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- W2041639449 abstract "Clinical data have accumulated showing that relative hypocortisolism, which may be regarded as a neuroendocrinological correlate of chronic stress, may be a characteristic of some functional pain syndromes. However, it has not been clarified yet whether deregulations of the hypothalamus–pituitary–adrenal (HPA) axis may directly alter pain perception and thus be causally involved in the pathophysiology of these disorders. To test this hypothesis, we performed a randomized placebo-controlled crossover trial in N = 20 healthy drug-free volunteers (median age 24 yrs) and analyzed the effects of metyrapone-induced hypocortisolism on quantitatively assessed basal mechanical pain sensitivity (1.5–13 m/s impact stimuli), perceptual wind-up (9 m/s impact stimuli at 1 Hz) and temporal summation of pain elicited by inter-digital web pinching (IWP; 10 N pressure stimuli for 2 min). Experimentally induced hypocortisolism significantly decreased pain detection thresholds and augmented temporal summation of IWP-induced pain (p < .05). The latter effect was dependent on the relative reduction in cortisol levels, and seemed to rely on a potentiated sensitization and not merely on the observed changes in basal pain sensitivity. Perceptual wind-up by contrast was reduced when cortisol synthesis was blocked (p < .05). This result is reminiscent of findings from animal studies showing a reversal of NMDA receptor activation by glucocorticoid receptor antagonists in neuropathic pain models. Our results speak in favor of a potential causal role of HPA axis alterations in pain chronicity." @default.
- W2041639449 created "2016-06-24" @default.
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- W2041639449 date "2010-06-01" @default.
- W2041639449 modified "2023-10-17" @default.
- W2041639449 title "Increased basal mechanical pain sensitivity but decreased perceptual wind-up in a human model of relative hypocortisolism" @default.
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- W2041639449 doi "https://doi.org/10.1016/j.pain.2010.03.026" @default.
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