• R F Schmidt.
• Physiologisches Institut der Bayerischen Julius-Maximilians-Universität, Röntgenring 9, D-8700, Würzburg.
• Schmerz. 1991 Mar 1;5(Supplement 1):S13-28.

AbstractPresent-day hypotheses about the origin of pain in deep tissues are based on the idea that pain is anindependent sensation with its own specialized apparatus of sensors, conduction pathways and centers. The sensors are callednociceptors ornocisensors, and the neuronal structures they activate are thenociceptive system. Accordingly, the reception, conduction and central nervous processing of noxious signals together are termednociception. All parts of the nociceptive system may be affected by pathophysiological processes which in turn may modify appreciably the perception of pain. Variouscomponents of pain are activated by noxious signals. The contributions of the sensory, affective, autonomic and motor components to the evaluation (cognitive component) and expression (psychomotor component) of the pain vary, depending on the nature of the pain. Again, all components may be modified by pathophysiological processes. It is also pointed out that an important aspect in evaluating pain is its duration, and various types ofacute and chronic (persistent, recurrent) pains and their mode of origin are discussed. Theneurobiology of joint pain is used to exemplify the processes of excitation (transduction) in nociceptors (nocisensors), the subsequent step of transformation, the peripheral conduction and central processing of noxious signals. Special emphasis will be given to the new finding that healthy tissues contain nociceptors with threshold so high that they cannot be excited by acute noxious stimuli ("sleeping" nociceptors). However,sensitization of these nociceptors as a consequence of pathological tissue alterations (e.g. by inflammation) will "awaken" them. Sensitization is probably brought about by algesic substances (mediators of inflammation, e.g. prostaglandins, bradykinin). The similarities and dissimilarities of joint pain versus other deep pain (originating from muscles, tendons or bones) are pointed out. The increase in sensory inflow resulting from the sensitization of peripheral nociceptors leads subsequently to acentral component in the sensitization which in turn modifies the perception of pain under these circumstances. Various processes such as expression of C-fos-like-protein, modification of the spinal composition of endogenous opioids, and release of neuropeptides may be involved in this newly detected phenomenon. Its possiblerelation to the development of chronic pain states is discussed. Finally an account is presented of pain produced by excitation of the nociceptive system proximal to the nociceptors. These pain states include pain resulting from pathophysiological impulse generation in nociceptive fibers (neuralgia orneuralgic pain) which usually projects into the region containing the sensory endings of these fibers (projected pain). Furthermore, brief descriptions of pain due to spinal root compression and ofcentral pain arising from various sites of the central nervous system are given.

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