Peripheral and Central Sensitization

Abstract

Neuronal excitation in nociception is not a static process of the kind “same stimulus–same response,” but rather underlies dynamic plasticity to adapt to different situations. (pain due to a stimulus that does not usually provoke pain) and (increased pain from a stimulus that usually provokes pain) both exemplify these dynamic changes, and are the result of a leftward shift of the stimulus–response curve to a specific (e.g., a mechanical or temperature) stimulus. Hyperalgesia/allodynia is typically divided into two types. While hyperalgesia occurring at the site of injury is termed primary hyperalgesia, enhanced pain sensitivity in surrounding uninjured skin is termed secondary hyperalgesia. Primary hyperalgesia is contributed to by sensitization of peripheral nerve endings (peripheral sensitization), whereas secondary hyperalgesia is due to changes in the spinal cord and higher brain areas (central sensitization). Depending on the provoking stimulus, hyperalgesia can be divided into heat hyperalgesia and mechanical hyperalgesia (subdivided in dynamic (provoked by light touch), punctuate (pinprick), and static (pressure) hyperalgesia).