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To investigate the associations between signs of painful temporomandibular disorders (TMD) and number of tender points (TPs) and fibromyalgia in adolescents, as well as the relationship between TPs and pressure-pain threshold (PPT) in individuals presenting with local, regional, or widespread pain as a way to investigate the presence of central sensitization (CS).
Peripheral nerve injury causes changes in expression of multiple receptors and mediators that participate in pain processing. We investigated the expression of microRNAs (miRNAs) – a class of post-transcriptional regulators involved in many physiological and pathophysiological processes – and their potential role in the development or maintenance of chronic neuropathic pain following lingual nerve injury in human and rat. We profiled miRNA expression in Sprague-Dawley rat and human lingual nerve neuromas using TaqMan low-density array (TLDA) cards. Expression of miRNAs of interest was validated via specific probes and correlated with nerve injury-related behavioural change in rat (time spent drinking) and clinical pain (VAS score). Target prediction was performed using publicly available algorithms; gene enrichment and pathway analysis were conducted with MetaCore. Networks of miRNAs and putative target genes were created with Cytoscape; interaction of miRNAs and target genomes in rat and human was displayed graphically using CircosPlot. rno-miR-138 was upregulated in lingual nerve of injured rats versus sham controls. rno-miR-138 and rno-miR-667 expression correlated with behavioural change at day 3 post-injury (with negative [rno-miR-138] and positive [rno-miR-667] correlations between expression and time spent drinking). In human, hsa-miR-29a was downregulated in lingual nerve neuromas of patients with higher pain VAS scores (painful group), versus patients with lower pain VAS scores (non-painful). A statistically significant negative correlation was observed between expression of both hsa-miR-29a and hsa-miR-500a, and pain VAS score. Our results show that following lingual nerve injury there are highly significant correlations between abundance of specific miRNAs, altered behaviour and pain scores. This study provides the first demonstration of correlations between human miRNA levels and VAS scores for neuropathic pain, and suggests a potential contribution of specific miRNAs to the development of chronic pain following lingual nerve injury. Putative targets for candidate miRNAs include genes related to interleukin and chemokine receptors and potassium channels.
Cold hyperalgesia is an indicator of widespread pain sensitivity and is associated with poor clinical outcomes. Menthol activates TRPM8, a cold-sensing receptor channel. This research evaluated topical menthol as a potential stimulus to be used in the clinical evaluation of cold hyperalgesia.
Migraine is characterized by an increased sensitivity to visual stimuli that worsens during attacks. Recent evidence has shown that feedforward volleys carrying incoming visual information induce high frequency (gamma) oscillations in the visual cortex, while feedback volleys arriving from higher order brain areas induce oscillatory activity at lower frequencies (theta/alpha/low-beta). We investigated visually induced high (feedforward) and low (feedback) frequency activations in healthy subjects and various migraine patients. Visual evoked potentials from 20 healthy controls and 70 migraine patients (30 inter-ictal and 20 ictal episodic migraineurs, 20 chronic migraineurs) were analysed in the frequency domain. We compared power in the theta-alpha-low beta and gamma range between groups, and searched for correlations between the low-to-high frequency activity ratio and number of monthly headache and migraine days. Compared to healthy controls, inter-ictal migraine patients had increased visually induced low frequency (feedback) activity. Conversely, ictal and chronic migraine patients showed an augmented gamma band (feedforward) power. The low-frequency-to-gamma (feedback/feedforward) activity ratio correlated negatively with monthly headache days and tended to do so with migraine days. Our findings show that visual processing is differentially altered depending on migraine cycle and type. Feedback control from higher order cortical areas predominates interictally in episodic migraine while migraine attacks and chronic migraine are associated with enhanced incoming afferent activity, confirming their similar electrophysiological profile. The presence of headache is associated with proportionally higher gamma (feedforward) activities. Perspective: This study provides an insight into the pathophysiology of migraine headache from the perspective of cortical sensory processing dynamics. Patients with migraine present alterations in feedback and feedforward visual signalling that differ with the presence of headache.
Recovery from severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection appears exponential, leaving a tail of patients reporting various long COVID symptoms including unexplained fatigue/exertional intolerance and dysautonomic and sensory concerns. Indirect evidence links long COVID to incident polyneuropathy affecting the small-fiber (sensory/autonomic) axons.
