Brain research
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Our recent magnetoencephalography study demonstrated that the mu rhythm can reliably indicate sensorimotor resonance during the perception of pain in others (Cheng, Y., Yang, C. Y., Lin, C. P., Lee, P. ⋯ Further, the mu suppression for pain empathy was positively correlated with the scoring on the personal distress subscale of the interpersonal reactivity index only in the female participants. The present findings suggest the existence of a gender difference in pain empathy in relation with the sensorimotor cortex resonance. The mu rhythm can be a potential biomarker of empathic mimicry.
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Case Reports
Vibrotactile detection thresholds for chest skin of amputees following targeted reinnervation surgery.
Recent advances in the design of prosthetic arms have helped upper limb amputees achieve greater levels of function. However, control of upper limb prostheses is limited by the lack of sensory feedback to the user. Targeted reinnervation, a novel surgical technique for amputees, offers the potential for returning this lost sensation. ⋯ For the two unilateral amputees, these thresholds were similar to measures on their contralateral chests, but greater than measures on their contralateral hands. Targeted reinnervation appears to result in near-normal vibration-detection ability with respect to the target tissue, suggesting the functional reinnervation of mechanoreceptors by the reinnervating afferents. The functional limb sensation following targeted reinnervation could be used to provide prosthesis users with a sense of touch.
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We have examined the effect of the peripheral application of glutamate and capsaicin to deep craniofacial tissues in influencing the activation and peripheral sensitization of deep craniofacial nociceptive afferents. The activity of single trigeminal nociceptive afferents with receptive fields in deep craniofacial tissues were recorded extracellularly in 55 halothane-anesthetized rats. The mechanical activation threshold (MAT) of each afferent was assessed before and after injection of 0.5 M glutamate (or vehicle) and 1% capsaicin (or vehicle) into the receptive field. ⋯ Following glutamate injection, capsaicin-evoked activity was greater than that evoked by capsaicin alone, whereas following capsaicin injection, glutamate-evoked responses were similar to glutamate alone. These findings indicate that peripheral application of glutamate or capsaicin may activate or induce peripheral sensitization in a subpopulation of trigeminal nociceptive afferents innervating deep craniofacial tissues, as reflected in changes in MAT and other afferent response properties. The data further suggest that peripheral glutamate and capsaicin receptor mechanisms may interact to modulate the activation and peripheral sensitization in some deep craniofacial nociceptive afferents.
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Higher-order processing of nociceptive input is distributed in corticolimbic regions of the brain, including the anterior cingulate, parieto-insular and prefrontal cortices, as well as subcortical structures such as the bed nucleus of stria terminalis and amygdala. In addition to their role in pain processing, these regions encode or modulate emotional, motivational and sensory responses to stress. Thus, pain and stress pathways in the brain intersect at cortical and subcortical forebrain structures. ⋯ Defeated rats exhibited a significant increase in cold preference after social defeat compared to the baseline. In the escape task, the rats exhibited increased escape from warm and nociceptive cold and heat temperatures. Thus, chronic social stress produces hyperalgesia for both hot and cold stimuli in male rats, suggesting a mutually facilitatory cross-regulation between central pathways regulating stress and pain.
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In this study, we evaluated the expression of MCP-1 in the rat dorsal root ganglion (DRG) and spinal cord following axotomy and chronic constriction injury (CCI) of the sciatic nerve and L5 spinal nerve ligation (L5 SNL) using an immunohistochemical approach. MCP-1 expression in the DRG peaked and declined before the full onset of pain hypersensitivity following nerve injury. Spinal expression of MCP-1 peaked when mechanical allodynia was maximal, but then declined rapidly despite the remarkable persistence of mechanical allodynia. ⋯ Despite increased MCP-1 in small and large DRG neurons, a remarkable increase in MCP-1-IR terminals was observed in the spinal superficial laminae following CCI and L5SNL, but not following axotomy; however, in the deeper laminae, a considerable increase in MCP-1-IR terminals, which may originate from the large and injured L5 DRG neurons, was found after L5 SNL. Our results demonstrate that MCP-1 synthesized in DRG neurons may or may not be transported to the spinal cord depending on the type of peripheral nerve injury. Additionally, increased MCP-1 in both intact L4 and injured L5 DRG neurons may contribute to neuropathic pain hypersensitivity following L5 SNL.