Pain
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Randomized Controlled Trial
Diffuse analgesic effects of unilateral repetitive transcranial magnetic stimulation (rTMS) in healthy volunteers.
We investigated the analgesic effects of unilateral repetitive transcranial magnetic stimulation (rTMS) of the motor cortex (M1) or dorsolateral prefrontal cortex (DLPFC) in two models of experimental pain in healthy volunteers. Two studies were carried out in parallel in two groups of 26 paid healthy volunteers. The effects of active or sham rTMS (frequency, 10Hz; intensity, 80% resting motor threshold) applied to the right M1 or DLPFC were compared in a double-blind randomized cross-over design. ⋯ By contrast, the second study showed that rTMS of M1 or DLPFC had no significant effect on the threshold or recruitment curve of the nociceptive flexion RIII reflex. Our findings demonstrate that unilateral rTMS of M1 or DLPFC induces diffuse and selective analgesic effects in healthy volunteers. The lack of effect on the RIII reflex suggests that such analgesic effects may not depend on the activation of descending inhibitory systems.
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Mu-opioid receptor (MOPr) agonists, such as morphine, produce greater antinociception in male compared to female rats. The ventolateral periaqueductal gray (vlPAG) appears to contribute to this sex-difference despite fewer vlPAG output neurons projecting to the rostral ventromedial medulla in male compared to female rats. This greater projection in female rats suggests that non-opioid activation of vlPAG output neurons should produce greater antinociception in female compared to male rats. ⋯ Antinociceptive potency was significantly greater in male compared to female rats following microinjection of morphine, DAMGO, and bicuculline, but not following microinjection of fentanyl or kainic acid. In no case did activation of the vlPAG produce greater antinocicepiton in female compared to male rats. These findings demonstrate that the vlPAG can produce comparable antinociception in female and male rats, but antinociception produced by inhibition of GABAergic neurons (whether by morphine or the GABA(A) receptor antagonist bicuculline) produces greater antinociception in males.
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This study examines the relationship between the severity of painful temporomandibular joint disorders (TMD) symptoms and current tobacco use in patients evaluated at a specialized orofacial pain clinic. Medical records, including responses to the Chronic Pain Grading Scale (CPGS), from 606 consecutive patients evaluated at the Mayo Clinic orofacial pain clinic with TMD by RDC-TMD criteria were retrospectively reviewed. Univariate analyses were performed comparing tobacco users and non-users. ⋯ In the subset of subjects who lacked a myofascial component of pain (N=333) this difference remained significant in the adjusted analysis (adjusted OR=4.56, 95% CI 1.46-14.24). Current tobacco use was associated with unfavorable demographic background variables and more pain interference in subjects with TMD presenting to a specialized orofacial pain clinic. These effects were more pronounced in cases where myofascial pain was not present.
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Some patients with myofascial pain from temporomandibular disorders (TMD) report pain in extra-trigeminal body regions. Our aim was to distinguish TMD as regional musculoskeletal pain syndrome (n=23) from a widespread pain syndrome (FMS; n=18) based on patients' tender point scores, pain drawings and quantitative sensory testing (QST) profiles. Referenced to 18 age- and gender-matched healthy subjects significant group differences for cold, pressure and pinprick pain thresholds, suprathreshold pinprick sensitivity and mechanical detection thresholds were found. ⋯ However, sensitive TMD patients had a short pain duration arguing against a transition from TMD to FMS over time. Data rather suggest an overlap in pathophysiology with FMS, e.g. a disturbance of central pain processing, in this subgroup of TMD patients. Those patients could be identified on the basis of their tender point count as an easy practicable screening tool.
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Previous research has demonstrated that the nociceptive flexion reflex (NFR) and pain-related evoked potentials are reduced in amplitude when elicited during the middle of the cardiac cycle. Despite these findings, suggesting a baroreceptor mechanism of antinociception during systole, pain intensity ratings reported in these studies were not modulated across the cardiac cycle. This discrepancy between the neurophysiological correlates of pain and its subjective experience was the focus of the current study that used a mixed block design to assess the effects of natural arterial baroreceptor activity on both the NFR and pain intensity and unpleasantness reports. ⋯ Finally, nociceptive responses did not differ among the R-wave to stimulation intervals for both painful and non-painful intensities. The observed phasic modulation of pain may be explained by a central nervous system alarm/defence reaction triggered by the unpredictability of the potentially damaging stimulation. The absence of systolic attenuation of nociceptive responding is compatible with previous evidence that baroreceptor modulation of the NFR is abolished under conditions of heightened arousal.