Strong noxious stimuli can sensitize central nociceptive neurons, such as spinothalamic tract (STT) cells. Central sensitization can be demonstrated by activating primary afferent neurons that are not sensitized or by local stimulation of the sensitized neurons, for example by iontophoretic release of an excitatory amino acid. Thus, central sensitization is independent of peripheral sensitization. During central sensitization, stimulation of mechan-oreceptors in an area surrounding the site of the initiating noxious stimulus produces an increased response in STT cells, a change that may help account for secondary mechanical allodynia. Similarly, mechanical stimulation of nociceptors in the secondary area produces a larger response after central sensitization than before, and this change can contribute to secondary mechanical hyperalgesia. Noxious stimuli applied in the vicinity of the original strong noxious stimulus may cause primary mechanical or heat hyperalgesia due to peripheral sensitization or a combination of peripheral and central sensitization. Central sensitization lasts for hours after its initiation, and it depends on the activation of signal transduction pathways by neurotransmit-ters released by the strong noxious stimulus.
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