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The blink reflex arc. The circuit for the oligosynaptic R1 component is depicted with a broken line, and the polysynaptic pathways for the R2i and R2c components with a continuous line. SON = supraorbital nerve, GG = gasserian ganglion, V PRINC = principal or main nucleus of the TN in the pons, FN = facial nerve, VII MOT = motor nucleus of the facial nerve in the lower pons.
Source publication
Chronic orofacial pain represents a diagnostic and treatment challenge for the clinician. Some conditions, such as atypical facial pain, still lack proper diagnostic criteria, and their etiology is not known. The recent development of neurophysiological methods and quantitative sensory testing for the examination of the trigeminal somatosensory sys...
Context in source publication
Context 1
... The same motor units fire during the R1 and the R2 responses, 50 but lid closure coincides with the beginning of the R2 response. 51 Figure 2 shows schematically the anatomy of the blink reflex arc. The sensory afferents involved in both the R1 and the R2 components are medium- sized myelinated tactile A fibers, 44,52 although A fibers also contribute to the generation of these components when higher stimulus intensities are used in experimental settings. ...
Similar publications
Background
Burning mouth syndrome (BMS) is a chronic and spontaneous oral pain with burning quality in the tongue or other oral mucosa without any identifiable oral lesion or laboratory finding. Pathogenesis and etiology of BMS are still unknown. However, BMS has been associated with other chronic pain syndromes including other idiopathic orofacial...
Citations
... For this purpose, thermal quantitative sensory testing (tQST) and skin biopsy for epithelial nerve fiber density are likely the most appropriate tests. Brainstem reflexes, the BR, masseter reflex, and masseter inhibitory reflex increase the diagnostic sensitivity in patients with orofacial pain of various origins (Valls-Solé et al., 1996;Wedekind et al., 2002;Jääskeläinen, 2004a;Galeotti et al., 2006;Teerijoki-Oksa et al., 2019), and these reflex recordings are recommended for orofacial pain diagnostics with level A evidence (Haanpaa et al., 2011). ...
... Les réponses réflexes peuvent être utilisées dans le diagnostic des lésions structurelles affectant les arcs réflexes des nerfs trijumeaux et faciaux, ainsi que leurs connexions dans le tronc cérébral, du mésencéphale jusqu'à la partie inférieure du bulbe rachidien [16][17][18][19][20] . [21] Le réflexe de clignement (ou blink reflex) peut être évoqué par la stimulation électrique des différentes branches du trijumeau. Les informations afférentes de l'arc réflexe (qui correspond au trajet parcouru par l'influx nerveux provoquant un réflexe) sont véhiculées par les fibres sensorielles trigéminales de la périphérie jusqu'à leurs connexions centrales au niveau des noyaux trigéminaux et faciaux du tronc cérébral, au niveau de la partie inférieure du pont et du bulbe rachidien. ...
... Le nerf facial sert d'arc efférent de manière bilatérale ; cette réponse motrice peut être enregistrée par des électrodes de surface placées bilatéralement sur les muscles orbiculaires des paupières [18] . La stimulation électrique du nerf sus-orbitaire induit de meilleures réponses réflexes que la stimulation du nerf infraorbitaire ou du nerf mentonnier [21] . Les réponses réflexes sont composées d'une réponse initiale ipsilatérale (R1), d'une latence comprise entre 10 et 12 ms, et de deux composantes ipsi-et controlatérales (R2i et R2c), de latences comprises entre 30 et 40 ms. ...
