primary and secondary hyperalgesia
Primary hyperalgesia refers to the sensitization process that enhances “pain” transmission via a peripheral mechanism. For example, in the setting of inflammation, there is synthesis of arachidonic acid, which is acted upon to produce prostaglandins. These lipid mediators in turn act on the terminals of primary afferent nociceptors and lower their threshold for firing. The nociceptors are sensitized. All of this occurs via a peripheral mechanism.
Secondary hyperalgesia refers to the sensitization that occurs because of changes in spinal cord processing. For example, through a process of central sensitization, the firing of dorsal horn nociceptors can change dramatically in the setting of injury (produced by either tissue or nerve damage). The threshold for activation of dorsal horn “pain” transmission neurons drops, their receptive field size increases, and they may become spontaneously active. Pain can now be produced by activation of uninjured, low threshold mechanoreceptive (A beta) afferents.