Nociceptive pain is caused by the ongoing activation of nociceptors in response to a noxious stimulus (e.g., injury, disease, inflammation). Pain arising from visceral organs is called visceral pain, whereas that arising from tissues such as skin, muscle, joint capsules, and bone is called somatic pain.

Somatic pain may be further categorized as superficial (cutaneous) or deep somatic pain. In contrast to neuropathic pain, the nervous system associated with nociceptive pain is functioning properly. Generally, there is a close correspondence between pain perception and stimulus intensity, and the pain is indicative of real or potential tissue damage.²

Neuropathic pain is defined by the International Association for the Study of Pain (IASP) as pain caused by damage or disease affecting the somatosensory nervous system. Compared with nociceptive pain, neuropathic pain is typically associated with sensory abnormalities, such as numbness and allodynia, more prominent pain paroxysms and, depending on the nerve(s) affected, neurological findings. ¹

Sensitization plays an important role in this process. Although central sensitization is relatively short lived in the absence of continuing noxious input, nerve injury triggers changes in the central nervous system that can persist indefinitely. Thus, central sensitization explains why neuropathic pain is often disproportionate to the stimulus (e.g., hyperalgesia, allodynia) or occurs when no identifiable stimulus exists.²

The IASP has defined nociplastic pain as “pain that arises from altered nociception despite no clear evidence of actual or threatened tissue damage causing the activation of peripheral nociceptors or evidence for disease or lesion of the somatosensory system causing the pain.”

Nociplastic pain is thought to be common and to play a role in many common chronic pain conditions such as fibromyalgia, low back pain, and headache. ³