Biomarkers in Temporomandibular Disorder and Trigeminal Neuralgia: A Conceptual Framework for Understanding Chronic Pain.
Ontology highlight
ABSTRACT:
SUBMITTER: Doshi TL
PROVIDER: S-EPMC7486013 | biostudies-literature | 2020
REPOSITORIES: biostudies-literature
Publications
Biomarkers in Temporomandibular Disorder and Trigeminal Neuralgia: A Conceptual Framework for Understanding Chronic Pain.
Doshi Tina L TL Nixdorf Donald R DR Campbell Claudia M CM Raja Srinivasa N SN
Canadian journal of pain = Revue canadienne de la douleur 20200123 1
In this review, we will explore the use of biomarkers in chronic pain, using the examples of two prototypical facial pain conditions: trigeminal neuralgia and temporomandibular disorder. We will discuss the main categories of biomarkers and identify various genetic/genomic, molecular, neuroradiological, and psychophysical biomarkers in both facial pain conditions, using them to compare and contrast features of neuropathic, non-neuropathic, and mixed pain. By using two distinct model facial pain ...[more]
Similar Datasets
Project description:Neuropathic pain is a common phenomenon that affects millions of people worldwide. Maxillofacial structures consist of various tissues that receive frequent stimulation during food digestion. The unique functions (masticatory process and facial expression) of the maxillofacial structure require the exquisite organization of both the peripheral and central nervous systems. Neuralgia is painful paroxysmal disorder of the head-neck region characterized by some commonly shared features such as the unilateral pain, transience and recurrence of attacks, and superficial and shock-like pain at a trigger point. These types of pain can be experienced after nerve injury or as a part of diseases that affect peripheral and central nerve function, or they can be psychological. Since the trigeminal and glossopharyngeal nerves innervate the oral structure, trigeminal and glossopharyngeal neuralgia are the most common syndromes following myofascial pain dysfunction syndrome. Nevertheless, misdiagnoses are common. The aim of this review is to discuss the currently available diagnostic procedures and treatment options for trigeminal neuralgia, glossopharyngeal neuralgia, and myofascial pain dysfunction syndrome.
| S-EPMC5554565 | biostudies-other
Project description:Purpose: In this study, we aimed to analyze lncRNA expression in the whole transcriptome of trigeminal ganglia (TG) and spinal trigeminal nucleus caudalis (Sp5C) in a chronic inflammatory TMJ pain mouse model. Chronic inflammatory TMJ pain was induced by intra-TMJ injection of complete Freund's adjuvant (CFA). The lncRNA expression patterns in the whole transcriptome of TG and Sp5C were profiled with RNA sequencing.
2022-06-01 | GSE188922 | GEO
Project description:We report a very rare case in which a patient believed to have auriculotemporal neuralgia due to the repeated recurrence of paroxysmal stabbing pain in the preauricular temporal region for four years developed occipital neuralgia, which finally improved with decompression of the greater occipital nerve (GON). The pain of occipital neuralgia has been suggested to be referred to the frontoorbital (V1) region through trigeminocervical interneuronal connections in the trigeminal spinal nucleus. However, the reports of such cases are very rare. In occipital neuralgia, the pain referred to the ipsilateral facial trigeminal region reportedly also occurs in the V2 and V3 distributions in addition to that in the V1 region. In the existing cases of referred trigeminal pain from occipital neuralgia, continuous aching pain is usually induced, but in the present case, typical neuralgic pain was induced and diagnosed as idiopathic auriculotemporal neuralgia. In addition, recurrent trigeminal pain occurred for four years before the onset of occipital neuralgia. If the typical occipital neuralgia did not develop in four years, it would be impossible to infer an association with the GON. This case shows that the clinical manifestations of referred trigeminal pain caused by the sensitization of the trigeminocervical complex by chronic entrapment of the GON can be very diverse.
| S-EPMC7463402 | biostudies-literature
Project description:BackgroundTrigeminal neuralgia, a severe chronic neuropathic pain disorder, is widely believed to be amenable to surgical treatments. Nearly 20% of patients, however, do not have adequate pain relief after surgery. Objective tools for personalized pre-treatment prognostication of pain relief following surgical interventions can minimize unnecessary surgeries and thus are of substantial benefit for patients and clinicians.PurposeTo determine if pre-treatment regional brain morphology-based machine learning models can prognosticate 1 year response to Gamma Knife radiosurgery for trigeminal neuralgia.MethodsWe used a data-driven approach that combined retrospective structural neuroimaging data and support vector machine-based machine learning to produce robust multivariate prediction models of pain relief following Gamma Knife radiosurgery for trigeminal neuralgia. Surgical response was defined as ≥ 75% pain relief 1 year post-treatment. We created two prediction models using pre-treatment regional brain gray matter morphology (cortical thickness or surface area) to distinguish responders from non-responders to radiosurgery. Feature selection was performed through sequential backwards selection algorithm. Model out-of-sample generalizability was estimated via stratified 10-fold cross-validation procedure and permutation testing.ResultsIn 51 trigeminal neuralgia patients (35 responders, 16 non-responders), machine learning models based on pre-treatment regional brain gray matter morphology (14 regional surface areas or 13 regional cortical thicknesses) provided robust a priori prediction of surgical response. Cross-validation revealed the regional surface area model was 96.7% accurate, 100.0% sensitive, and 89.1% specific while the regional cortical thickness model was 90.5% accurate, 93.5% sensitive, and 83.7% specific. Permutation testing revealed that both models performed beyond pure chance (p < 0.001). The best predictor for regional surface area model and regional cortical thickness model was contralateral superior frontal gyrus and contralateral isthmus cingulate gyrus, respectively.ConclusionsOur findings support the use of machine learning techniques in subsequent investigations of chronic neuropathic pain. Furthermore, our multivariate framework provides foundation for future development of generalizable, artificial intelligence-driven tools for chronic neuropathic pain treatments.