Les troubles neurologiques orofaciaux sont principalement provoqués par des lésions du sys-tème nerveux périphérique à la suite, par exemple, d'une chirurgie (avulsion des troisièmes molaires, implantologie) ou d'un traumatisme. Les autres causes sont généralement le reflet d'une atteinte du système nerveux central (origine inflammatoire, tumorale, ischémique, etc.). Cliniquement, il s'agit soit de symptômes sensitifs positifs (paresthésies, dysesthésies, douleur, etc.) et/ou négatifs (diminution ou perte de la perception sensorielle). Les symptômes peuvent être présents seuls, ou en association, chez un même patient et avoir des caractéristiques (intensité, localisation, étendue, association avec d'autres signes ou symptômes, etc.) qui fluctuent avec le temps. Ainsi, l'examen clinique est un préalable indispensable afin d'établir un diagnostic. Toutefois, cet examen n'est pas suffisant pour définir exactement les caractéristiques des troubles neurologiques, notamment la localisation des lésions (périphérique, et/ou centrale). L'analyse du système somatosensoriel à l'aide de divers outils (imagerie, électrophysiologie et/ou psychophysiques) permet ainsi, d'une part, d'établir un diagnostic pertinent et, d'autre part, de mettre en place le traitement le plus approprié pour le patient. © 2022 Elsevier Masson SAS. Tous droits réservés.
... In recent decades, it has been shown that several neuropathic mechanisms may contribute to the primary BMS pathophysiology. Indeed, neurophysiologic, psychophysical and functional imaging studies [9][10][11][12][13] have suggested pathophysiological alterations at different levels of the neuraxis, and BMS is currently considered to be a neuropathic pain affecting the central and peripheral nervous systems [1,14]. ...
Abstract: The pathophysiology of primary burning mouth syndrome (BMS) has been extensively debated but is poorly understood despite a large number of hypotheses attempting to explain its etiopathogenic mechanisms. The aim of the present work was to systematically review papers that could provide arguments in favour of the neuropathic and psychogenic components of primary BMS for a better understanding of the disease. This systematic review (SR) was registered in PROS‐ PERO (CRD42021224160). The search was limited to articles in English or French from 1990 to 01 December 2020. A total of 113 articles were considered for data extraction. We divided them into four subgroups: pharmacological and nonpharmacological management studies (n = 23); neuro‐ physiological studies (n = 35); biohistopathological studies (n = 25); and questionnaire‐based studies (n = 30). Several of these studies have shown neuropathic involvement at various levels of the neu‐ raxis in BMS with the contribution of quantitative sensory testing (QST), functional brain imaging, and biohistopathological or pharmacologic studies. On the other hand, the role of psychological factors in BMS has also been the focus of several studies and has shown a link with psychiatric disorders such as anxiety and/or depression symptoms. Depending on the patient, the neuropathic and psychogenic components may exist simultaneously, with a preponderance of one or the other, or exist individually. These two components cannot be dissociated to define BMS. Consequently, BMS may be considered nociplastic pain.
... Heat pain thresholds were determined by dropping the highest and lowest trials and then averaging the remaining 3 trials. 30 To determine group differences in pain thresholds and in pain ratings from individual conditions from the sustained pain task, we used a Mann-Whitney test. To examine group differences in the pain-rating curve, we fit linear mixed-effects models (using the R package lmerTest, with Satterthwaite degrees of freedom method) with participant as a random effect and temperature as a fixed effect. ...
Introduction:
Individuals with autism spectrum disorder (ASD) often exhibit differences in pain responsivity. This altered responsivity could be related to ASD-related social communication difficulties, sensory differences, or altered processing of pain stimuli. Previous neuroimaging work suggests altered pain evaluation could contribute to pain-related anxiety in ASD.
Objectives:
We hypothesized that individuals with ASD would report increased pain sensitivity and endorse more pain-related anxiety, compared to typically developing controls.
Methods:
We recruited 43 adults (ASD, n = 24; typically developing, n = 19) for 3 heat pain tasks (applied to the calf). We measured heat pain thresholds using a method of limits approach, a pain-rating curve (7 temperatures between 40 and 48°C, 5 seconds, 5 trials each), and a sustained heat pain task with alternating low (42°C) and high (46°C) temperatures (21 seconds, 6 trials each). Individual differences in pain-related anxiety, fear of pain, situational pain catastrophizing, depressive symptoms, and autism-related social communication were assessed by self-report.
Results:
There were no group differences in pain thresholds. For suprathreshold tasks, mean pain ratings were higher in ASD across both the pain-rating curve and the sustained heat pain tasks, but responses in the ASD group were more varied. Pain anxiety (PASS-Total) and pain-related fear (FOP-III-Total) were higher in the ASD group and were positively associated with pain ratings.
