痛觉过敏

The concept of preemptive analgesia is to decrease the incidence of hyperalgesia and allodynia by reducing central sensitization.

预先镇痛是通过防止中枢敏感化来降低伤害性刺激引起的痛觉过敏和异常痛觉。

METHODS: Ninety-two patients with diabetic neuropathy, postherpetic neuralgia, or postsurgical/posttraumatic neuropathic pain with allodynia, hyperalgesia, or pinprick hypesthesia were randomly assigned to receive one of four creams (placebo, 2% amitriptyline, 1% ketamine, or 2% amitriptyline-1% ketamine combined).

92名出现痛觉超敏、痛觉过敏或针刺感觉减退的糖尿病神经病变、疱疹感染后神经痛或手术后/外伤后神经性疼痛患者被随机分组，分别使用下列四种霜剂中的一种进行治疗：安慰剂、2%阿米替林、1%氯胺酮或2%阿米替林＋1%氯胺酮联用。

BACKGROUND: Chronic pain, including hyperalgesia and algesthesia paresthesia, is pathological phenomenons making the patients felt unendurable and lacking of clinical treatments.

背景：慢性痛包括痛觉过敏和痛觉感觉异常，是患者感到难以忍受和临床缺乏治疗手段的一种病理现象。

The treatment group was given Qizhengxiaotong Emplastrum(0.75 g/kg),and the model group and blank group were given normal saline solution(0.5 mL/each)externally for 5 days on 10th day after the establishment of ...

末次给药后测量各组小鼠的痛行为，包括机械性痛觉超敏和热刺激痛觉过敏；将小鼠股骨进行X线摄片，影像学评估骨破坏；用免疫组化法检测各组局灶皮肤组织肿瘤坏死因子α、内皮素-1(ET-1)、白介素-1β(IL-1β)水平及脊髓后角P物质受体、c-fos及GFAP阳性反应神经元的表达。

Inflammation causes the induction of cyclooxygenase-2 (Cox-2), leading to the release of prostanoids, which sensitize peripheral nociceptor terminals and produce localized pain hypersensitiity.

炎症导致COX-2的产生，从而导致前列腺素的释放，释放的前列腺素使得外周痛觉末梢敏感化，从而产生了局部的痛觉过敏。

Inflammation causes the induction of cyclooxygenase-2 (Cox-2), leading to the release of prostanoids, which sensitize peripheral nociceptor terminals and produce localized pain hypersensitivity.

炎症导致COX-2的产生，从而导致前列腺素的释放，释放的前列腺素使得外周痛觉末梢敏感化，从而产生了局部的痛觉过敏。

These results suggestthat the antiallodynic and antihyperalgesic effect of NTP onneuropathic pain induced by spinal nerve ligation is mediatedprincipally through the action at supraspinal sites and throughactivation of spinal noradrenergic systems, possibly via thedescending inhibitory pathway.

这些结果提示 NTP 对脊神经结扎导致神经性疼痛的抗痛觉超敏和抗痛觉过敏作用主要是脊髓上作用和去甲肾上腺素能系统的激活介导的，可能是通过下行抑制通路起作用。

Perceptual wind-up (increased pain perception to constant intensity sensory stimuli at frequencies 0.3 Hz) is used as a proxy for central sensitisation to inestigate pain syndromes where pain hypersensitiity is important.

在痛觉过敏重要的情况下，感觉兴奋性升级现象（痛觉增加至恒定的强度，感觉刺激的频率达0.3Hz）被用来作为中枢促感觉剂的表现形式，来研究疼痛症状。

The latedischarges decreased from 9.29 ± 0.97 to 6.71 ± 0.68 with the A-fiberconditioning stimulus increasing from 1 to 5 (n〓8, P〓0. 05).(7) The intervalbetween the conditioning stimulus and test stimulus (C-T interval) wasincreasing, the inhibition tended to plateau off. At shorter time intervalsthe inhibition became more effective. When C-T interval was limited in 50ms,the inhibitory effects was the strongest, here, the late discharges reducedfrom 12.57±1.21to 2.29±0.42 (n=11, P＜0. 01).(8) Behavior research showedthat the rat model of snake venom exhibited neuropathic pain with heathyperalgesia, cold and mechanical allodynia, which corresponding to the acuteelectrophysiological findings.

