• Linn K Kuehl, Gilles P Michaux, Steffen Richter, Hartmut Schächinger, and Fernand Anton.
• Institute of Psychobiology, Department of Clinical Physiology, University of Trier, Johanniterufer 15, Trier, Germany.
• Pain. 2010 Jun 1; 149 (3): 539-46.

AbstractClinical 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 24yrs) and analyzed the effects of metyrapone-induced hypocortisolism on quantitatively assessed basal mechanical pain sensitivity (1.5-13m/s impact stimuli), perceptual wind-up (9m/s impact stimuli at 1Hz) and temporal summation of pain elicited by inter-digital web pinching (IWP; 10N pressure stimuli for 2min). 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.

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