Constant pain can really get on your nerves – literally! The phenomenon of pain sensitivity enhancement is responsible for this. In the case of persistent pain impulses, it brings about permanent changes in the neurons responsible for transmitting the pain signals. This leads to an increase in pain sensitivity and the sensation of pain can even persist long after the actual pain signals has faded out.
Strong and Weak
Pain sensitivity enhancement is a feature of both weak and strong pain, but the model used to explain how this phenomenon arises is based solely on the testing of strong pain impulses. In reality, though, low level pain does not give rise to all of the neural processes which are postulated by the previous explanatory model.
Now, a team under Prof. Jürgen Sandkühler of the Department of Neurophysiology at the Medical University of Vienna has published findings in the June 2006 edition of SCIENCE which explain the existence of pain amplification even at low levels of pain. Commenting on the research, Prof. Sandkühler said: "We were able to show in a controlled laboratory system that the amplification arises even when the pain is quite weak. We actually used electrical impulses that were 50 times weaker than those previously employed to induce this response. Weak pain signals like these are symptomatic of the healing of wounds and of inflammation."
Prof. Sandkühler's group was also able to identify the cells responsible for this previously unknown phenomenon. They are located in the lamina I of the spinal dorsal horn, and ensure that signals from peripheral pain fibres are transmitted to spinal nerve tracts leading to the brain.
As part of this large-scale project, Sandkühler and his team were also able to indicate which cellular mechanism is behind low-level pain enhancement. Cells were loaded with dyes which emit light when exposed to sufficient concentrations of calcium ions. This made it possible to show that the concentration of calcium ions in these lamina I cells also increases dramatically in response to weak pain impulses. This is one of a multitude of cases in which calcium ions are involved in cellular signal transmissions. Here, the calcium ions activate enzymes which amplify the pain impulses.
These new findings are of fundamental importance for pain therapy. As Sandkühler put it: "Treating patients with pain killers for a short period of time after an operation, for example, is not an effective means of avoiding pain enhancement. Pain therapy must be continued without interruption until the pain has largely subsided."
In order that these recommendations may be implemented quickly, Prof. Sandkühler is playing a part in organising an expert meeting on the topic. The "Risk Assessment in Pain Therapy" symposium will take place on 10th November 2006, with the aim of evaluating the opportunities and risks of current therapeutic procedures in the light of these new findings. In cooperation with IGOST (the Interdisciplinary Society for Orthopaedic Pain Therapy), Sandkühler has succeeded in attracting representatives of DGSS (the German Society for the Study of Pain), ÖSG (the Austrian Pain Society) and internationally renowned pain researchers to this event in Vienna. This should mean that the findings of this FWF project can soon feed through into specific recommendations for clinical therapy.
Till C. Jelitto | alfa
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