Department of Medical Psychology, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands Pain and Nociception Neuroscience Research Group, Department of Anaesthesiology, Pain and Palliative Medicine, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands Department of Dermatology, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands.
Pain. 2010 May;149(2):332-337. doi: 10.1016/j.pain.2010.02.026. Epub 2010 Mar 11.
Pain can be endogenously modulated by heterotopic noxious conditioning stimulation (HNCS) through a mechanism which is known as diffuse noxious inhibitory control (DNIC). Since DNIC can be impaired in patients suffering from chronic pain, a comparable impaired itch inhibition may exist in patients suffering from chronic itch. The aim of the present study was to investigate whether heterotopic pruritic conditioning stimulation (HPCS) would display an impaired modulation of itch in patients suffering from chronic itch compared with healthy subjects. To this end, electrical stimuli were applied before and after histamine application (HPCS) to female patients with psoriasis and healthy female control subjects. Subjects reported the intensity of electrically evoked itch before and after HPCS. In order to replicate earlier findings for DNIC, electrically evoked pain was additionally investigated before and after cold stimulation (HNCS). As expected, the intensity of itch evoked by the electrical stimulus was significantly less after than before HPCS in healthy subjects, and the same was found for the intensity of electrically evoked pain after compared to before HNCS. Contrarily, in the patients levels of electrically evoked itch were significantly higher after than before HPCS, and no significant difference in pain intensity before and after HNCS was observed. In line with pain modulation, results suggest that there is a DNIC analogous mechanism for itch, i.e., diffuse pruritic inhibitory control (DPIC), which is impaired in patients with chronic itch, possibly due to a dysregulation of descending itch modulatory systems.
疼痛可以通过一种称为弥散性痛觉抑制控制（DNIC）的机制，由异位有害性条件刺激（HNCS）内源性调节。由于慢性疼痛患者的 DNIC 可能受损，因此患有慢性瘙痒的患者可能存在类似的瘙痒抑制受损。本研究旨在探讨与健康受试者相比，慢性瘙痒患者的异位瘙痒条件刺激（HPCS）是否会显示出瘙痒调节受损。为此，对患有银屑病的女性患者和健康女性对照者在应用组胺前后施加电刺激（HPCS）。受试者在 HPCS 前后报告电诱发瘙痒的强度。为了复制先前关于 DNIC 的发现，还在冷刺激（HNCS）前后研究了电诱发疼痛。正如预期的那样，与 HPCS 前相比，健康受试者的电刺激诱发的瘙痒强度在 HPCS 后明显降低，HNCS 前后电诱发疼痛的强度也是如此。相反，在患者中，与 HPCS 前相比，电诱发瘙痒的强度在 HPCS 后明显升高，而 HNCS 前后疼痛强度无显著差异。与疼痛调节一致的结果表明，瘙痒存在类似的 DNIC 机制，即弥散性瘙痒抑制控制（DPIC），在慢性瘙痒患者中受损，可能是由于下行瘙痒调节系统失调所致。
