Pain research has been enriched by remarkable discov- eries during the past three decades leading to an unprecedented understanding of underlying mecha- nisms. But in spite of these discoveries, little has been translated into effective pain therapy. Pain research should take a page from cancer research. Instead of searching for a single drug panacea, we should dwell on the differences in pain conditions and pursue multiple treatment approaches. There will not be one magic bullet for all pains. Rather, to effectively characterize and treat the broad spectrum of pain experiences, we will need to take advantage of the latest technical approaches in genomics and proteomics. For those of us following the field, the discoveries have been nothing short of breathtaking. Specialized receptors that signal the presence of tissue damage have been identified in skin, viscera, and other tissues; and molecular biology tools have been used to clone them. We have learned that pathways in the brain that transmit information related to pain are subject to modulation by chemical mediators that can enhance or suppress these ascending signals. Included among these mediators are the morphine-like substances, the endorphins, whose receptors in the brain have been cloned. We also know that the presence of persistent nerve impulses related to tissue damage lead to plastic changes in nociceptive pathways and to an amplification of the perceived pain.
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