Pain
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Postherpetic neuralgia is an exceptionally drug-resistant neuropathic pain. To investigate the pathophysiological mechanisms underlying postherpetic neuralgia we clinically investigated sensory disturbances, pains and itching, with an 11-point numerical rating scale in 41 patients with ophthalmic postherpetic neuralgia. In all the patients we recorded the blink reflex, mediated by non-nociceptive myelinated Abeta-fibers, and trigeminal laser evoked potentials (LEPs) related to nociceptive myelinated Adelta- and unmyelinated C-fiber activation. ⋯ Our study shows that postherpetic neuralgia impairs all sensory fiber groups. The neurophysiological-clinical correlations suggest that constant pain arises from a marked loss of nociceptive afferents, whereas paroxysmal pain is related to Abeta-fiber demyelination. These findings might be useful for a better understanding of pain mechanisms in postherpetic neuralgia.
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In chronic musculoskeletal pain conditions, the balance between supraspinal facilitation and inhibition of pain shifts towards an overall decrease in inhibition. Application of a tonic painful stimulus results in activation of diffuse noxious inhibitory controls (DNIC). The aims of the present experimental human study were (1) to compare DNIC, evoked separately, by hypertonic saline (6%)-induced muscle pain (tibialis anterior) or cold pressor pain; (2) to investigate DNIC evoked by concomitant experimental muscle pain and cold pressor pain, and (3) to analyze for gender differences. ⋯ When cold pressor and muscle pain were applied concomitantly the PPT increases were smaller when compared to the individual sessions. This study showed for the first time that two concurrent conditioning tonic pain stimuli (muscle pain and cold pressor pain) cause less DNIC compared with either of the conditioning stimuli given alone; and males showed greater DNIC than females. This may explain why patients with chronic musculoskeletal pain have impaired DNIC.
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A few experimental observations have suggested that diffuse noxious inhibitory control (DNIC)-type inhibition acts preferentially on the pain system if this is in a sensitised state, e.g. after slow temporal summation (wind-up). However, firm evidence is still missing. Furthermore, sex-related factors, which seem to affect temporal summation as well as DNIC effects, might thus also modulate the interaction of these two processes. ⋯ Sex differences were not observed for temporal summation, DNIC inhibition or for the interaction of the two processes, although women exhibited significantly lower pressure pain thresholds and higher ratings for the tonic heat stimuli. In conclusion, DNIC-type inhibition apparently does not preferentially act on a sensitised pain system after slow temporal summation. Considering the sex of the subjects does not change this insight.