gms | German Medical Science

54. Jahrestagung der Norddeutschen Orthopädenvereinigung e. V.

Norddeutsche Orthopädenvereinigung

16.06. bis 18.06.2005, Hamburg

Significant changes of pain processing in SII and cingulum induced by chronic painful osteoarthritis of the knee

Meeting Abstract

  • corresponding author M. Quante - Klinik und Poliklinik für Allgemeine Orthopädie/Universitätsklinikum Münster, Orthopädie, Münster
  • M. Hauck - Hamburg
  • J. Lorenz - Hamburg
  • S. Hille - Hamburg
  • E. Hille - Hamburg

Norddeutsche Orthopädenvereinigung. 54. Jahrestagung der Norddeutschen Orthopädenvereinigung e.V.. Hamburg, 16.-18.06.2005. Düsseldorf, Köln: German Medical Science; 2005. Doc05novK1.04

The electronic version of this article is the complete one and can be found online at:

Published: June 13, 2005

© 2005 Quante et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( You are free: to Share – to copy, distribute and transmit the work, provided the original author and source are credited.




Chronic pain is discussed to induce ongoing changes in pain processing. In patients with chronic painful osteoarthritis of the knee (PO). This might have relevance for prognosis of conservative and surgical treatment. Aim of this study was to evaluate changes in pain processing in PO patients. In particular parameters of cortical plasticity were evaluated concerning their reversability in a pain free status.

Materials and Methods

Cortical pain processing (induced by a well established experimental pain model) in 12 patients with PO was recorded by 64-channel electroencephalography and 32-channel magnetencephalography. Interactions between experimental pain and PO (latency and amplitude of localized cortical activity, individual pain ratings) were documented in 3 different PO states: before, while and after induction of PO.


Compared to previous data from healthy subjects (hs) patients showed a loss/decrease in pain induced modulation of pain sensitivity and a corresponding loss of modulation of SII activity. Cingulum activity shows a significant reduction induced by PO, smaller than known from hs. Recovery of cingulum activity after PO appears slowy and smaller than in hs.


For the first time we showed that PO leads to a loss of pain dependant reduction in SII- activity and of pain modulation on the subjective level, known from healty subjects. Adaptation of cingulum activity known from interaction with acute pain is reduced in PO. There is some evidence that changes persist after adequate treatment of PO. Thus PO patients show a relevant and ongoing impairment of their pain system.