J Orofac Pain
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To examine the relationship between depression and somatization and pain during muscle and joint palpation as well as limitations related to mandibular functioning (LRMF) in patients with temporomandibular disorders. ⋯ The results suggest that depression and somatization are related to the self-report of MP. In addition, severe somatization may be associated with an increase in jaw disability.
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This article reviews the utility of psychophysical approaches in the assessment of posttraumatic neuropathic trigeminal pain. Methods of quantitative sensory testing are derived from psychophysical principles and provide a widely accepted means for characterizing sensory dysfunction in patients who experience injury to the trigeminal nerve. No published study, however, has sought to compare sensory findings from trigeminal nerve-injured patients who develop neuropathic pain with those from trigeminal nerve-injured patients who remain pain-free. ⋯ In addition, trigeminal nerve-injured patients with pain may be more likely to report cold allodynia than patients without pain and to exhibit signs of central sensitization such as allodynia to light brushing tactile stimuli and abnormal temporal summation of pain. New studies using state-of-the-art psychophysical methods are needed to search for sensory markers that bear on the development of pain. Moreover, the relationship between psychophysical indices of central sensitization and measures of clinical pain should be addressed to obtain a better understanding of the underlying pathophysiology.
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This article reviews the utility of neurophysiological recordings and quantitative sensory testing (QST) in providing sensitive, quantitative, and objective tests for the diagnosis and localization of damage to the trigeminal nerve. Electromyography and recordings of the masseter reflex and compound muscle action potential evoked by transcranial magnetic stimulation or direct electrical stimulation of the masseteric nerve can be of value in evaluating the function of a motor neurons supplying the muscles of mastication. Orthodromic recording of the sensory action potential and trigeminal somatosensory-evoked potential recording with the near-nerve stimulation technique are sensitive tools for the investigation of trigeminal sensory Abeta afferents, whereas recordings of polysynaptic trigeminal brainstem reflexes and tactile QST are less sensitive. ⋯ In a study of the diagnostic value of neurography, blink reflex and thermal QST, and various commonly used clinical sensory tests, neurophysiologic tests and thermal QST had better sensitivity (50% to 88% vs 40% to 59%) and negative predictive values (78% to 100% vs 70% to 74%) compared to clinical examination, whereas the specificity (55% to 100%) and positive predictive values (48% to 73%) were similar. At 1 year after trigeminal nerve injury, the risk of a false negative finding with clinical sensory testing was 94%, whereas the combination of nerve conduction recordings and thermal QST increased the diagnostic yield to 100% in patients with long-standing postsurgical sensory alteration. In conclusion, clinical neurophysiological recordings and QST improve the diagnostic accuracy for trigeminal neuropathy.
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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.
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Nerve signals arising from sites of tissue or nerve injury lead to long-term changes in the central nervous system and contribute to hyperalgesia and the amplification and persistence of pain. These nociceptor activity-dependent changes are referred to as central sensitization. Central sensitization involves an increase in the excitability of medullary dorsal horn (subnucleus caudalis) and spinal dorsal horn neurons brought about by a series of events including neuronal depolarization; removal of the voltage-dependent magnesium block of the N-methyl-D-aspartate (NMDA) receptor; release of calcium from intracellular stores; phosphorylation of the NMDA, alpha amino-3-hydroxy-5-methyl-4-isoxazole-propionate (AMPA), and neurokinin (NK) 1 receptors via activation of protein kineses; a change in the neuron's excitability; and an increase in synaptic strength. ⋯ In contrast, the ventral pole of the Vi/Vc is unique. In addition to its role in the nociceptive sensory processing of deep tissues, it is involved bilaterally in somatovisceral and somatoautonomic processing, activation of the pituitary-adrenal axis, and descending modulatory control. The findings support our overall hypothesis that the ventral pole of Vi/Vc is involved in the coordination of bilateral sensorimotor functions of the trigeminal system associated with the response to deep tissue injury.