OPIOID RESPONSIVENESS OF CANCER PAIN SYNDROMES CAUSED BY NEUROPATHIC OR NOCICEPTIVE MECHANISMS - A COMBINED ANALYSIS OF CONTROLLED, SINGLE-DOSE STUDIES

We performed a combined analysis of the results from four controlled s ingle-dose relative-potency studies to assess the impact of inferred p ain mechanism on the response to an opioid drug. A total of 168 patien ts received 474 administrations of either morphine or heroin, and we a ssessed the analgesic response during a 6-hour period with visual anal og scales. We summarized this as a total pain relief(TOTPAR) score. Tw o experienced pain clinicians reviewed information about pain characte ristics and designated each case according to the inferred pain mechan ism (neuropathic, nociceptive, or mixed) and the degree of confidence in the inferred mechanism (definite versus probable/possible). They gr ouped the cases as follows: nociceptive pain only (n = 205), neuropath ic pain only (n = 49), and mixed (n = 220). We compared pain relief ac hieved by patients with different mechanisms, with TOTPAR adjusted for significant covariates (duration of prior opioid administration, dose s of opioid administered in the previous 48 hours, pain intensity at t he start of the study, BUN:creatinine ratio, and dose of administered opioid). The adjusted mean TOTPAR score of the group with any neuropat hic pain was significantly lower than that of the group with nocicepti ve pain only (26.1 versus 20.4, p = 0.02). The score of the group with definite nociceptive pain alone (adjusted mean TOTPAR = 28.0) was sig nificantly higher than scores of the groups with possible/probable noc iceptive pain (TOTPAR = 19.9), mixed mechanisms (TOTPAR = 20.2), defin ite neuropathic pain alone (TOTPAR = 20.6), and possible/probable neur opathic pain alone (TOTPAR = 22.9). In pairwise comparisons, there wer e no significant differences in the adjusted mean TOTPAR scores among the latter four groups. Among the patients with neuropathic pain, the dose-response relationship was significant. These data support the pos tulate that opioid responsiveness is a continuum with extensive overla p in the responsiveness of pains mediated by neuropathic, nociceptive, and mixed pain mechanisms.