此时轻刷WDR神经元的感受野不能引起其活动改变，但伤害性齿镊夹捏仍可引起WDR神经元放电增多；〓5〓晚成分放电的潜伏期缩短，即宁静期的时程变短，由给蛇毒前的118.83〓3.67ms降至50.72〓1.36ms〓n〓32，P〓0.01〓；〓6〓在正常动物，如果预先给予只激活A纤维的弱条件电刺激〓mA，100μs〓可抑制随后的伤害性检验刺激所诱发的WDR神经元的晚成分放电，当条件刺激个数从1增加至5时，每次伤害性检验刺激所诱发的晚成分放电数从9.29〓0.97个降至6.71〓0.68个〓n〓8，P〓0.05〓；〓7〓固定条件刺激数为1个，当条件刺激与检验刺激之间的间隔增大时，A纤维条件刺激对WDR神经元晚成分放电的抑制作用逐渐减弱，当条件刺激与检验刺激之间的间隔在50 ms以内时，抑制效应最为显著，此时，晚成分放电数由正常时的12.57〓1.21个降至2.29〓0.42个〓n〓11，P〓0.01〓；〓8〓与急性研究中的WDR神经元电活动的变化结果相匹配，利用蛇毒制备的大鼠模型在行为学上表现为热痛觉过敏、冷觉的痛性感觉异常及机械痛觉过敏等慢性痛症状。

At the same time, most WDR neurons failedto respond to the light brush applied to the receptive fields, but they couldbe intensively excited by the noxious pinch.(5) The latency of the latedischarges was shortened from 118.83 ± 3.67ms to 50.72 ± 1.36ms (n〓32, P〓0. 01).(6) Preceding graded number of A〓fiber conditioning inputs (〓mA, 100 μs) delayed the C-activity evoked by the following nociceptive teststimulus activating both A- and C-fiber applied to the sciatic nerve. The latedischarges decreased from 9.29 ± 0.97 to 6.71 ± 0.68 with the A-fiberconditioning stimulus increasing from 1 to 5 (n〓8, P〓0. 05).(7) The intervalbetween the conditioning stimulus and test stimulus (C-T interval) wasincreasing, the inhibition tended to plateau off. At shorter time intervalsthe inhibition became more effective. When C-T interval was limited in 50ms,the inhibitory effects was the strongest, here, the late discharges reducedfrom 12.57±1.21to 2.29±0.42 (n=11, P＜0. 01).(8) Behavior research showedthat the rat model of snake venom exhibited neuropathic pain with heathyperalgesia, cold and mechanical allodynia, which corresponding to the acuteelectrophysiological findings.

此时轻刷WDR神经元的感受野不能引起其活动改变，但伤害性齿镊夹捏仍可引起WDR神经元放电增多；〓5〓晚成分放电的潜伏期缩短，即宁静期的时程变短，由给蛇毒前的118.83〓3.67ms降至50.72〓1.36ms〓n〓32，P〓0.01〓；〓6〓在正常动物，如果预先给予只激活A纤维的弱条件电刺激〓mA，100μs〓可抑制随后的伤害性检验刺激所诱发的WDR神经元的晚成分放电，当条件刺激个数从1增加至5时，每次伤害性检验刺激所诱发的晚成分放电数从9.29〓0.97个降至6.71〓0.68个〓n〓8，P〓0.05〓；〓7〓固定条件刺激数为1个，当条件刺激与检验刺激之间的间隔增大时，A纤维条件刺激对WDR神经元晚成分放电的抑制作用逐渐减弱，当条件刺激与检验刺激之间的间隔在50 ms以内时，抑制效应最为显著，此时，晚成分放电数由正常时的12.57〓1.21个降至2.29〓0.42个〓n〓11，P〓0.01〓；〓8〓与急性研究中的WDR神经元电活动的变化结果相匹配，利用蛇毒制备的大鼠模型在行为学上表现为热痛觉过敏、冷觉的痛性感觉异常及机械痛觉过敏等慢性痛症状。

Plunder melds and run with this jewel!

掠夺melds和运行与此宝石！

My dream is to be a crazy growing tree and extend at the edge between the city and the forest.

此刻，也许正是在通往天国的路上，我体验着这白色的晕旋。