Neuropathic pain: what do we do with all these theories?

Only a generation ago there were few ideas as to what might cause neuropath ic pain, and even fewer relevant data. Ln contrast, we can currently point to hundreds of distinct cellular changes that are triggered by nerve injury and that might be relevant to the emergence of pain symptomatology. The nu mber may soon increase to thousands. It is essential, therefore, to redirec t efforts towards the development of experimental strategies for testing wh ich of these are essential parts of the pain process and which are tangenti al. In this paper I point out four such strategies: tin-Ling, deletion, pre vention and genetic heterogeneity, and summarize how one neuropathic pain t heory, the ectopic pacemaker hypothesis, holds up to scrutiny.