Abstract

The sensations w e call pain-pricking, buring, aching, stinging, and soreness-are the m ost distinctive of all the sensory modalities. Pain is a submodality of somatic sensation like touch, pressure, and position sense and serves an important protective function: It w arns of injury that should be avoid or treated. U nlike other somatic subm odalities pain has an urgent and primitive quality, a quality responsible for the affective and emotional aspect of pain perception. Moreover, the intensity w ith w hich pain is felt is affected by surrounding conditions, and the same stim ulus can produce different responses in different individuals under similar conditions. A cute, nociceptive pain results from the complex convergence of m any signals traveling up and down the neuraxis and serves to warn us of impending harm. the painful sensations ultim ately leave the periphery and travel centrally, carried by the axons of the primary sensory neurons, the dorsal root ganglia, which are relatively quiescent unless specifically stim ulated by sensory input. H owever, if inflammation or injury damages the neural structures, pain sensation (neuropathic pain) may continue long after the noxious stimuli subside. The pain response can then harm rather than help the individual. Injured dorsal root ganglia m ay become hyperexitable and display considerable spontaneous electrical activity. Such increased activity results from the expression of a dramatically different constellation of m any cell-specific m olecules in injured cells compared w ith norm al ones. U nlikely, the operation of complex neuronal circuits m ay be m arkedly altered. Chronic pain sensation result from such injury. Considerable advances have been m ade in the last decade, w hich have given some insight into the m echanisms responsible for the development of chronic pain. U nderstanding the changes that follow injury at a cellular and m olecular level m ay help lead to new therapeutic interventions.