Pain measurement

Increasing evidence from laboratory methods in humans and animals indicates that pain arises from, and is modulated by, a number of mechanisms. In add ition, these mechanisms are not static but change as pain persists. Recent human studies have demonstrated new aspects of pain processing at all level s of the central nervous system. Studies of the influence of analgesic agen ts on a large number of experimental pain measures have shown a preferentia l effect of opioids for attenuating the central integration of prolonged st imuli while local anesthetics may be more effective for brief stimulation. Studies of NK1 antagonists in man have shown results similar to those found with animals. There is little effect on brief stimulation of A delta and C -fiber nociceptors, including conditions Mat can evoke central summation. H owever, these antagonists, which block Me effects of substance P, are effec tive in more persistent states such as postsurgical pain. Persistent pain c an also alter the function of the large diameter A beta touch afferents, ra nging from increased tactile sensitivity in inflammatory conditions to fran k allodynia following nerve injury or focal nociceptor stimulation. Recent advances in evaluation of supraspinal pain processing in humans have demons trated pain-related activation using both methods that assess synchronized neural activity and methods that infer this activity in the whole brain by local changes in regional cerebral blood flow. These methods have begun to identify brain regions associated with the multiple dimensions and processi ng of painful stimulation and the modulation of these processes by pharmaco logical agents and non-pharmacological interventions.