Unravelling the mechanisms involved in neuropathic pain requires the use of laboratory animal models that replicate as far as possible, with the above caveats, the different pathophysiological changes present in patients. For reasons of reproducibility and simplicity, most studies of neuropathic pain are based upon animal models of traumatic nerve injury, usually in the rat sciatic nerve (Figure 1.2).
sensation have begun to encode painful stimuli, while in hyperalgesia the structures which normally subserve nociception have become hyperexcitable.
Before exploring what is known about the pathophy-siology of neuropathic pain, three major caveats as to the nature of the existing literature need to be stated. First, the overwhelming bulk of the literature related to neuropathic pain mechanisms has emerged from rodent studies in which the major outcome measure is hypersensitivity of spinal withdrawal reflexes evoked by sensory stimuli. Thus, in this chapter, it will actually only be possible to discuss the putative mechanisms of evoked hypersensitivity, a relatively minor component of the spectrum of clinical neuropathic pain. Second, since it is also not currently possible to directly measure pain in experimental animals, the putative pain mechanisms which are to be discussed can only be interpreted in the
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