Conclusions:
Our results suggest that both sensory and cognitive experiences of pain are heightened and interact reciprocally in adults with ASD. Future studies are needed to evaluate the impact of pain-related anxiety on treatment-seeking and pain behaviors, given higher levels of pain-related anxiety in ASD.
... However, QualST did not detect a significant difference between 10 min and 2 hr after block anaesthesia, whereas QST revealed a return towards normal baseline stimulus perception at the 2-hr interval. Notably, other studies have shown glaring discrepancies between QualST and QST results (Agbaje, De Laat, Politis, et al., 2017;Jääskeläinen, 2004;Teerijoki-Oksa et al., 2003. Most studies report that qualitative (clinical) sensory testing has a high specificity and a low sensitivity Teerijoki-Oksa et al., 2019). ...
Background and objective: Orofacial quantitative sensory testing (QST) is an increasingly valuable psychophysical tool for evaluating neurosensory disorders of the orofacial region. Here, we aimed to evaluate the current evidence regarding this testing method and to discuss its future clinical potential. Data treatment: We conducted a literature search in Medline, Embase and Scopus for English-language articles published between 1990 and 2019. The utilized search terms included QST, quantitative, sensory testing and neurosensory, which were combined using the AND operator with the terms facial, orofacial, trigeminal, intraoral and oral. Results: Our findings highlighted many methods for conducting QST—including method of levels, method of limits and mapping. Potential stimuli also vary, and can include mechanical or thermal stimulation, vibration or pinprick stimuli. Orofacial QST may be helpful in revealing disease pathways and can be used for patient stratification to validate the use of neurosensory profile-specific treatment options. QST is reportedly reliable in longitudinal studies and is thus a candidate for measuring changes over time. One disadvantage of QST is the substantial time required; however, further methodological refinements and the combination of partial aspects of the full QST battery with other tests and imaging methods should result in improvement.
Conclusions: Overall, orofacial QST is a reliable testing method for diagnosing pathological neurosensory conditions and assessing normal neurosensory function. Despite the remaining challenges that hinder the use of QST for everyday clinical decisions and clinical trials, we expect that future improvements will allow its implementation in routine practice.
... It was introduced by the German Research Network on Neuropathic Pain in 2006 and is already strongly substantiated in its value, being that it can clarify if a neurosensory deficit is present or not. [13][14][15][16][17][18][19] However, for the time being, it remains unclear how these tests evolve in the transition from the acute to the chronic phases of trigeminal nerve damage and if they can predict prognosis and treatment outcomes in PTTN. 17,20,21 Magnetic resonance neurography (MRN) is an MRI technique in which dedicated sequences are used to enhance the visualization of the peripheral nervous system and its pathology. ...
Objectives
To perform a systematic review of published studies on diagnostic accuracy of magnetic resonance neurography (MRN) versus clinical neurosensory testing (NST) for post-traumatic trigeminal neuropathy (PTTN) in patients reporting neurosensory disturbances (NSD).
Methods
Human studies except case reports, reviews, systematic reviews and meta-analyses were included. PubMed, Embase, Web of Science and Cochrane Library were consulted. Risk of bias assessment was conducted using the QUADAS-2 tool. Predetermined data extraction parameters were noted and summarized.
Results
Eight studies met eligibility criteria of which seven were retrospective, representing 444 subjects. Most studies were at high risk of bias with low applicability concerns. Populations and objectives were divergent with a large variation in timing (3 days-17 years post injury) and parameters (multiple coil designs, fat suppression techniques, additional contrast agent) of MRI acquisition. T 2 -weighted 3T imaging with short echo times (2.2–100 ms) and fat suppression was applied in seven studies, techniques varied. Determination of sensitivity and specificity could not be performed due to the methodological variation between studies and lacking comparative data between index and reference tests. Based on limited data, PTTN correlated reasonably well between clinical assessment, intraoperative findings and MRN abnormalities (k = 0.57). Increased signal intensity correlated with persistency of neurosensory disturbances in one study. Intra- (ICC 0.914–0.927) and interobserver (k = 0.70–0.891) MRN variability was considered good to excellent. One retrospective study showed substantial impact of MRN on clinical decision making in one third of patients.
