Enhanced medial prefrontal-default mode network functional connectivity in chronic pain and its association with pain rumination.

Rumination is a form of thought characterized by repetitive focus on discomforting emotions or stimuli. In chronic pain disorders, rumination can impede treatment efficacy. The brain mechanisms underlying rumination about chronic pain are not understood. Interestingly, a link between rumination and functional connectivity (FC) of the brain's default mode network (DMN) has been identified within the context of mood disorders. We, and others, have also found DMN dysfunction in chronic pain populations. The medial prefrontal cortex (mPFC) is a key node of the DMN that is anatomically connected with the descending pain modulatory system. Therefore, we tested the hypothesis that in patients with chronic pain, the mPFC exhibits abnormal FC related to the patient's degree of rumination about their pain. Seventeen patients with idiopathic temporomandibular disorder (TMD) and 17 age- and sex-matched healthy controls underwent resting state functional MRI, and rumination about pain was assessed through the rumination subscale of the Pain Catastrophizing Scale. Compared with healthy controls, we found that TMD patients exhibited enhanced mPFC FC with other DMN regions, including the posterior cingulate cortex (PCC)/precuneus (PCu) and retrosplenial cortex. We also found that individual differences in pain rumination in the chronic pain patients (but not in healthy controls) were positively correlated to mPFC FC with the PCC/PCu, retrosplenial cortex, medial thalamus, and periaqueductal/periventricular gray. These data implicate communication within the DMN and of the DMN with the descending modulatory system as a mechanism underlying the degree to which patients ruminate about their chronic pain.

Symptoms resembling temporomandibular joint disorder caused by a pleomorphic adenoma.

Pleomorphic adenoma is a benign neoplasm of the salivary glands. It is the most common type of salivary gland tumour and the tumour most commonly found in the parotid gland. Clinical diagnosis of a parotid gland neoplasm can be difficult, particularly when the lesion is located deep within the gland. Although usually asymptomatic, pleomorphic adenoma may exhibit symptoms mimicking those of conditions such as temporomandibular joint disorder. This case report highlights the difficulties of diagnosing this type of tumour and the importance of communication between physicians and dentists to ensure an accurate diagnosis.

Assessment of Concordance between Chairside Ultrasonography and Digital Palpation in Detecting Myofascial Trigger Points in Masticatory Myofascial Pain Syndrome.

INTRODUCTION: Masticatory myofascial pain is a musculoligamentous syndrome that can mimic odontogenic pain. Pain referral to odontogenic structures can be traced to hyperirritated myofascial trigger points (MTrPs). This pragmatic study evaluated the concordance between ultrasonography and palpation in detecting MTrPs in the masseter and temporalis muscles. METHODS: Fifty-seven patients suspected to have temporomandibular disorder were included. MTrPs were palpated manually by expert clinicians. Ultrasonography was then performed by a blind sonographer. The quantity of MTrPs and the involved muscle sections, the pain occurrence, and the location of the MTrPs within the muscle sections were compared using the mean difference (MD) and concordance statistics (Cohen κ and the interclass correlation coefficient [ICC]) as applicable. RESULTS: Ultrasonography located MTrPs as 2.1 ± 1.3 mm2 hypoechoic nodules at a depth of 7 ± 3.3 mm. Ultrasonography moderately agreed with palpation on the quantity of MTrPs per patient (MD = 1; 95% confidence interval [CI], 0.06-1.9; ICC = 0.56; 95% CI, 0.32-0.72). Palpation detected marginally more involved muscle sections per patient (MD = 0.7; 95% CI, 0.06-1.34.05; ICC = 0.64; 95% CI, 0.44-0.77) with more pain occurrence per patient (MD = 1.4; 95% CI, 0.56-2.28; ICC = 0.13; 95% CI, -0.26 to 0.41). There was a discordance in the location of the MTrPs within the muscle sections per patient (κ = -0.46; 95% CI, -0.77 to -0.14). CONCLUSIONS: Ultrasonography and palpation concurred moderately to substantially on the quantity of MTrPs and the involved muscle sections but disagreed on the location of the MTrPs within the muscle sections. Ultrasonography has the potential as a chairside diagnostic aid to help clinicians determine an accurate diagnosis, enhance patient experience during examination, and avoid unnecessary treatments that can mitigate the risk of iatrogenic damage.

