Felsby S, Nielsen J, Arendt-Nielsen L, Jensen T S
Department of Neurology, Aarhus University Hospital, and Pain Research Center, Aarhus University, DK-8000 Aarhus C Denmark Laboratory of Experimental Pain Research, Aalborg University, DK-9000 Aalborg Denmark Department of Anaesthesiology, Aarhus Amtssygehus, Aarhus University Hospital, DK-8000 Aarhus C Denmark.
Pain. 1996 Feb;64(2):283-291. doi: 10.1016/0304-3959(95)00113-1.
Ten patients (4 female, 6 male) aged 34-67 years suffering from peripheral neuropathic pain participated in a double-blind placebo-controlled study where ketamine or magnesium chloride were administered by a 10 min bolus infusion (ketamine: 0.84 mumol/kg = 0.2 mg/kg, magnesium: 0.16 mmol/kg) followed by a continuous infusion (ketamine: 1.3 mumol/kg/h = 0.3 mg/kg/h, magnesium: 0.16 mmol/kg/h). Ongoing pain determined by VAS score, area of touch-evoked allodynia, detection and pain thresholds to mechanical and thermal stimuli were measured before and during drug infusion. Ketamine produced a significant reduction of spontaneous pain (57%) and of the area of allodynia (33%). Magnesium chloride reduced pain (29%) and area of allodynia (18%) insignificantly. Following ketamine there was a significant correlation between the reduction in ongoing pain and reduction in area of touch-evoked allodynia. Detection and pain thresholds to mechanical and thermal stimuli were not significantly changed by the drugs. These findings suggest that both ongoing pain and touch-evoked pain (allodynia) in neuropathic pain are inter-related phenomena, which may be mediated by the same mechanism and involving a N-methyl-D-aspartate receptor.
10名年龄在34至67岁之间、患有周围神经性疼痛的患者（4名女性，6名男性）参与了一项双盲安慰剂对照研究，在该研究中，通过10分钟的推注输注给予氯胺酮或氯化镁（氯胺酮：0.84 μmol/kg = 0.2 mg/kg，镁：0.16 mmol/kg），随后进行持续输注（氯胺酮：1.3 μmol/kg/h = 0.3 mg/kg/h，镁：0.16 mmol/kg/h）。在药物输注前和输注期间，测量由视觉模拟评分法（VAS）确定的持续性疼痛、触觉诱发痛觉过敏区域、对机械和热刺激的检测阈值和疼痛阈值。氯胺酮使自发性疼痛显著降低（57%），痛觉过敏区域显著减小（33%）。氯化镁使疼痛（29%）和痛觉过敏区域（18%）有不显著的降低。给予氯胺酮后，持续性疼痛的减轻与触觉诱发痛觉过敏区域的减小之间存在显著相关性。药物对机械和热刺激的检测阈值和疼痛阈值没有显著改变。这些发现表明，神经性疼痛中的持续性疼痛和触觉诱发疼痛（痛觉过敏）都是相互关联的现象，可能由相同的机制介导，且涉及N-甲基-D-天冬氨酸受体。
