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Central sensitization
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=== Inflation of the central sensitization concept === These experiments referred to central sensitization as an activity-dependent increase in the excitability of spinal neurons. It was related to peripheral tissue damage and mostly confined to the area surrounding the site of injury.<ref name="Hansson2014">{{Cite journal | last = Hansson | first = Per | date = Oct 2014 | title = Translational aspects of central sensitization induced by primary afferent activity: What it is and what it is not | url = http://dx.doi.org/10.1016/j.pain.2014.07.016 | journal = Pain | volume = 155 | issue = 10 | pages = 1932–1934|doi=10.1016/j.pain.2014.07.016|issn=0304-3959|quote=|via=}}</ref> Though the secondary hyperalgesia it elicited lasted beyond the initial stimulus, this effect was usually short-lived and sometimes disappeared within the time-span of a day.<ref name="Woolf2011">{{Cite journal | last = Woolf | first = Clifford J. | date = Mar 2011 | title = Central sensitization: Implications for the diagnosis and treatment of pain | url =http://dx.doi.org/10.1016/j.pain.2010.09.030 | journal = Pain | volume = 152 | issue = Supplement | pages = S2–S15|doi=10.1016/j.pain.2010.09.030|issn=0304-3959}}</ref> Since then the concept of central sensitization has gone through a significant expansion.<ref name=":11">{{Cite journal | last = Gracely | first = Richard | last2 = Schweinhardt | first2 = Petra | date = 2015-07-02 | title = Programmed Symptoms: Disparate Effects United by Purpose | url =http://dx.doi.org/10.2174/1573397111666150619095125 | journal = Current Rheumatology Reviews | volume = 11 | issue = 2 | pages = 116–130|doi=10.2174/1573397111666150619095125|issn=1573-3971|quote= | authorlink = Richard Gracely | author-link2 = Petra Schweinhardt|via=}}</ref> It became widespread, lasting and unrelated to an identifiable nociceptive input form the periphery. Clifford Woolf who championed the broadening of the definition, now defines central sensitization as the “genus of all forms of pain sensitization that arise within the central nervous system”.<ref>{{Cite journal | last = Woolf | first = Clifford J. | date = Oct 2014 | title = What to call the amplification of nociceptive signals in the central nervous system that contribute to widespread pain? | url = http://dx.doi.org/10.1016/j.pain.2014.07.021 | journal = Pain | volume = 155 | issue = 10 | pages = 1911–1912|doi=10.1016/j.pain.2014.07.021|issn=0304-3959}}</ref> Woolf argues that the increase in excitability of the spinal cord he discovered in the 1980s represented only one example of what should be regarded as central sensitization.
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