Perceived helplessness is associated with individual differences in the central motor output system.

Learned helplessness is a maladaptive response to uncontrollable stress characterized by impaired motor escape responses, reduced motivation and learning deficits. There are important individual differences in the likelihood of becoming helpless following exposure to uncontrollable stress but little is known about the neural mechanisms underlying these individual differences. Here we used structural MRI to measure gray and white matter in individuals with chronic pain, a population at high risk for helplessness due to prolonged exposure to a poorly controlled stressor (pain). Given that self-reported helplessness is predictive of treatment outcomes in chronic pain, understanding such differences might provide valuable clinical insight. We found that the magnitude of self-reported helplessness correlated with cortical thickness in the supplementary motor area (SMA) and midcingulate cortex, regions implicated in cognitive aspects of motor behavior. We then examined the white matter connectivity of these regions and found that fractional anisotropy of connected white matter tracts along the corticospinal tract was associated with helplessness and mediated the relationship between SMA cortical thickness and helplessness. These data provide novel evidence that links individual differences in the motor output pathway with perceived helplessness over a chronic and poorly controlled stressor.

Masticatory Myofascial Pain Syndrome: Implications for Endodontists.

INTRODUCTION: Masticatory myofascial pain syndrome can present similarly to other dental conditions in odontogenetic structures. Endodontists should be familiar with the symptomology and pathophysiology of masticatory myofascial pain syndrome to avoid misdiagnosis, incorrect treatment, and medicolegal repercussions. The aim of this review was to provide a foundational summary for endodontists to identify and correctly manage masticatory myofascial pain syndrome. METHODS: A narrative review of the literature was performed through a MEDLINE search and a hand search of the major myofascial pain textbooks. RESULTS: Masticatory myofascial pain syndrome is a musculoligamentous syndrome that can present similarly to odontogenic pain or refer pain to the eyebrows, ears, temporomandibular joints, maxillary sinus, tongue, and hard palate. Currently, the most comprehensive pathophysiology theory describing masticatory myofascial pain syndrome is the expanded integrated hypothesis. The most widely accepted diagnostic guidelines for masticatory myofascial pain syndrome are the Diagnostic Criteria for Temporomandibular Disorders; however, their diagnostic capability is limited. There is no hierarchy of treatment methods because each patient requires a tailored and multidisciplinary management aimed at regaining the muscle's range of motion, deactivating the myofascial trigger points, and maintaining pain relief. CONCLUSIONS: The pain patterns for masticatory myofascial pain syndrome are well-known; however, there is a lack of consensus on the most proper method of trigger point diagnosis or pain quantification. The diagnostic strategies for masticatory myofascial pain syndrome vary, and the diagnostic aids are not well developed.

Contribution of chronic pain and neuroticism to abnormal forebrain gray matter in patients with temporomandibular disorder.

Cortical plasticity is thought to occur following continuous barrage of nociceptive afferent signals to the brain. Hence, chronic pain is presumed to induce anatomical and physiological changes in the brain over time. Inherent factors, some pre-dating the onset of chronic pain, may also contribute to brain abnormalities present in patients. In this study we used structural MRI to examine whether patients with chronic temporomandibular (TMD) pain have abnormalities in gray matter (GM) within brain areas implicated in pain, modulation and sensorimotor function. We found that patients with TMD have cortical thickening in the primary somatosensory cortex (S1), frontal polar and the ventrolateral prefrontal cortex (PFC). These findings provide a structural basis for previous findings of TMD pain and cognitive sluggishness in TMD. We then examined the contribution of TMD characteristics to GM abnormalities. We found that 1) GM in the sensory thalamus positively correlated to TMD duration, 2) cortical thickness in the primary motor (M1) and the anterior mid-cingulate cortices (aMCC) were negatively correlated to pain intensity, and 3) pain unpleasantness was negatively correlated to cortical thickness in the orbitofrontal cortex (OFC). These findings suggest that an individual's TMD pain history contributes to GM in the brain. Lastly, we examined the contribution of a potential pre-existing vulnerability due to neuroticism. In the TMD patients, we found that there was an abnormal positive correlation between neuroticism and OFC thickness, in contrast to the negative correlation found in the healthy controls. Therefore, neuroticism may contribute to TMD pathophysiology. In sum, our data suggest that GM in the brain of patients with chronic TMD pain can be shaped by both personality and pain characteristics.

