Davis Karen D
Division of Neurosurgery, University of Toronto, The Toronto Hospital (Western Division), MP14-322, 399 Bathurst Street, Toronto, Ontario, M5T 2S8 Canada.
Pain. 1998 Mar;75(1):47-57. doi: 10.1016/S0304-3959(97)00203-0.
Little is known concerning the mechanisms underlying the perception of cold pain in humans. An appreciation of these mechanisms is important to understand and possibly treat those disorders in which cold stimuli evoke unpleasant sensations. To study cold pain, I have conducted psychophysical experiments on 16 healthy subjects. A peltier-type stimulator (20 x 25 mm) was used to deliver stimuli to sites on the thenar eminence (glabrous skin) and volar forearm (hairy skin) of each arm. Each trial consisted of a 90 s, 2 degrees C stimulus that was preceded and followed by a 35 degrees C stimulus. A computer-based visual analog scale was used to collect continuous pain ratings throughout each trial. In experiment 1, nine subjects rated the overall evoked pain intensity (four trials/skin type) and the prickle component (four trials/skin type). Typically, subjects perceived the cold-evoked pain as prickly, cold/freezing and achy. The pain intensity and quality was similar for glabrous and hairy skin sites within individual subjects. Pain intensity gradually rose to a plateau by approximately 60 s into each trial. The prickle component differed amongst subjects due to its variable time course. Subjects consistently reported an intense, brief jab of prickle at both hairy and glabrous sites during the rewarming phase. In experiment 2, nine subjects rated the pain intensity during the cold stimulus before and during a compression-ischemic block of Abeta/Adelta fiber conduction. The dominant sensation evoked by the cold stimulus in the hairy and glabrous skin during the block was a sharp, hot/burning pain. The block did not consistently affect the total pain at the hairy sites. However, most subjects reported more pain during the block at the glabrous sites. These data suggest that noxious cold stimuli affect a mosaic of primary afferent input and central processing resulting in a complex pain experience which may differ in glabrous and hairy skin.
关于人类冷痛感知背后的机制，我们所知甚少。了解这些机制对于理解并可能治疗那些冷刺激引发不适感的疾病至关重要。为了研究冷痛，我对16名健康受试者进行了心理物理学实验。使用珀尔帖式刺激器（20×25毫米）向每只手臂的鱼际隆起（无毛皮肤）和掌侧前臂（有毛皮肤）部位施加刺激。每次试验包括一个90秒、2摄氏度的刺激，前后分别有一个35摄氏度的刺激。在每次试验过程中，使用基于计算机的视觉模拟量表收集连续的疼痛评分。在实验1中，9名受试者对总体诱发疼痛强度（每种皮肤类型进行4次试验）和刺痛成分（每种皮肤类型进行4次试验）进行评分。通常，受试者将冷诱发的疼痛感知为刺痛、冷/冰冻和酸痛。在个体受试者中，无毛和有毛皮肤部位的疼痛强度和性质相似。每次试验中，疼痛强度在大约60秒时逐渐上升至平稳状态。由于刺痛成分的时间进程不同，受试者之间存在差异。在复温阶段，受试者在有毛和无毛部位均一致报告有强烈、短暂的刺痛。在实验2中，9名受试者在阻断Aβ/Adelta纤维传导的压迫性缺血过程之前和期间，对冷刺激期间的疼痛强度进行评分。在阻断过程中，有毛和无毛皮肤的冷刺激诱发的主要感觉是尖锐的、热/灼痛。阻断并未始终影响有毛部位的总体疼痛。然而，大多数受试者报告在阻断期间无毛部位的疼痛更强烈。这些数据表明，有害冷刺激会影响初级传入输入和中枢处理的组合，导致复杂的疼痛体验，这在无毛和有毛皮肤中可能有所不同。