| S-EPMC8184658 | biostudies-literature
Project description:Classical trigeminal neuralgia (TN) is a severe neuropathic facial pain disorder associated with increased risks of anxiety and depression. Converging evidence suggests that chronic pain pathophysiology involves dysfunctional pain-related and emotion-related networks. However, whether these systems are also among the culprit networks for TN remains unclear. Here, we aimed to assess TN-related anatomical and functional brain anomalies in pain-related and emotion-related networks. We investigated differences in gray matter (GM) volume and the related resting-state functional connectivity (rsFC) between 29 classical TN patients and 34 matched healthy controls. Relationships between brain measurement alterations, clinical pain and emotional states were identified. A longitudinal observation was further conducted to determine whether alterations in the brain could renormalize following pain relief. Reduced GM volumes in the bilateral amygdala, periaqueductal gray (PAG) and right insula were found in TN patients compared with healthy control subjects. Whole-brain rsFC analyses with the four above-mentioned anatomical regions as seeds identified three significantly altered functional circuits, including amygdala-DLPFC, amygdala-mPFC and amygdala-thalamus/putamen circuitry. The amygdala-DLPFC and amygdala-mPFC circuits were associated with clinical pain duration and emotional state ratings, respectively. Further longitudinal analysis found that rsFC strength abnormalities in two fronto-limbic circuits (left amygdala/left DLPFC and right amygdala/right PFC) were resolved after pain relief. Together, structural and functional deficits in pain-related and emotion-related networks were associated with TN patients, as demonstrated by our multimodal results. Pain relief had protective effects on brain functional connectivity within fronto-limbic circuits. Our study provides novel insights into the pathophysiology of TN, which may ultimately facilitate advances in TN intervention.
| S-EPMC5890150 | biostudies-literature
Project description:IntroductionClassical trigeminal neuralgia (CTN) is a kind of trigeminal neuralgia which is due to neurovascular compression. The common neurological treatment CTN drug called carbamazepine is the main measure, although it usually has side effects and a high-rate of relapse. As a critical alternative therapy, electroacupuncture (EA) has been shown to benefit for neuropathic pain. The aims of this study are to observe the therapeutic effect and safety of EA for CTN, to evaluate whether EA has the advantage over carbamazepine in the analgesia of CTN. Furthermore, we would to establish a standardized, effective, and convenient therapy program of EA.Methods and analysisOne hundred twenty patients diagnosed with CTN will be randomized for a 4-week intervention. The interventions will be different according to the four groups (EA + carbamazepine group, sham EA + carbamazepine group, EA + placebo group and sham EA + placebo group). EA therapy will be performed in specific acupoints with a dilute wave (2/100 Hz) for 60 minutes. Carbamazepine tablets will be taken orally with 0.1 g each time, thrice daily. Sham EA and placebo intervention will not receive EA and drug treatment. The main outcomes are the change from baseline intensity of pain at 6 months (pain evaluation by visual analogue score) and the change from baseline brief introduction of 2-week pain to evaluate pain comprehensively. The data management and statistical analysis will be conducted by third party statisticians. Incidence of adverse events will be investigated.Ethics and disseminationEthics approval was obtained from the Clinical Trial Ethics Committee of The Third Affiliated Hospital of Zhejiang Chinese Medical University (NO. ZSLL-KY-2017-033) and Jiaxing Hospital of Traditional Chinese Medicine (NO. 2018-JZLK-002). The results will be disseminated by presentation at peer-reviewed journals.
| S-EPMC7440061 | biostudies-literature
Project description:Trigeminal neuralgia (TN), marked by chronic pain from neural damage, is closely associated with inflammation. The role of OTULIN, a key regulator in inflammation and autophagy, is not fully understood in TN. The regulatory mechanism of OTULIN, a key protein involved in modulating inflammatory responses and autophagy processes, remains incompletely elucidated, particularly in the context of TN and neuroinflammation. An infraorbital nerve ligation-induced rat model of TN was used. OTULIN's expression was modulated using adenovirus vectors and short hairpin RNA. The impact on pain and inflammatory responses was assessed via quantitative real-time polymerase chain reaction, western blot, immunofluorescence, and transcriptomic analysis. Enhanced OTULIN expression significantly increased head withdrawal thresholds and reduced pain sensitivity and neuroinflammatory markers in the model. Conversely, silencing OTULIN exacerbated pain and inflammation. Transcriptomic data revealed OTULINs influence on both inflammatory and autophagy pathways, specifically in suppressing NLR family pyrin domain containing 3 (NLRP3) inflammasome and promoting autophagy. In vitro experiments demonstrated OTULIN's inhibition of inflammatory markers in microglia and neurons. OTULIN is crucial in modulating TN, reducing neuropathic pain and neuroinflammation by activating the autophagy pathway and inhibiting the NLRP3 inflammasome.
