Endogenous mechanisms of sensory modulation

We provide evidence supporting the idea that the relationship between tissu e damage, or the threat of tissue damage, and the response to such stimuli is variant and dependent on neuronal networks by which attentional, emotion al and cognitive components of pain experience activate endogenous descendi ng modulatory systems. Most previous studies have focused on responses to t ransient noxious stimuli with little information on the influence of descen ding modulation on behavioral responses to persistent pain and hyperalgesia after tissue or nerve injury. Utilizing correlative behavioral and neurona l studies we have demonstrated that (1) behavioral context modulates neuron al activity in nociceptive and non-nociceptive somatosensory pathways, supp orting the hypothesis that responses in these pathways are not immutable; ( 2) descending modulation influences behavior and neuronal activity at spina l cord levels after inflammation and persistent pain; and (3) there are des cending facilitatory as well as inhibitory influences on behavior and spina l cord neuronal activity that may impact on persistent pain particularly of deep muscle and visceral origin. Cortical as well as subcortical pathways are available by which dorsal horn activity can be modulated by attentional , motivational and cognitive factors. It appears that the same neuronal mec hanisms in the forebrain and brain stem are available for behavioral modula tion in a learned task involving the threat of tissue damage (transient nox ious stimuli) as are available in the development and amplification of pers istent pain produced by inflammation. These parallel brain mechanisms empha size the saliency of pain experience as an important learned behavior for t he survival of the organism, similar to sequential goal-directed behaviors in an operant task. (C) 1999 International Association for the Study of Pai n. Published by Elsevier Science B.V.