J Orofac Pain
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Evaluating sensory nerve damage is a challenging and often frustrating process. Diagnosis and follow-up is usually based on the patient's history and gross physical evaluation in addition to simple sensory tests such as brushing or pin prick. ⋯ In this article specific clinical uses of QST are described and its clinical applicability is demonstrated. Future studies should be directed at exploring the use of QST in the diagnosis and classification of further nerve pathologies.
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The purpose of this article is to review the pharmacological treatment of neuropathic trigeminal pain by means of a systematic review. A number of randomized controlled trials and important historical and uncontrolled studies in trigeminal neuralgia and postherpetic neuralgia were identified. ⋯ It does not respond to the usual drugs used for other neuropathic pains. The drug therapy of trigeminal postherpetic neuralgia is similar to that of other neuropathic trigeminal pain conditions.
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Comparative Study
Comparison of algometry and palpation in the recognition of temporomandibular disorder pain complaints.
To determine the construct validity of algometry and to compare it with that of palpation, and to compare tenderness of masticatory muscle sites and the temporomandibular joint (TMJ) on palpation and on algometry. ⋯ Construct validity of algometry in the recognition of TMD pain complaints is comparable to that of palpation, and differences in tenderness on palpation and on algometry are found between masticatory muscle sites and the TMJ.
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Previous work suggests that hyperexcitability of central nociceptive neurons may play a role in the pain of temporomandibular disorders (TMD). The aim of this study was to test this theory by assessing differences, between myalgic TMD patients and pain-free controls, in temporal summation of mechanically evoked pain and aftersensations following repetitive noxious stimulation. ⋯ A generalized hyperexcitability of central nociceptive processing in this TMD patient group is indicated by their more pronounced temporal summation of pain and greater aftersensations following repetitive noxious digital stimulation versus controls. Such hyperexcitability may contribute to the pathophysiology of TMD pain.
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Transmission of noxious-stimulus-evoked inputs in the spinal and trigeminal systems is mediated primarily through excitatory glutamatergic synapses using alpha amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA), kainate and N-methyl-D-aspartate (NMDA) subtypes of glutamate receptors. Glutamatergic synapses exhibit multiple forms of short-lasting and long-lasting synaptic plasticity. Persistent enhancement of nociceptive transmission, known as "central sensitization," is a form of lasting plasticity that is similar mechanistically to long-term potentiation of glutamatergic transmission in other regions of the central nervous system. ⋯ Central sensitization is thus an expression of increased synaptic gain at glutamatergic synapses in central nociceptive-transmission neurons and thereby contributes importantly to pain hypersensitivity. In addition, recent evidence has revealed a new player in the mechanisms underlying pain hypersensitivity following nerve injury--microglia. Understanding of the roles of microglia may lead to new strategies for the diagnosis and management of neuropathic pain.