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OBJECTIVE: The aim was to assess sensitization using quantitative sensory testing in mechanical and thermal modes in individuals with and without osteoarthritis (OA) of the knee. Pain thresholds were correlated with functionality, symptoms of depression and intensity of pain. METHODS: Thirty control volunteers and 30 patients with OA of the knee were assessed. Punctate pain thresholds using Von Frey filaments and thermal pain thresholds using a Thermal Sensory Analyzer were evaluated in the periarticular region of the knee and forearm. Using a digital pressure algometer, pressure pain thresholds were assessed in the periarticular region of the knee and on the root exit zone on the lumbar and sacral spine. RESULTS: Punctate, pressure, and thermal pain thresholds differed significantly between participants with and without OA (p < 0.05). Values in those with OA were consistent with pain sensitization. Pressure pain thresholds also showed moderate and negative correlations with data on functionality, symptoms of depression and intensity of pain (-0.36 < r > -0.56), contributing up to 30% of their variability. CONCLUSIONS: Allodynia and hyperalgesia were demonstrated in the OA group, suggesting central sensitization in patients with mild to moderate severity of joint damage. Correlation between mechanical hypersensitivity and psychosocial factors seems to be small, despite of its significance.

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Aim To provide an overview of mechanisms underlying craniofacial pain; to highlight peripheral and central adaptations that may promote chronification of pain in craniofacial pain states such as migraine and temporomandibular disorders (TMD). Background Pain is a common symptom associated with disorders involving craniofacial tissues including the teeth and their supporting structures, the temporomandibular joint and the muscles of the head. Most acute painful craniofacial conditions are easily recognized and well managed, but others, especially those that are chronic (e.g., migraine, TMD and trigeminal neuropathies), present clinical challenges. Preclinical studies have provided substantial information about the anatomical and physiological mechanisms related to the initiation and modulation of nociceptive signals in the trigeminal system. While knowledge of the mechanisms underlying chronic craniofacial pain remains limited, both clinical and preclinical investigations suggest that changes in afferent inputs to the brain as well as in brain structure and modulatory pathways occur in chronic pain. Collectively, these changes result in amplification of nociception that promotes and sustains craniofacial chronic pain states. Conclusions The increased understanding gained of the physiological and pathological processing of nociception in the trigeminal system has provided new perspectives for the mechanistic understanding of acute craniofacial pain conditions and the peripheral and central adaptations that are related to pain chronification. Such knowledge may contribute to improvements in currently available treatments as well as to the development of novel analgesic therapies.

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Emerging evidence proposes a link between immune changes and pain, which is consistent with the inflammation theory and the increased incidence of neurodegenerative diseases. Flavonoids have long been used because of their anti-inflammatory potential activity and they are considered a promising alternative to alleviate neuropathic pain. The aim of this study was to investigate the antihyperalgesic effect of hesperidin and the presence of pro-inflammatory cytokines evaluated at peripheral and central levels in the chronic constriction injury as model of neuropathic pain in rats. Mechanical and thermal hyperalgesia were assessed in the aesthesiometer and plantar tests, respectively, as related to the presence of cytokines concentrations (TNF-α, IL-1ß and IL-6) in sciatic nerve and segments of the spinal cord after 15 days chronic constriction injury model in rats receiving vehicle or hesperidin. Antihyperalgesic response of hesperidin (100 mg/kg) was associated to the presence of cytokines mainly at several sections of the spinal cord suggesting not only peripheral but also its involvement in central sensitization in the experimental neuropathic pain.

