Group differences in pain modulation: pain-free women compared to pain-free men and to women with TMD

Abstract

Previously reported differences in sensitivity to experimental pain stimuli between the sexes, as well as between temporomandibular disorder (TMD) patients and healthy control subjects, may be attributable in part to group differences in two pain modulatory mechanisms: the baroreceptor reflex arc and the endogenous opioid system. Twenty-two pain-free (PF) men, 20 PF women and 20 women with TMD underwent two testing sessions in which heat pain and ischemic arm pain threshold and tolerance were measured during both sessions, but followed relaxation during one session and laboratory stress tasks during the other. Blood pressure (BP) and plasma -endorphin (E) concentration were measured during a baseline rest and during the stress or relaxation periods. PF men's threshold and tolerance for heat pain, but not for ischemic pain, exceeded that of PF women's during both sessions. PF women and TMD women did not differ in sensitivity to either pain modality; however, significantly lower ischemic pain threshold (IPTh) was linked to oral contraceptive use in PF women but not TMD patients. In the men alone, higher baseline systolic BP (SBP) was correlated with higher heat pain threshold on both days and heat pain tolerance on the stress day. Conversely, in TMD women, higher baseline SBP was correlated with lower ischemic pain tolerance (IPTol) on both days; BP and pain sensitivity were not related in PF women. In men, but not in PF or TMD women, stress systolic and diastolic BP were positively correlated with heat pain threshold and tolerance and higher diastolic reactivity to stress were correlated with higher heat pain and IPTh and tolerance. On the stress day, higher baseline E level was strongly associated with higher IPTol in PF women but marginally associated with lower IPTol in TMD women. Thus, it appears that a BP-related analgesic mechanism (probably baroreceptor-mediated) predominates in PF men, while an endogenous opioid mechanism predominates in PF women. Stress enhances the expression of these central mechanisms. Female TMDs appear unable to effectively engage normal pain-inhibitory systems; opioid receptor desensitization and/or downregulation are probably implicated, because TMDs' production of E appears normal.

Trait anger expressiveness and pain-induced beta-endorphin release: Support for the opioid dysfunction hypothesis

“…This approach, however, was not feasible. That the plasma BE measure assessed has some relevance to pain is suggested by the significant inverse correlations observed between BE change and pain responses both in the current study and in previous work (e.g., Bragdon et al, 2002;Cleeland et al, 1984;Guasti et al, 1996;Miller et al, 1993;Rosa et al, 1988;Sheps et al, 1995;Szyfelbein et al, 1985). At the very least, results do confirm diminished peripheral opioid release in high anger-outs following noxious stimuli, even if the correspondence with central BE release is unclear.…”

“…The target of this study was plasma beta-endorphin (BE), an endogenous mu opioid receptor agonist with known analgesic properties (Millan, 2002). Circulating plasma BE has previously shown associations with acute pain responses (e.g., Bragdon et al, 2002;Cleeland et al, 1984;Guasti et al, 1996;Miller et al, 1993;Rosa et al, 1988;Sheps et al, 1995;Szyfelbein et al, 1985). Therefore, plasma BE levels were assessed at baseline and again following three laboratory acute pain stimuli in a series of subjects participating in a larger study examining alpha-2 adrenergic pain regulatory mechanisms.…”

Pain catastrophizing, physiological indexes, and chronic pain severity: tests of mediation and moderation models

“…Finally, although prior work suggests that blood pressure-related analgesia may be impaired in chronic pain patients (Bragdon et al 2002;Bruehl et al 2002;Bruehl and Chung 2004), the current findings indicate that some patients do exhibit effective blood pressure-related anal-gesia. These contrasting findings could reflect key methodological differences across these studies.…”

“…From a "person × situation" perspective, it perhaps may have been more appropriate to examine links between pain catastrophizing and chronic pain using interviews probing for difficulties adjusting to pain, interference with social and work functioning, issues of loss and so forth. The ability to test whether catastrophizing affects pain through physiological reactivity may have been limited because of the unrestricted topics patients could describe in the interviews.Finally, although prior work suggests that blood pressure-related analgesia may be impaired in chronic pain patients (Bragdon et al 2002;Bruehl et al 2002;Bruehl and Chung 2004), the current findings indicate that some patients do exhibit effective blood pressure-related anal-gesia. These contrasting findings could reflect key methodological differences across these studies.…”

Associations between Sensorimotor, Autonomic and Central Neuropathies in Diabetes Mellitus

“…Impairment of CPM are previously reported in chronic painful conditions such as fibromyalgia, painful osteoarthritis, temporomandibular joint disease, chronic low back pain, inflammatory bowel disease and chronic pancreatitis, where it is considered to predispose development and persistence of chronic pain [24][25][26][27][28][29][30]. DM patients with clinical suspicion of sensorimotor neuropathy may have concomitant peripheral Aδ-and C-neuropathy and consequently decreased afferent transmission.…”