Are mechanisms mediating acute pain different from those mediating late-onset pain?
Although there are examples of changes that occur in the acute phase that may be prolonged, such as the surprisingly long-term inflammatory changes reported in post-herpetic neuralgia (Watson et al., 1991), it seems improbable that mechanisms implicated in acute pain can usually account for pain that develops after a prolonged period. Processes that mediate acute pain occur rapidly and are followed by a cascade of events that take place within minutes, hours and days, and affect widespread regions of the nervous system (Wall, 1984). It seems implausible that in the majority of painful conditions those molecular changes that ensue in the wake of acute damage and inflammation (for reviews, see Zimmermann and Herdegen, 1996; Woolf and Costigan, 1999), or the development of physiological phenomena such as central sensitization (for a review, see Li et al., 1999), could develop de novo months or years after the initiating event. What happens to the acute-phase processes during the long pain