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ABSTRACT BACKGROUND AND OBJECTIVES: Trigeminal neuralgia is one of the most common neuropathic pains that compromise head and neck. It manifests as shock or burning pain normally evoked by non-noxious facial stimulations. Its etiopathology is not totally understood, but it is known that different mechanisms contribute to the establishment and maintenance of pain. This study aimed to address current contexts of epidemiology, diagnosis, management and pathophysiological mechanisms underlying trigeminal neuralgia in peripheral and central nervous systems. CONTENTS: Inflammation and release of inflammatory mediators, neuropeptides and neurotrophic factors, as well as degenerative changes of nervous fibers caused by direct nervous injury are relevant peripheral mechanisms which lead to altered sensitivity of nociceptive neurons, development of spontaneous and exacerbated activity, allodynia and hyperalgesia. Among central mechanisms, exacerbated activation of central nociceptive neurons, neuroplasticity, changes in electrophysiological properties and neuronal hyperexcitability, in addition to changes in modulatory pain controls, lead to pain establishment and maintenance. CONCLUSION: Several mechanisms are involved in neuropathic pains, both in peripheral and central levels, although specific trigeminal neuralgia events are not totally described. Studies concerning its specific neurobiology are needed to understand functional and behavioral changes, which can contribute to trigeminal neuralgia clinical management and treatment.

RESUMO JUSTIFICATIVA E OBJETIVOS: A neuralgia do trigêmeo é uma das dores neuropáticas mais comumente encontradas na região de cabeça e pescoço e manifesta-se como crises de choque ou queimação geralmente desencadeadas por estímulos não dolorosos na região da face. A sua etiopatogenia não é totalmente conhecida, mas sabe-se que diversos mecanismos contribuem para seu estabelecimento. O objetivo deste estudo foi abordar os contextos atuais de epidemiologia, diagnóstico, tratamento e mecanismos fisiopatológicos subjacentes à neuralgia do trigêmeo nos sistemas nervoso periférico e central. CONTEÚDO: A inflamação e a liberação de mediadores inflamatórios, neuropeptídeos e fatores neurotróficos, assim como alterações degenerativas das fibras nervosas decorrentes da lesão nervosa direta são mecanismos periféricos relevantes que, em conjunto ou isoladamente, levam à sensibilidade alterada dos neurônios nociceptivos, com desenvolvimento de atividade espontânea e exacerbada e, consequentemente, dor espontânea e hiperalgesia. Dentre os mecanismos centrais, a ativação exacerbada de neurônios nociceptivos centrais, a neuroplasticidade, as alterações nas propriedades eletrofisiológicas e a hiperexcitabilidade neuronal, além das modificações nos controles modulatórios da dor, são eventos que levam à instalação e à manutenção da dor. CONCLUSÃO: Diversos mecanismos estão envolvidos nas dores neuropáticas, tanto a nível periférico quanto central, apesar dos eventos específicos da neuralgia do trigêmeo não estarem totalmente elucidados. Estudos que abordem a sua neurobiologia específica são necessários para a compreensão das alterações funcionais e comportamentais presentes, com claras repercussões no tratamento e manuseio clínico da neuralgia do trigêmeo.

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El dolor agudo postoperatorio constituye un importante desafío para el anestesiólogo y un derecho para los pacientes. No obstante, en la actualidad éste continúa presente en un alto porcentaje de pacientes, a pesar de los esfuerzoz en la difusión de su evaluación y en el uso de diferentes terapias. una importante e interesante forma de cambiar estas cifras puede ser la investigación de la fisiopatología del dolor agudo postoperatorio y la difusión de los resultados. En los últimos años se ha profundizado en el conocimiento de la fisiopatología del dolor agudo postoperatorio, donde se ha determinado que existen cambios capaces de enfrentar la noxa quirúrgica, conocidos como neuroplasticidad, una de cuyas principales expresiones es el mecanismo de sensibilización. Se presenta a continuación una revisión de los principales mecanismos involucrados en el desarrollo y mantención de esta neuroplasticidad.

Accute postoperative pain is a great challenge for anesthesiologists and a right for patients. However, there is still an important percentage of patients with accute postoperative pain, despite all the efforts that have been made to divulge the existing evaluation methods and the use of different therapies. Research of physiopathology of accute postoperative pain might be a relevant and interesting way to change such percentage as well as the publication of the results from that research. In the last years, researchers have gained deeper knowledge in the field of physiopathology of accute postoperative pain and found there are some changes with the capacity to face the surgical noxa known as neuroplasticity, being one of the most important expressions the sensitizazation mechanism. A review of the most important mechanisms that play a part in the development and maintenance of this neuroplasticity is presented below.

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