Chronic postsurgical pain (CPSP) is a phenomenon which is now recognised and whose reality and importance have been demonstrated by a large number of epidemiological studies. There are a number of risk factors for the persistence of pain after surgery, some of which are related to the patients themselves and others to the type of operation carried out. The role of anaesthesia is to prevent the occurrence of adverse phenomena associated with surgery. This is done while the operation is taking place. When considering the problem of CPSP, however, it seems possible that anaesthesia plays a preventative role but in some circumstances also facilitates the development of the phenomenon. Alteration of the physiological response to pain through the development of the phenomena of hyperalgesia and allodynia, resulting in an exacerbation of the experience of pain, is in fact one of the mechanisms that may facilitate the establishment of CPSP [1]. There seems to be a relationship between the area of immediate postoperative mechanical periwound allodynia and the incidence of CPSP: the larger the area, the higher the risk of chronic pain [2]. The ultimate aim of reducing or preventing these processes of allodynia and hyperalgesia could therefore be to prevent CPSP. Although these hypersensitisation processes are a direct consequence of the tissue injuries caused by surgery and the release of pro-inflammatory mediators at the surgical site, they are also dependent on the administration of opiates for analgesic purposes [3]. The way in which opiates are administered during the perioperative period may therefore play a role in the long-term consequences of anaesthesia and analgesia in causing CPSP.

The exacerbation of pain when stopping treatment with opiates is a phenomenon that has been recognised for some time, and it was long thought to be linked to chronic opiate administration. It has been known for several years now that this is not the case and that the same phenomenon can be observed after the administration of opiates for a short period corresponding to the time of the operation itself. It appears that opiates have a dual role, at once inhibiting and facilitating nociceptive transmission, the latter effect continuing for longer than the former one [3, 4]. In animals, hypersensitivity to pain caused by a surgical lesion or inflammation is potentiated by the administration of an opioid and this occurs in a dose-dependent way [5–7]. Increasing the dose of the opioid also increases not only the amplitude of the hyperalgesic type response but also its duration. This process of hypersensitisation to pain causes activation of NMDA type post-synaptic receptors, while concomitant administration of an agent that blocks NMDA receptors, such as ketamine, attenuates the occurrence of the phenomenon [5–7]. Opioids inhibit nociception by stimulating mainly μ-type opioid receptors. They also activate facilitatory systems which are triggered by NMDA receptors. Passage of calcium into the cell via NMDA receptors activates a protein kinase Cγ which, by phosphorylating the NMDA receptors themselves, triggers the activation of more of these receptors. The administration of opiates can therefore be considered to induce a vulnerability to pain which seems not only to persist during the days following a mechanical trauma (such as an operation in man), but may also extend beyond that period. To prevent this, two strategies may be used: reducing the quantity of opiates administered due to a sparing effect resulting from the use of other analgesic agents, and concomitant administration of agents capable of blocking the hyperalgesia by blocking the NMDA receptors.