Conclusion
Currently, there is insufficient scientific knowledge to support or refute the use of MRN. Based on limited data, MRN seems promising and reliable in detection and grading of PTTN. Methodological issues underline the importance for prospective blinded studies with standardization of signal intensity calculation and rigorous reporting of MRI acquisition parameters.
... The details of the pathophysiology of BMS are an enigma. Recent studies suggest that BMS has a neuropathic component, in which trigeminal somatosensory function is modulated by the chorda tympani and glossopharyngeal nerves and trigeminal reflexes are altered [1][2][3][4][5][6]. Some reports implicate peripheral neuropathic pathophysiological mechanisms [7][8][9], while others suggest that central neuropathic mechanisms are primarily involved [2,3,10,11]. ...
Objectives
A standardized battery of quantitative sensory tests developed by the German Research Network on Neuropathic Pain (DFNS) was used to assess the association between somatosensory dysfunction and disease duration in patients with burning mouth syndrome (BMS).
Materials and methods
The 28 female participants with BMS were classified according to disease duration: ≤ 6 months (subchronic BMS, n = 15) and > 6 months (chronic BMS, n = 13); 29 age- and sex-matched healthy volunteers (control group) were recruited from staff of a dental hospital. The DFNS quantitative sensory testing protocol was applied at the ulnar surface of the right forearm and the tip of the tongue. Values for BMS patients and controls were compared and analyzed.
Results
The mechanical detection threshold (MDT) was significantly higher (i.e., loss of sensation) at the tongue tip in the chronic BMS group than in the control group (p = 0.011), whereas mechanical pain sensitivity (MPS) at the forearm was significantly higher (i.e., gain of sensation) in the chronic BMS group than in the control group (Z score = − 2.13 and 1.99, respectively). Multivariate analyses revealed that BMS patients could be discriminated from controls by using pressure pain threshold at the tongue (79.3%) (in the subchronic BMS group) and by MDT and MPS at the tongue tip and MPS at the forearm (96.6 and 89.7%, respectively) (in the chronic BMS group).
Conclusions
In BMS patients with long disease duration, MDT showed loss of sensation.
Clinical relevance
Increased MPS suggests that a neuropathic mechanism in the peripheral and central nervous systems is involved in BMS development.
... Furthermore, a study reported that because BMS patients frequently suffer from taste disturbance and other similar problems, dysfunction of the chorda tympani nerve may be involved [26]. Other researchers support the hypothesis that BMS may be a neuropathic pain involving the central nervous system [4,9,27]. It is probably true that some central sensitization might be related to BMS, as are other functional somatic syndromes [28,29], however, recent evidence shows its limitations, especially for elderly patients [30,31]. ...
... After checking for the above, the final diagnose depends mainly on the patients' subjective symptoms and history. Most of the complaints of BMS patients' are focused on their tongue, usually a tingling/burning/numbing sensation or feeling [27]. Symptoms related to the palate, lip, or gingiva are also observed, however, facial skin is not usually affected. ...
Burning Mouth Syndrome (BMS), a chronic intraoral burning sensation or dysesthesia without clinically evident causes, is one of the most common medically unexplained oral symptoms/syndromes. Even though the clinical features of BMS have been astonishingly common and consistent throughout the world for hundreds of years, BMS remains an enigma and has evolved to more intractable condition. In fact, there is a large and growing number of elderly BMS patients for whom the disease is accompanied by systemic diseases, in addition to aging physical change, which makes the diagnosis and treatment of BMS more difficult. Because the biggest barrier preventing us from finding the core pathophysiology and best therapy for BMS seems to be its heterogeneity, this syndrome remains challenging for clinicians. In this review, we discuss currently hopeful management strategies, including central neuromodulators (Tricyclic Antidepressants - TCAs, Serotonin, and Norepinephrine Reuptake Inhibitors - SNRIs, Selective Serotonin Reuptake Inhibitors - SSRIs, Clonazepam) and solutions for applying non-pharmacology approaches. Moreover, we also emphasize the important role of patient education and anxiety management to improve the patients’ quality of life. A combination of optimized medication with a short-term supportive psychotherapeutic approach might be a useful solution.
