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).