Central sensitization has provided a mechanistic explanation for many of the temporal, spatial, and threshold changes in pain sensibility in acute and chronic clinical pain settings and has highlighted the fundamental contribution of changes in the CNS to the generation of abnormal pain sensitivity. The pain in these situations arises spontaneously, can be elicited by normally innocuous stimuli (allodynia), is exaggerated and prolonged in response to noxious stimuli (hyperalgesia), and spreads beyond the site of injury (secondary hyperalgesia).

In many clinical syndromes, pain is no longer protective. 369 Since then, we have learned that a number of different forms of functional, chemical, and structural plasticity can sensitize the central nociceptive system to produce pain hypersensitivity under both normal and pathological circumstances, some of which are persistent. This sensitization is the expression of use-dependent synaptic plasticity triggered in the central nervous system (CNS) by the nociceptor input and was the first example of central sensitization, discovered 26 years ago. The nociceptor-induced sensitization of the somatosensory system is adaptive in that it makes the system hyperalert in conditions in which a risk of further damage is high, for example, immediately after exposure to an intense or damaging stimulus.

132, 376, 380 In the absence of ongoing tissue injury, this state of heightened sensitivity returns over time to the normal baseline, where high-intensity stimuli are again required to initiate nociceptive pain the phenomenon is long lasting but not permanent. An additional important phenomenon that further enhances this protective function is the sensitization of the nociceptive system that occurs after repeated or particularly intense noxious stimuli, so that the threshold for its activation falls and responses to subsequent inputs are amplified.

374 Nociception, the detection of noxious stimuli, 282 is a protective process that helps prevent injury by generating both a reflex withdrawal from the stimulus and as a sensation so unpleasant that it results in complex behavioral strategies to avoid further contact with such stimuli. Instead, central sensitization produces pain hypersensitivity by changing the sensory response elicited by normal inputs, including those that usually evoke innocuous sensations.Īcute nociceptive pain is that physiological sensation of hurt that results from the activation of nociceptive pathways by peripheral stimuli of sufficient intensity to lead to or to threaten tissue damage (noxious stimuli). Because central sensitization results from changes in the properties of neurons in the central nervous system, the pain is no longer coupled, as acute nociceptive pain is, to the presence, intensity, or duration of noxious peripheral stimuli. Central sensitization is responsible for many of the temporal, spatial, and threshold changes in pain sensibility in acute and chronic clinical pain settings and exemplifies the fundamental contribution of the central nervous system to the generation of pain hypersensitivity. The net effect of central sensitization is to recruit previously subthreshold synaptic inputs to nociceptive neurons, generating an increased or augmented action potential output: a state of facilitation, potentiation, augmentation, or amplification. Central sensitization represents an enhancement in the function of neurons and circuits in nociceptive pathways caused by increases in membrane excitability and synaptic efficacy as well as to reduced inhibition and is a manifestation of the remarkable plasticity of the somatosensory nervous system in response to activity, inflammation, and neural injury.

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