تجزیه و تحلیل از درد محرک برانگیخته در بیماران مبتلا به اختلالات درد فکی گیجگاهی عضلات جونده
|کد مقاله||سال انتشار||تعداد صفحات مقاله انگلیسی||ترجمه فارسی|
|76218||2001||11 صفحه PDF||سفارش دهید|
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Publisher : Elsevier - Science Direct (الزویر - ساینس دایرکت)
Journal : Pain, Volume 92, Issue 3, June 2001, Pages 399–409
The pathophysiological mechanisms of myofascial temporomandibular disorders (TMD) are still under investigation. The hypothesis that TMD pain is caused by a generalized sensitization of higher order neurons in the nociceptive pathways combined with a decreased efficacy of endogenous inhibitory systems has recently gained support in the literature. This study was designed to further investigate the somatosensory sensibility within and outside the craniofacial region. Twenty-two patients fulfilled the research diagnostic criteria for TMD for myofascial pain (Dworkin and LeResche, J Craniomandib Disord Facial Oral Pain 6 (1992) 301) and 21 age- and sex-matched subjects served as a control group. The somatosensory sensibility to a deep tonic input was tested by standardized infusions of hypertonic saline into the masseter and anterior tibialis muscle. Furthermore, pressure pain thresholds (PPTs) and heat pain thresholds (HPTs) were assessed with phasic stimuli at the same sites before and following the infusions. Myofascial TMD patients reported infusion of hypertonic saline to be more painful on 10 cm visual analogue scales (peak pain 8.8±0.4 cm) than control subjects (6.8±0.5 cm, t-test: P=0.003) in the masseter but not in the anterior tibialis (7.4±0.5 vs. 6.6±0.5 cm, P=0.181). The perceived area of experimental masseter pain measured on drawings was marginally larger in TMD patients (2.6±0.5 arbitrary units (a.u.)) than in control subjects (1.4±0.2 a.u., Mann–Whitney: P=0.048) but no differences were observed for the anterior tibialis (P=0.771). The PPTs were lower in the myofascial TMD patients compared to the control group, both in the masseter (analysis of variance (ANOVA): P=0.002) and in the anterior tibialis (P=0.005), whereas there were no significant differences in HPT (ANOVAs: P=0.357, P=0.101). There were no significant correlations between measures of somatosensory sensibility and measures of clinical pain intensity, pain duration, graded chronic pain scores or somatization or depression scores (Pearson: R<0.304, P>0.172). The present study in a well-defined group of myofascial TMD patients found that the responsiveness to both tonic and phasic deep stimuli, but not to phasic superficial inputs at the pain threshold level, in the craniofacial region was higher compared with a control group. These findings suggest that myofascial TMD pain is associated with a facilitation of stimulus-evoked pain primarily, but not exclusively related to the painful region.