orofacial region). There was no relationship between vibration thresholds over the masseter and pain threshold at other orofacial sites, including the contralateral masseter. Vibrotactile and pain thresholds were uncorrelated in control participants without chronic pain (n = 18). The results indicate that in TMD, a localized relationship exists between pain sensitivity and the sensitivity of a low-frequency vibrotactile channel.     

Effects of 4-Week Diacutaneous Fibrolysis on Myalgia,Mouth Opening,and Level of Functional Severity in Women With Temporomandibular Disorders: A Randomized Controlled Trial

ObjectiveThe purpose of this study was to assess the effects of 4-week protocol of diacutaneous fibrolysis (DF) compared with simulated DF (sham-DF) on myalgia and mouth opening.MethodsIn a sham randomized controlled trial, 34 women with temporomandibular disorders and myofascial pain were randomly divided as intervention group (IG) and sham-DF group (SG). The IG received 4 weeks of real DF, and the SG received sham. Pain was assessed through the visual analog scale and pressure pain thresholds (PPTs) on the temporomandibular joint (TMJ), and over the temporal and masseter muscles. The Mandibular Function Impairment Questionnaire was used to classify the participants regarding to the severity of the functional limitation related to TMD.ResultsPain scores decreased for both groups, but the IG showed lower values at week 4, with between-group differences. Bilateral temporal PPT showed higher values at week 4, with between-group differences. The SG had lower PPTs but the IG had higher PPTs, both compared to baseline results. The time-by-group interaction and the frequency of participants above 40 mm of mouth opening showed a significant difference for the IG over time with higher results at the 4-week assessment compared to its own baseline. Both groups showed lower MFIQ scores from baseline to 4-week assessment. There was a lower frequency of a moderate level of severity for the IG. No differences were observed for TMJ or for the masseter muscles PPT.ConclusionImprovements were observed for visual analog scale scores and PPTs on temporal muscles. There was a group-by-time interaction in the IG, suggesting a possible potential use of DF for mouth opening.     

Patterns of experimentally induced pain in pericranial muscles

Nociceptive mechanisms in the craniofacial muscle tissue are poorly understood. The pain pattern in individual pericranial muscles has not been described before. Experimental muscle pain was induced by standardized infusions of 0.2 ml 1 m hypertonic saline into six craniofacial muscles (masseter, anterior temporalis, posterior temporalis, trapezius, splenius capitis and sternocleidomastoid) in 20 healthy subjects. The pressure pain thresholds (PPTs) were determined before and after infusions. The subjects continuously reported intensity of saline-induced pain on an electronic visual analogue scale (VAS) and the perceived area of pain was drawn on anatomical maps. The pain areas were measured and the localization determined by a new centre-of-gravity method. The PPTs were lowest on the sternocleidomastoid muscle (anova: P<0.001), but the saline-evoked VAS pain scored highest following injection into the masseter muscle (anova: P<0.05). The centre-of-gravity measures demonstrated significantly different localization of the pain areas (anova: P<0.001). The trigeminally vs. the cervically innervated muscles had significantly different patterns of spread and referral of pain according to trigeminally vs. cervically innervated dermatomes (P<0.005). In conclusion, there appear to be characteristic pain patterns and pain sensitivity in different craniofacial muscles in healthy volunteers, which may be of importance for further research on different craniofacial pain conditions.     

Headache service quality: evaluation of quality indicators in 14 specialist-care centres

Dopaminergic pathways could be involved in the pathophysiology of myofascial temporomandibular disorders (M-TMD). This study investigated plasma levels of dopamine and serotonin (5-HT) in patients with M-TMD and in healthy subjects. Fifteen patients with M-TMD and 15 age- and sex-matched healthy subjects participated. The patients had received an M-TMD diagnosis according to the Research Diagnostic Criteria for TMD. Perceived mental stress, pain intensity (0–100-mm visual analogue scale), and pressure pain thresholds (PPT, kPa) over the masseter muscles were assessed; a venous blood sample was taken. Dopamine in plasma differed significantly between patients with M-TMD (4.98 ± 2.55 nM) and healthy controls (2.73 ± 1.24 nM; P < 0.01). No significant difference in plasma 5-HT was observed between the groups (P = 0.75). Patients reported significantly higher pain intensities (P < 0.001) and had lower PPTs (P < 0.01) compared with the healthy controls. Importantly, dopamine in plasma correlated significantly with present pain intensity (r = 0.53, n = 14, P < 0.05) and perceived mental stress (r = 0.34, n = 28, P < 0.05). The results suggest that peripheral dopamine might be involved in modulating peripheral pain. This finding, in addition to reports in other studies, suggests that dopaminergic pathways could be implicated in the pathophysiology of M-TMD but also in other chronic pain conditions. More research is warranted to elucidate the role of peripheral dopamine in the pathophysiology of chronic pain.