Evidence for up-regulated central nociceptive processing in patients with masticatory myofascial pain.

J Orofac Pain

Department of Biomedical Sciences, Research Center for Neuroendocrine Influences on Pain, Brotman Facial Pain Center, University of Maryland, Baltimore, MD 21201, USA.

Published: April 2004

Aims: 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.

Methods: Sixteen series of 10 repetitive, mildly noxious mechanical stimuli were applied to the fingers of 25 female TMD patients with masticatory myofascial pain and 25 age-matched, pain-free female subjects. All subjects rated the pain intensity and unpleasantness evoked by the first, fifth, and tenth stimuli in the series and their aftersensations at 15 seconds and 1 minute following the last stimulus. Data were analyzed by 3-way repeated-measures analysis of variance.

Results: Pain and unpleasantness ratings increased with repetition of the stimulation (P < .0001). In addition, there was a significant trial number x group interaction for the pain intensity ratings, such that TMD patients provided higher ratings than controls for the tenth stimulus (P < .001). The increase in unpleasantness ratings with repetitive stimulation was also higher for the patient group (P < .0001). Moreover, TMD patients rated the intensity of aftersensations as higher (P < .005) and reported painful aftersensations at significantly greater frequency (P < .05).

Conclusion: 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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