Trigeminal neuralgia caused by intracranial epidermoid tumour: report of a case.

Trigeminal neuralgia is a recognized complication in patients with intracranial tumours affecting the trigeminal nerve. This case report describes an epidermoid tumour at the cerebellopontine angle in a middle-aged man with otherwise classical unilateral trigeminal neuralgia. The case highlights the difficulties of diagnosis and the importance of a multidisciplinary approach when trigeminal neuralgia occurs concurrently with a brain tumour.

Modulation of Jaw Muscle Motor Response and Wake-Time Parafunctional Tooth Clenching With Music.

AIMS: To evaluate the effects of Guided Music Listening (GML) on masticatory muscles and on the amplitude of wake-time tooth clenching in individuals with higher vs lower frequency of clenching episodes. METHODS: The electromyographic (EMG) activity of the right masseter was recorded during three 20-minute music (relaxing, stress/tension, and favorite) tasks and a control no-music task in 10 (mean age ± standard deviation [SD] = 21.4 ± 3.0 years) and 11 (22.6 ± 2.9 years) healthy volunteers with higher (HP) vs lower (LP) frequency of tooth-clenching episodes, respectively. EMG episodes greater than 10% of the maximum voluntary contraction (EMG activity of the masseter during tooth clenching) and below 10% (EMG activity during rest) were analyzed. Nonparametric tests were used to assess between-group and within-group (between-task) differences in primary outcome measures. RESULTS: In both groups, EMG activity during rest was the greatest during the stress/tension task, and it was the lowest during the favorite task in the LP group and the relaxing task in the HP group (all P < .001). In the HP group, the amplitude of clenching episodes was significantly lower during the favorite and stress/tension tasks than during the relaxing task (all P < .05), while in the LP group, it was significantly lower during the stress/tension task than during the control task (P = .001). The experiment did not affect the frequency or duration of clenching episodes. CONCLUSION: GML modulates masticatory muscle activity. The response to GML depends on the frequency of clenching and the type of music.

Abnormal gray matter aging in chronic pain patients.

Widespread brain gray matter (GM) atrophy is a normal part of the aging process. However, recent studies indicate that age-related GM changes are not uniform across the brain and may vary according to health status. Therefore the aims of this study were to determine whether chronic pain in temporomandibular disorder (TMD) is associated with abnormal GM aging in focal cortical regions associated with nociceptive processes, and the degree to which the cumulative effects of pain contributes to age effects. We found that patients have accelerated whole brain GM atrophy, compared to pain-free controls. We also identified three aberrant patterns of GM aging in five focal brain regions: 1) in the thalamus, GM volume correlated with age in the TMD patients but not in the control group; 2) in the anterior mid- and pregenual cingulate cortex (aMCC/pgACC), the TMD patients showed age-related cortical thinning, whereas the controls had age-related cortical thickening; and 3) in the dorsal striatum and the premotor cortex (PMC). Interestingly, the controls but not the patients showed age-related GM reductions. Finally, a result of particular note is that after accounting for the effects of TMD duration, age remained as a significant predictor of GM in the PMC and dorsal striatum. Thus, abnormal GM aging in TMD may be due to the progressive impact of TMD-related factors in pain-related regions, as well as inherent factors in motor regions, in patients with TMD. This study is the first to show that chronic pain is associated with abnormal GM aging in focal cortical regions associated with pain and motor processes.