| S-EPMC11339468 | biostudies-literature
Project description:Trigeminal neuralgia (TN) is a severe and disabling facial pain condition and is characterized by intermittent, severe, electric shock-like pain in one (or more) trigeminal subdivisions. This pain can be triggered by an innocuous stimulus or can be spontaneous. Presently available therapies for TN include both surgical and pharmacological management; however, the lack of a known etiology for TN contributes to the unpredictable response to treatment and the variability in long-term clinical outcomes. Given this, a range of peripheral and central mechanisms underlying TN pain remain to be understood. We acquired functional magnetic resonance imaging (fMRI) data from TN patients who (1) rested comfortably in the scanner during a resting state session and (2) rated their pain levels in real time using a calibrated tracking ball-controlled scale in a pain tracking session. Following data acquisition, the data was analyzed using the conventional correlation analysis and two artificial intelligence (AI)-inspired deep learning methods: convolutional neural network (CNN) and graph convolutional neural network (GCNN). Each of the three methods yielded a set of brain regions related to the generation and perception of pain in TN. There were 6 regions that were identified by all three methods, including the superior temporal cortex, the insula, the fusiform, the precentral gyrus, the superior frontal gyrus, and the supramarginal gyrus. Additionally, 17 regions, including dorsal anterior cingulate cortex (dACC) and the thalamus, were identified by at least two of the three methods. Collectively, these 23 regions are taken to represent signature centers of TN pain and provide target areas for future studies seeking to understand the central mechanisms of TN.
| S-EPMC10232768 | biostudies-literature
Project description:BackgroundClassic trigeminal neuralgia (TN) is caused by vessels compressing the trigeminal nerve root entry zone. The cause is usually impingement of the superior cerebellar artery, anterior inferior cerebellar artery, or a vein. Other rare causes have been reported including aneurysmal compression, skull base tumors, and vascular malformations. An enlarged suprameatal tubercle (EST) as a cause of TN has not yet been described.Case presentationWe report the first case of 37 year old female patient presented with severe TN involving the three branches of trigeminal nerve who failed medical treatment and underwent multiple balloon compression for left TN with minimal improvement. The severity of pain was assessed using Barrow Neurological Institute (BNI) pain intensity score. Patient had brain MRI with CISS sequence and CT scan for the brain. After careful revision of her imaging studies, patient found to have prominent and heavily calcified left supra meatal tubercle. Her preoperative BNI score was 5.Patient had left retrosigmoid craniotomy and drilling of left suprameatal tubercle. No other structures were seen in contact with left trigeminal nerve root entry zone. Patient had significant improvement on her pain, postoperative BNI score was 1 until the last follow-up 4 years.ConclusionEST is a rare cause of TGN and should be suspected as the offending compressing structure when no other causes seen on imaging studies.
| S-EPMC8141507 | biostudies-literature
Project description:Temporomandibular joint disorder (TMJD) is known for its mastication-associated pain. TMJD is medically relevant because of its prevalence, severity, chronicity, the therapy-refractoriness of its pain, and its largely elusive pathogenesis. Against this background, we sought to investigate the pathogenetic contributions of the calcium-permeable TRPV4 ion channel, robustly expressed in the trigeminal ganglion sensory neurons, to TMJ inflammation and pain behavior. We demonstrate here that TRPV4 is critical for TMJ-inflammation-evoked pain behavior in mice and that trigeminal ganglion pronociceptive changes are TRPV4-dependent. As a quantitative metric, bite force was recorded as evidence of masticatory sensitization, in keeping with human translational studies. In Trpv4(-/-) mice with TMJ inflammation, attenuation of bite force was significantly less than in wildtype (WT) mice. Similar effects were seen with systemic application of a specific TRPV4 inhibitor. TMJ inflammation and mandibular bony changes were apparent after injections of complete Freund adjuvant but were remarkably independent of the Trpv4 genotype. It was intriguing that, as a result of TMJ inflammation, WT mice exhibited significant upregulation of TRPV4 and phosphorylated extracellular-signal-regulated kinase (ERK) in TMJ-innervating trigeminal sensory neurons, which were absent in Trpv4(-/-) mice. Mice with genetically-impaired MEK/ERK phosphorylation in neurons showed resistance to reduction of bite force similar to that of Trpv4(-/-) mice. Thus, TRPV4 is necessary for masticatory sensitization in TMJ inflammation and probably functions upstream of MEK/ERK phosphorylation in trigeminal ganglion sensory neurons in vivo. TRPV4 therefore represents a novel pronociceptive target in TMJ inflammation and should be considered a target of interest in human TMJD.
| S-EPMC3722361 | biostudies-literature