Koltzenburg M, Torebjörk H E, Wahren L K
Department of Neurology, University of Würzburg, Germany.
Brain. 1994 Jun;117 ( Pt 3):579-91. doi: 10.1093/brain/117.3.579.
Brush-evoked pain (mechanical allodynia, dynamic mechanical hyperalgesia) is a hallmark of neuropathic and inflammatory pain states. Here we have examined the neural mechanisms that induce and maintain this component of mechanical hyperalgesia. The principle finding of these experiments is that the severity of brush-evoked pain correlates with the intensity of background pain in patients suffering from chronic painful neuropathies and in normal subjects with acute experimental chemogenic pain. In experiments on nine normal subjects topical application of mustard oil for 5 min evoked strong burning pain and hyperalgesia to light mechanical stimuli. Differential nerve blocks (by compression of the superficial radial nerve) revealed that the brush-evoked pain was transmitted by A beta-fibres, which normally encode non-painful tactile sensations, while the burning pain was signalled by C-fibres. Psychophysical measurements showed that mustard oil treatment resulted in a pronounced sensitization of nociceptors to heat so that subsequent innocuous changes of skin temperature from 35 to 40 degrees C resulted in a proportional increase of burning background pain. Changes in the magnitude of ongoing burning pain were closely correlated (r = 0.81) to the intensity of brush-evoked pain. While conduction block of A-fibres eliminated only touch-evoked pain, blockade of C-fibre excitation instantaneously abolished both ongoing and touch-evoked pain. In nine patients with chronic neuralgia (15 years mean duration) ongoing and brush-evoked pain were examined. In six patients, differential block of A beta-fibres eliminated touch-evoked pain, but ongoing pain persisted when only C-fibres were conducting. Complete relief of both ongoing and stimulus-induced pain was obtained in two patients with intravenous regional guanethedine block and in two other individuals by local anaesthetic blocks of nerves supplying the symptomatic skin, indicating that input from primary afferents was necessary for the maintenance of the pains and that ongoing pain was not self-perpetuated by central mechanisms alone. Quantitative sensory tests revealed heat hyperalgesia in four patients. In those individuals, an increase of skin temperature produced a graded increase of their ongoing pain which was closely correlated (r = 0.94) with the level of brush-evoked pain. In the remaining five patients there was no heat hyperalgesia and consequently no aggravation of pain by increases of skin temperature. Nevertheless when the intensity of the background pain fluctuated spontaneously there were also parallel changes (r = 0.88) of the severity of brush-evoked pain.(ABSTRACT TRUNCATED AT 400 WORDS)
刷擦诱发的疼痛（机械性异常性疼痛、动态机械性痛觉过敏）是神经性和炎性疼痛状态的一个标志。在此，我们研究了诱发并维持这种机械性痛觉过敏成分的神经机制。这些实验的主要发现是，在患有慢性疼痛性神经病变的患者以及患有急性实验性化学源性疼痛的正常受试者中，刷擦诱发疼痛的严重程度与背景疼痛的强度相关。在对9名正常受试者进行的实验中，局部涂抹芥子油5分钟会诱发强烈的灼痛以及对轻微机械刺激的痛觉过敏。差异性神经阻滞（通过压迫桡浅神经）显示，刷擦诱发的疼痛由Aβ纤维传导，Aβ纤维通常编码无痛性触觉，而灼痛则由C纤维传导。心理物理学测量表明，芥子油处理导致伤害感受器对热明显敏感，以至于随后皮肤温度从35℃到40℃的无害变化会导致灼痛背景疼痛成比例增加。持续灼痛程度的变化与刷擦诱发疼痛的强度密切相关（r = 0.81）。虽然A纤维的传导阻滞仅消除了触摸诱发的疼痛，但C纤维兴奋的阻滞立即消除了持续疼痛和触摸诱发的疼痛。对9名慢性神经痛患者（平均病程15年）的持续疼痛和刷擦诱发疼痛进行了检查。在6名患者中，Aβ纤维的差异性阻滞消除了触摸诱发的疼痛，但当仅C纤维传导时，持续疼痛仍然存在。两名接受静脉区域胍乙啶阻滞的患者以及另外两名接受供应有症状皮肤神经的局部麻醉阻滞的患者，其持续疼痛和刺激诱发的疼痛均完全缓解，这表明初级传入神经的输入对于疼痛的维持是必要的，并且持续疼痛并非仅由中枢机制自我维持。定量感觉测试显示4名患者存在热痛觉过敏。在这些个体中，皮肤温度升高会使他们的持续疼痛分级增加，这与刷擦诱发疼痛的程度密切相关（r = 0.94）。在其余5名患者中没有热痛觉过敏，因此皮肤温度升高不会加重疼痛。然而，当背景疼痛强度自发波动时，刷擦诱发疼痛的严重程度也会出现平行变化（r = 0.88）。（摘要截取自400字）
