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      Changes in somatosensory perception induced by trigeminal injury after Maxillofacial Surgical Procedures Translated title: Cambios en la percepción somatosensorial inducidos por lesiones trigeminales causadas por procedimientos quirúrgicos maxilofaciales

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          Abstract

          Abstract Evidence has been reported that shows that somatosensory perception can be altered by a trigeminal injury resulting from maxillofacial surgical procedures. However, the surgical procedures that most frequently cause trigeminal lesions and the risk factors are unknown. In the same way, there is little information on what has been determined in preclinical models of trigeminal injury. This article integrates relevant information on trigeminal injury from both clinical findings and primary basic science studies. This review shows that the age and complexity of surgical procedures are essential to induce orofacial sensory alterations.

          Translated abstract

          Resumen Se han reportado evidencias que demuestran que la percepción somatosensorial puede ser alterada por la lesión trigeminal producto de procedimientos quirúrgicos maxilofaciales. Sin embargo, se desconoce cuáles son los procedimientos quirúrgicos que más frecuentemente producen lesiones trigeminales, y los factores de riesgo. De la misma forma hay poca información sobre lo que se ha determinado en modelos preclínicos de lesión trigeminal. El objetivo de este artículo es integrar información relevante sobre la lesión trigeminal desde los hallazgos clínicos como los principales estudios de ciencia básica. Esta revisión demuestra que la edad y el tipo de procedimiento son fundamentales para inducir alteraciones sensoriales orofaciales, así como los procesos neurobiológicos que subyacen a estos padecimientos.

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          Most cited references47

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          Neuropathic pain

          Neuropathic pain is caused by a lesion or disease of the somatosensory system, including peripheral fibres (Aβ, Aδ and C fibres) and central neurons, and affects 7-10% of the general population. Multiple causes of neuropathic pain have been described and its incidence is likely to increase owing to the ageing global population, increased incidence of diabetes mellitus and improved survival from cancer after chemotherapy. Indeed, imbalances between excitatory and inhibitory somatosensory signalling, alterations in ion channels and variability in the way that pain messages are modulated in the central nervous system all have been implicated in neuropathic pain. The burden of chronic neuropathic pain seems to be related to the complexity of neuropathic symptoms, poor outcomes and difficult treatment decisions. Importantly, quality of life is impaired in patients with neuropathic pain owing to increased drug prescriptions and visits to health care providers, as well as the morbidity from the pain itself and the inciting disease. Despite challenges, progress in the understanding of the pathophysiology of neuropathic pain is spurring the development of new diagnostic procedures and personalized interventions, which emphasize the need for a multidisciplinary approach to the management of neuropathic pain.
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            Brainstem Pain-Control Circuitry Connectivity in Chronic Neuropathic Pain.

            Preclinical investigations have suggested that altered functioning of brainstem pain-modulation circuits may be crucial for the maintenance of some chronic pain conditions. While some human psychophysical studies show that patients with chronic pain display altered pain-modulation efficacy, it remains unknown whether brainstem pain-modulation circuits are altered in individuals with chronic pain. The aim of the present investigation was to determine whether, in humans, chronic pain following nerve injury is associated with altered ongoing functioning of the brainstem descending modulation systems. Using resting-state functional magnetic resonance imaging, we found that male and female patients with chronic neuropathic orofacial pain show increased functional connectivity between the rostral ventromedial medulla (RVM) and other brainstem pain-modulatory regions, including the ventrolateral periaqueductal gray (vlPAG) and locus ceruleus (LC). We also identified an increase in RVM functional connectivity with the region that receives orofacial nociceptor afferents, the spinal trigeminal nucleus. In addition, the vlPAG and LC displayed increased functional connectivity strengths with higher brain regions, including the hippocampus, nucleus accumbens, and anterior cingulate cortex, in individuals with chronic pain. These data reveal that chronic pain is associated with altered ongoing functioning within the endogenous pain-modulation network. These changes may underlie enhanced descending facilitation of processing at the primary synapse, resulting in increased nociceptive transmission to higher brain centers. Further, our findings show that higher brain regions interact with the brainstem modulation system differently in chronic pain, possibly reflecting top-down engagement of the circuitry alongside altered reward processing in pain conditions.SIGNIFICANCE STATEMENT Experimental animal models and human psychophysical studies suggest that altered functioning of brainstem pain-modulation systems contributes to the maintenance of chronic pain. However, the function of this circuitry has not yet been explored in humans with chronic pain. In this study, we report that individuals with orofacial neuropathic pain show altered functional connectivity between regions within the brainstem pain-modulation network. We suggest that these changes reflect largely central mechanisms that feed back onto the primary nociceptive synapse and enhance the transfer of noxious information to higher brain regions, thus contributing to the constant perception of pain. Identifying the mechanisms responsible for the maintenance of neuropathic pain is imperative for the development of more efficacious therapies.
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              Activation of glia and microglial p38 MAPK in medullary dorsal horn contributes to tactile hypersensitivity following trigeminal sensory nerve injury.