Acute stress reduces responses to static evoked pain stimuli (stress-induced analgesia [SIA]). Whether SIA inhibits temporal summation of pain, a dynamic evoked pain measure indexing central sensitization, has been little studied and mechanisms were not evaluated.
To analyze cervical tenderness scores (CTS) in patients with various temporomandibular disorders (TMD) and in controls and to examine associations of CTS with demographic and clinical parameters.
The neural mechanisms responsible for the initiation and expression of migraines remain unknown. Though there is growing evidence of changes in brainstem anatomy and function between attacks, very little is known about brainstem function and structure in the period immediately prior to a migraine. The aim of this investigation is to use brainstem-specific analyses of diffusion weighted images to determine if the brainstem pain processing regions display altered structure in individuals with migraine across the migraine cycle, and in particular immediately prior to a migraine. Diffusion tensor images (29 controls, 36 migraineurs) were used to assess brainstem anatomy in migraineurs compared with controls. We found that during the interictal phase, migraineurs displayed greater mean diffusivity in the region of the spinal trigeminal nucleus, dorsomedial/dorsolateral pons and midbrain periaqueductal gray matter/cuneiform nucleus. Remarkably, the mean diffusivity returned to controls levels during the 24-hour period immediately prior to a migraine, only to increase again within the three following days. Additionally, fractional anisotropy was significantly elevated in the region of the medial lemniscus/ventral trigeminal thalamic tract in migraineurs compared with controls over the entire migraine cycle. These data show that regional brainstem anatomy changes over the migraine cycle, with specific anatomical changes occurring in the 24 hours prior to onset. These changes may contribute to the activation of the ascending trigeminal pathway by either an increase in basal traffic or by sensitising the trigeminal nuclei to external triggers, with activation ultimately resulting in perception of head pain during a migraine attack. It has been hypothesised that modulation of brainstem pain pathways may be critical for the initiation of migraine attacks. There is some evidence that altered brainstem function, possibly involving increased astrocyte activation, occurs immediately prior to a migraine attack. We sought to obtain evidence to support this theory. Using diffusion tensor imaging, we found that immediately prior to a migraine, mean diffusivity decreased in the spinal trigeminal nucleus, dorsomedial/dorsolateral pons and midbrain periaqueductal gray matter/nucleus cuneiform. Mean diffusivity then increased again immediately following the migraine attack. Decreased mean diffusivity before a migraine is consistent with increased astrocyte activation, since astrocyte processes enlarge during activation. These changes may underlie changes in brainstem function that are essential for the generation of a migraine.
Epidemiological studies have to a little extent addressed the potential fluctuations of chronic pain over time, and there is a lack of information about the long-term course of pain using repeated measurements. We wanted to identify different trajectories of pain during eight waves of follow-up over four years among individuals in the general population reporting pain lasting at least six months at baseline. Secondarily, we wanted to investigate whether biopsychosocial factors at baseline were associated with the different pain trajectories. Longitudinal Latent Class Analysis (LLCA) was performed to classify 1905 random participants from a larger population-based study (HUNT3) into groups based on their longitudinal pain severity reporting. A five-class solution gave the best fit. The terms chosen to describe the pain trajectories were: "fluctuating" (n = 586 [31 %]), "persistent mild" (n = 449 [24 %]), "persistent moderate" (n = 414 [22 %]), "persistent severe" (n = 251 [13 %]), and "gradual improvement" (n = 205 [11 %]). In a multinomial logistic regression model using "gradual improvement" as the reference category, the "persistent moderate", "persistent severe", and "fluctuating" pain groups were associated with chronic widespread pain (CWP), elevated levels of catastrophizing, and poorer mental health. The "persistent mild" group was associated with sleep difficulties only. This study finds that although most individuals have a stable pain course, individuals in the largest distinct trajectory reports pain that fluctuate between mild and moderate levels, thus fluctuating under and above the chronic pain definition using moderate pain or more as a criterion. Perspective: When examining the long-term course of chronic pain in the general population, five trajectories emerge. Although most individuals have stable pain, the largest distinct trajectory fluctuated under and above the chronic pain cut-off, using moderate pain or more as a criterion. A dichotomous categorization of chronic pain may be overly simplistic.