Neurophysiology of pain

Abstract

The nociceptive system supports two sensory functions, pain and itch. Itch has often been regarded as a minor form of pain. Recently, it has been shown, however, that the pruritic system is supported by its own peripheral and central neuronal pathways which are closely associated, although antagonistic in some respect. Both the pruritic and the algesic system have their own primary nociceptive afferents. These nociceptive afferents are unique among sensory receptors in their capacity to become sensitized following exposure to noxious stimuli. Consequences of sensitization are increased spike discharges to stimulation and decreased thresholds. These phenomena may be formally conceptualized as leftward shift of the stimulus response function. Hyperalgesia was traditionally seen as the perceptual correlate of sensitization of the algogenic system. The respective sensory phenomena in the pruritic system have been called hyperknesis. Both hyperalgesia and hyperknesis encompass decrease in sensory thresholds and increased sensation (pain or itch) to suprathreshold stimuli, together with spontaneous pain or itch. However, at least in the pain system, the simple conception of hyperalgesia as a linear corollary of sensitization of a uniform nociceptor population is inadequate in the light of the diversity of hyperalgesias which are subserved by various peripheral and central neuronal mechanisms, to different degrees. Likewise, different forms of hyperknesis exist which are dependent either on peripheral or on central nervous mechanisms. The pathophysiology of different forms of hyperalgesia and hyperknesis in dermatological diseases will be discussed.