Therefore, the highly significant reduction in head pain referral during the cervical intervention could be a clinical correlate of lessening central sensitization of the TCN. In particular, it is conceivable that palpation and stretch of dysfunctional cervical paraspinal tissues elicits tenderness that lessens

as remodeling occurs.[35, see more 36, 39] This could explain why tenderness ratings decreased during the cervical intervention and not the arm for, presumably, participants’ arm tissues were not dysfunctional and subject to remodeling. However, the perception of pain is not only determined by the intensity of the afferent pain signal (nociception).[45] Nociceptive inputs to the dorsal horn of the spinal cord are also influenced by potent endogenous

descending inhibitory and facilitatory processes from supraspinal regions. This bidirectional, central control incorporates a frontal, limbic, brainstem, and spinal cord neuronexus46-49 that is driven primarily by noxious inputs and associated emotional responses. Importantly, this includes spinal cord activity because the spinally mediated nociceptive flexion reflex is influenced by central pain modulation processes.[50] While the exact mechanisms responsible for emotional modulation of pain are not fully understood, heightened anxiety appears to increase sensitivity to pain (hyperalgesia),51-68 while moderate fear inhibits pain (hypoalgesia).51,69-77 Pexidartinib in vitro This suggests that anticipation of an unpredictable, threatening intervention could result in enhanced pain, while hypoalgesia results from exposure to a predictable, threatening MCE公司 event

(fear).[51] As we did not assess the participants’ psychological state, we are unsure whether this changed over the course of the experiment. Nevertheless, it seems unlikely that psychological factors had a major influence on our findings for the following reasons. First, participants were included only if usual head pain could be produced when stressing either the AO or C2-3 segments – the “inclusion/exclusion” session. In the case of head pain referral, both segments were examined (prior to the experimental sessions) to ascertain which segment reproduced usual head pain most clearly. Thus, participants experienced reproduction of their usual head pain, which ceased immediately on cessation of the technique (ie, essentially, participants were “cued” to believe that the procedures were not threatening). Second, participants, armed with the knowledge that they could terminate the experimental session at any time, were in control, further lessening the role of psychological factors.78-83 Third, pain ratings to the supraorbital stimuli were comparable for the cervical and arm interventions, and remained unchanged across the trials.