J Orofac Pain
-
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.
-
Neuropathic trigeminal pain conditions are more common than is generally appreciated. Sites inside the mouth as well as involvement of extraoral tissues are common manifestations of these disorders. There is a general lack of recognition of the complex characteristics of neuropathic trigeminal pain that frequently lead to mischaracterization of the nature of the complaint. ⋯ Relative to etiology, the records review revealed that most onsets were associated with a specific dental treatment or odontogenic symptom that resulted in a dental diagnosis or treatment. Initial treatment modalities that either caused the pain or were used to address painful symptoms commonly included replacement of restorations, endodontic therapy, apicectomy, extraction, splint therapy, and occlusal equilibration. Correct diagnosis, and particularly early definitive diagnosis, of neuropathic trigeminal pain is crucial to avoid invasive and potentially more damaging forms of treatment.
-
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.
-
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.
-
To examine the jaw-stretch reflex after injection of local anesthetic (LA) into painful temporomandibular joints (TMJs), since the functional role of jaw-stretch reflexes in patients with painful temporomandibular disorders is still not well understood. ⋯ These results do not support the notion of asymmetries in the jaw-stretch reflex in patients with TMJ pain, but they do suggest that the reflex sensitivity can be influenced by nociceptive activity from the TMJ area.