论文部分内容阅读
Tactile allodynia,defined as a pain or a nociceptive response provoked by an innocuous mechanical stimulus,in addition to hyperalgesia and spontaneous pain,is one of the common features of peripheral neuropathy in hu-mans following peripheral nerve injury.In many respects it is the development of exquisite sensitivity to light touch that many patients with post herpetic neuralgia,partial nerve trauma,and metabolic and inflammatory neuropa-thies find particularly unbearable.It is a pain hypersensi-tivity that is,moreover,resistant to most current forms of therapy.An enormous breakthrough in our understanding of the pathophysiology of neuropathic pain in general,and tactile allodynia in particular,has come through the rec-ognition that the mechanical hypersensitivity is mediated by low-threshold,large myelinated Aβfibers.These high-ly specialized sensory fibers normally never produce pain and are responsible for the detection of light touch,move- ment of hairs,pressure,flutter,and vibration [1] .However,after nerve damage,activation of these afferents elicits pain.The major question then is what mechanisms are responsible for converting sensory processing within the somatosensory system such that low-threshold Aβmechanoreceptors elicit pain?
Tactile allodynia, defined as a pain or a nociceptive response provoked by an innocuous mechanical stimulus, in addition to hyperalgesia and spontaneous pain, is one of the common features of peripheral neuropathy in hu-mans following peripheral nerve injury. Many respects it is the development of exquisite sensitivity to light touch that many patients with post herpetic neuralgia, partial nerve trauma, and metabolic and inflammatory neuropa-thies find particular unbearable. It is a pain hypersensi-tivity that is, moreover, resistant to most current forms of therapy. An enormous breakthrough in our understanding of the pathophysiology of neuropathic pain in general, and tactile allodynia in particular, has come through the rec-ognition that the mechanical hypersensitivity is mediated by low-threshold, large myelinated Aβ fibbers. These high-ly specialized sensory fibers normally never produce pain and are responsible for the detection of light touch, move ment of hairs, pressure, flutter, and vibra tion [1]. After, after nerve damage, activation of these afferents elicits pain. major is then responsible for converting sensory processing within the somatosensory system such that low-threshold Aβmechanoreceptors elicit pain?