Discussion:
The principle of central sensitization, as described by Woolf in 1983, is a manifestation of the somatosensory plasticity of the central nervous system (10, 37).
Central nociceptive sensitization develops as a result of sustained nociceptor activity in physiological conditions but also in pathological situations following inflammatory attacks, nerve damage, or trauma (38).
The mechanisms involved in the development of central nociceptive sensitization are quite complicated. They involve disrupting inter and intracellular neuronal signalling using numerous membrane receptors and various intracellular transduction pathways, resulting in changes in genetic expressions.
Changing cell phenotypes is one aspect of maintaining central nociceptive sensitization (38,39 and 40). A growing number of studies indicate that epigenetic changes may be involved in pathophysiology (41).
Woolf summarises central sensitization as the lowering of cortical nociceptive thresholds (10-13). These lower pain thresholds will have multiple clinical consequences and lead to so-called co-morbidities (11, 24). Therefore, myofascial pain, autonomic disorders with hyperalgesia, urinary, rectal and sexual dysfunction, neuropathic pain, and visceral pain are more or less associated (42).