... In recent decades, quantitative sensory testing protocols had been developed to elucidate the mechanisms involved in orofacial pain conditions [51][52][53][54]. Sensory abnormalities appear most often after trauma or in neuropathic conditions [6,7,24,[55][56][57][58][59][60][61]. ...
Purpose: The objective of this study was to review the literature to find scientific evidence about the mechanisms involved in orofacial sensory interaction, including trigeminal and special sensory modalities. Views: Conscious sensory perception depends on peripheral external and internal stimuli, which are integrated and processed in central neural centres in order to promote the sensory experience through learning and memory. In the orofacial region, besides somatosensory inputs, there are special sensory modalities (gustation, olfaction, vision and audition) that interact with trigeminal ascendant inputs in a way that makes this area of the body unique. Moreover, the trigeminal nerve may have an important role due to the complex functions of this region, including breathing, feeding and detecting threats. In recent decades the development of equipment accurate enough to detect sensory thresholds has produced a wide range of evidence about orofacial interaction, which allows for the possible development of a unified underlying theory on this issue. Conclusions: The trigeminal system seems to mediate olfactory and gustative sensations in cortical associative centres, and sensory peripheral neural inputs are modulated by physiological and pathological conditions. Future experimental studies should seek to clarify the mechanisms involved in this interaction, and the role of pathological states in abnormalities of sensory thresholds and perception.
... Нейровизуализационные обследования часто не выявляют патологии у пациентов с симптомами ПИЛБ или выявляют случайные находки, не имеющие отношения к клиническим проявлениям [9]. В работах S. Jääskeläinen [10] при изучении электрофизиологических показателей у пациентов с атипичной лицевой болью было показано, что электрофизиологические тесты могут быть более чувствительными, чем магнитно-резонансная томография (МРТ), для выявления патологических нарушений у этих больных [10]. H. Forssell и соавт. ...
... Нейровизуализационные обследования часто не выявляют патологии у пациентов с симптомами ПИЛБ или выявляют случайные находки, не имеющие отношения к клиническим проявлениям [9]. В работах S. Jääskeläinen [10] при изучении электрофизиологических показателей у пациентов с атипичной лицевой болью было показано, что электрофизиологические тесты могут быть более чувствительными, чем магнитно-резонансная томография (МРТ), для выявления патологических нарушений у этих больных [10]. H. Forssell и соавт. ...
Aim:
To study neurophysiological characteristics of persistent idiopathic facial pain (PIFP) in comparison to trigeminal neuralgia.
Material and methods:
Forty-five patients with PIFP at the age from 25 to 74 years (42 women and 3 men), 25 patients with trigeminal neuralgia at the age from 25 to 84 (15 women and 10 men) and 20 healthy volunteers were examined. Multimodal evoked potentials (EP): brainstem auditory (BAEPs), trigeminal (TEPs) and sympathetic skin responses (SSRs) evoked potentials were recorded. EEG with functional tests (hyperventilation, rhythmical photic stimulation and test with eye opening) was recorded as well.
Results:
The neurophysiological pattern of PIFP includes: 1) shortening of the latent period (LP) and an increase in peak amplitudes of short-latent components of the BAEPs on both sides in combination with signs of brainstem structure dysfunction (fusion of II-III or III-IV peaks, bifurcation of peaks and lengthening of inter-peaks intervals); 2) normal parameters of the TEPs; 3) an increase in the amplitude of autonomic components (sympathetic and parasympathetic without signs of predominance of the tone of this or that system), intensification of the autonomic reaction; 4) disorganization and acuity of the alpha rhythm, smoothing of zonal differences, presence of bilateral tapering alpha-, theta- or alpha-theta waves on the EEG.
Conclusion:
Patients with PIFP have significant changes in EP and EEG connected with brainstem structure dysfunction and irritation of subcortical structures and autonomic disorders.
