Pain
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Clinical Trial
Ethnic identity predicts experimental pain sensitivity in African Americans and Hispanics.
The aim of this study was to examine experimental pain sensitivity in three ethnic groups, African Americans, Hispanic Americans and non-Hispanic White Americans, and to determine whether ethnic identity is differentially associated with pain sensitivity across ethnic groups. Participants included sixty-three African American, sixty-one Hispanic and eighty-two non-Hispanic white participants who were assessed using three experimental pain measures: thermal, cold-pressor and ischemic. Participants' ethnic identity was assessed using the Multi-group Ethnic Identity Measure (MEIM). ⋯ Statistically controlling for ethnic identity rendered some of the group differences in pain range non-significant. These findings indicate that ethnic identity is associated with pain sensitivity in ethnic minority groups, and may partially mediate group differences in pain perception. The results of the present investigation provide evidence of ethnic group differences in responses to experimental pain across multiple noxious stimuli, with both minority groups exhibiting greater sensitivity to laboratory evoked pain compared to non-Hispanic White Americans.
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Activation of histamine H3 receptors (H3Rs) reduces inflammation and nociception, but the existence of H3Rs on peripheral innervation has never been demonstrated. Here we use antibodies to locate H3Rs in whisker pads, hairy and glabrous hind paw skin, dorsal root ganglia (DRGs), and spinal cords of rats, wild type mice, and H3R knockout (H3KO) mice. Although H3Rs have been hypothesized to be on C and sympathetic fibers, H3R-like immunoreactivity (H3R-LI) was only detected on presumptive periarterial A delta fibers and on A beta fibers that terminated in Meissner's corpuscles and as lanceolate endings around hair follicles. ⋯ Low levels of H3R-LI were also present on A beta fibers penetrating superficial and into deeper laminae. The distribution of H3R-LI was similar in rats and wild type mice, but was eliminated or strongly reduced in A delta fibers and A beta fibers, respectively, in H3KO mice. Taken with recently published behavioral results, the present findings suggest that periarterial, peptidergic, H3R-containing A delta fibers may be sources of high threshold mechanical nociception.
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Comparative Study
Role of gender norms and group identification on hypothetical and experimental pain tolerance.
Previous research indicates that men typically tolerate more pain in experimental settings than women. One likely explanation for these group differences in pain tolerance is conformity to traditional, gender group social norms (i.e., the ideal man is masculine and tolerates more pain; the ideal woman is feminine and tolerates less pain). According to self-categorization theory, norms guide behavior to the degree that group members adopt the group identity. ⋯ The experimental outcome revealed that high-identifying men tolerated more painful stimulation than high-identifying women. Further, high-identifying men tolerated more pain than low-identifying men. These results highlight the influence of social norms on behavior and suggest the need to further explore the role of norms in pain reporting behaviors.
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This study evaluated the contribution of condition-specific helplessness and loss to depression in fibromyalgia (FM). Two models were tested. The first model examined whether loss, measured by the West Haven-Yale Multidimensional Pain Inventory (WHYMPI) Interference Scale, would mediate the relationship between disability and depression. ⋯ In Model 1, loss fully mediated the relationship between disability and depression. In Model 2, condition-specific helplessness mediated the relationship between pain and depression, but the contribution of loss was not significant. The findings confirm the importance of helplessness and demonstrate that the cognitive meaning of having FM plays a more central role in predicting depressive symptomatology than illness-related stressors, such as pain or disability.
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Comparative Study
Spinal NK-1 receptor expressing neurons mediate opioid-induced hyperalgesia and antinociceptive tolerance via activation of descending pathways.
Opioids can induce hyperalgesia in humans and in animals. Mechanisms of opiate-induced hyperalgesia and possibly of spinal antinociceptive tolerance may be linked to pronociceptive adaptations occurring at multiple levels of the nervous system including activation of descending facilitatory influences from the brainstem, spinal neuroplasticity, and changes in primary afferent fibers. Here, the role of NK-1 receptor expressing cells in the spinal dorsal horn in morphine-induced hyperalgesia and spinal antinociceptive tolerance was assessed by ablating these cells with intrathecal injection of SP-saporin (SP-SAP). ⋯ Thus, NK-1 receptor expressing neurons play a critical role in sustained morphine-induced neuroplastic changes which underlie spinal excitability reflected as thermal and tactile hypersensitivity to peripheral stimuli, and to reduced antinociceptive actions of spinal morphine (i.e., antinociceptive tolerance). Ablation of these cells likely eliminates the ascending limb of a spinal-bulbospinal loop that engages descending facilitation and elicits subsequent spinal neuroplasticity. The data may provide a basis for understanding mechanisms of prolonged pain which can occur in the absence of tissue injury.