              Glial activation is known to contribute to pain hypersensitivity following spinal sensory nerve injury. In this study, we investigated mechanisms by which glial cell activation in medullary dorsal horn (MDH) would contribute to tactile hypersensitivity following inferior alveolar nerve and mental nerve transection (IAMNT). Activation of microglia and astrocytes was monitored at 2 h, 1, 3, 7, 14, 28, and 60 days using immunohistochemical analysis with OX-42 and GFAP antibodies, respectively. Tactile hypersensitivity was significantly increased at 1 day, and this lasted for 28 days after IAMNT. Microglial activation, primarily observed in the superficial laminae of MDH, was initiated at 1 day, maximal at 3 days, and maintained until 14 days after IAMNT. Astrocytic activation was delayed compared to that of microglia, being more profound at 7 and 14 days than at 3 days after IAMNT. Both tactile hypersensitivity and glial activation appeared to gradually reduce and then return to the basal level by 60 days after IAMNT. There was no significant loss of trigeminal ganglion neurons by 28 days following IAMNT, suggesting that degenerative changes in central terminals of primary afferents might not contribute to glial activation. Minocycline, an inhibitor of microglial activation, reduced microglial activation, inhibited p38 mitogen-activated protein kinase (MAPK) activation in microglia, and significantly attenuated the development of pain hypersensitivity in this model. These results suggest that glial activation in MDH plays an important role in the development of neuropathic pain and activation of p38 MAPK in hyperactive microglia contributes to pain hypersensitivity in IAMNT model.
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                Author and article information

                Journal
                odovtos
                Odovtos International Journal of Dental Sciences
                Odovtos
                Facultad de Odontología. Universidad de Costa Rica (San José, San José, Costa Rica )
                1659-1046
                2215-3411
                August 2022
                : 24
                : 2
                : 14-25
                Affiliations
                [1] orgnameUniversidad Nacional Autónoma de México orgdiv1Facultad de Estudios Superiores Iztacala orgdiv2Clínica Universitaria de Salud Integral Almaraz Mexico
                [2] orgnameUniversidad Nacional Autónoma de México orgdiv1Facultad de Estudios Superiores Iztacala orgdiv2Programa de Maestría y Doctorado en Ciencias Médicas Odontológicas y de la Salud Mexico
                [3] orgnameUniversidad Nacional Autónoma de México orgdiv1Facultad de Estudios Superiores Iztacala orgdiv2Clínica Universitaria de Salud Integral Almaraz Mexico isaac.perez@ 123456unam.mx
                Article
                S2215-34112022000200014 S2215-3411(22)02400200014
                10.15517/ijds.2022.50505
                010a33a4-1fe6-448a-bccd-5e14d904cedc

                This work is licensed under a Creative Commons Attribution-NonCommercial 3.0 International License.

                History
                : 11 February 2022
                : 10 January 2022
                Page count
                Figures: 0, Tables: 0, Equations: 0, References: 47, Pages: 12
                Product

                SciELO Costa Rica

                Categories
                New perspective article

                Trigeminal injury,Nervio trigémino,Alteraciones sensoriales,Percepción somatosensorial,Ccirugía orofacial,Lesión trigeminal,Dolor neuropático,Trigeminal nerve,Sensory alterations,Somatosensory perception,Orofacial surgery,Neuropathic pain

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