In normal joint and muscle, pain is only elicited by intense tissue-threatening (noxious) stimuli. Inflammation and other deep tissue pathologies cause a state of hyperalgesia and pain that often becomes chronic. Under these conditions, pain is elicited by physiological stimuli.
Muscle and joint nerves possess nociceptors which are exclusively or preferentially excited by noxious stimuli, and silent nociceptors which do not respond to stimuli under normal conditions.
During pathological processes, such as inflammation muscle and joint nociceptors, are sensitized to mechanical stimuli. This peripheral sensitization is an important mechanism of primary hyperalgesia. Peripheral sensitization is induced and maintained by inflammatory mediators acting on the nociceptive terminals, and by changes of the intrinsic response properties of the neurons.
In the central nervous system, nociceptive stimulation of deep tissue is encoded in neurons exclusively driven by deep input, and by neurons that show convergent inputs from deep tissue and skin. Peripheral sensitization induces a state of hyperexcitability in the central nociceptive system (central sensitization) that increases the gain of central nociceptive processing at spinal, thalamic, and cortical levels. Spinal hyperexcitability contributes to primary and accounts for secondary hyperalgesia. Descending systems control the nociceptive processing at the spinal level. During peripheral inflammation descending inhibition increases and reduces central sensitization. Descending facilitation may support secondary hyperalgesia.
Pain treatment should target peripheral, as well as central, sensitization.
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