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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The trapezius muscle often develops pain as the result of repetitive and stressful work tasks although it is unclear to what extent this pain is due to alterations in muscle concentrations of algesic/nociceptive substances. Twenty women with chronic neck- and shoulder pain (TM) whose work required highly repetitive work tasks and 20 pain-free female colleagues (CON) were studied during and after a full 8-hour workday. We collected microdialysates from their dominant/most painful trapezius muscle; concentrations of serotonin, glutamate, lactate, pyruvate, potassium, bradykinin, and cytokines and blood flow were determined. ⋯ No differences in EMG, task exposure level, mental stress, or urine-cortisol in the groups were found. These findings support the idea that peripheral nociceptive processes are activated in occupationally active subjects, who are diagnosed with trapezius myalgia. In contrast, no sign of low blood flow or increased stress or muscle activity markers were found in TM.
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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.
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Provoked vestibulodynia (PVD) is a common form of chronic vulvar pain with unknown aetiology. Central pain regulatory mechanisms have been suggested to be disrupted in PVD, and consequently, PVD may be associated with anatomical changes in pain modulatory brain areas. Here, we compared total gray matter volumes and regional gray matter densities between 14 medication-free young women with relatively short-standing PVD (1 to 9 yrs) and 14 control subjects using whole brain voxel-based morphometry (VBM). ⋯ These results point at the morphological alterations in supra-spinal pain modulatory circuitry, which might contribute to the clinical symptoms of patients with PVD. Previous VBM studies in older subjects with a longstanding chronic pain condition have demonstrated gray matter decreases in similar areas. We therefore speculate that gray matter density might increase in young pain patients with short disease duration and decrease in older subjects with longstanding disease, similarly to some psychiatric conditions, in which bi-directional changes of gray matter have been observed.
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Osteoarthritis (OA) is a major healthcare burden of increasing prevalence. It has been demonstrated that the relationship between pain and sleep produces changes in sleep patterns and pain perception. However, electrophysiological studies in animal models of pain are limited. ⋯ These changes in sleep pattern occurred mostly between days 10 and 28. In the dark period, sleep disturbances were also characterized by decreased sleep efficiency, slow-wave sleep, and paradoxical sleep, although sleep was only initially fragmented. Thus, pain associated with the rat OA model causes alterations in sleep architecture by disrupting the sleep pattern.