Pain
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The contribution of four cortical areas (S1, S2, insular cortex and gyrus cinguli) to pain processing was assessed by functional magnetic resonance imaging (fMRI). Phasic (mechanical impact) and tonic stimuli (squeezing) were applied to the back of a finger, both at two different strengths. Stimuli were adjusted to inflict weak and strong pain sensations. ⋯ Though the insular cortex was often bilaterally activated, no significant differences between stimulus quality or intensity were found. Our results provide evidence for a contribution of the S2 projection area and of the cingulate cortex to the processing of the intensity dimension of phasic mechanical pain. Such evidence was not found for the S1 area, which probably receives dominant input from non-nociceptive mechanoreceptors.
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Chemical cauterization of the central cornea with silver nitrate was assessed as a superficial injury model of tissue sensitization accompanying acute inflammation. Adult male Sprague-Dawley rats were anesthetized with halothane gas, and the centers of their right corneas treated with a silver nitrate applicator stick (75% silver nitrate, 25% potassium nitrate) to produce a discrete lesion 1 mm in diameter. Edema of the corneal stroma and elevated immune cell counts became significant 4 h after cauterization, and were still evident after 48 h. ⋯ A significant increase in stimulus-induced blinking was evident 2 h after cauterization. Chemical sensitization peaked at 6 h, and was no longer significant at 12 h. We conclude that silver nitrate cauterization produces acute corneal inflammation and hyperalgesia, and may prove a useful model for the study of primary afferent nociceptors.