Many have suspected that there is fast pain in the evoked aspect of central pain.
Slow or chronic pain is mediated by NMDA reeptors. Fast pain is mediated by AMPA reeptors. For some time, it was settled that the slow pain, ie. the spontaneous burning of central pain was mediated by NMDA receptors.
There have always been indicators that perhaps AMPA was also involved in CP. What else could explain the quick rise or evocation in burning with light touch or cold. The problem was that the experiments were always done in models of PERIPHERAL nerve injury pain, never in central pain.
Gwak, et al have completed this portion of the puzzle by showing that spinal AMPA receptor inhibition attenuates mechanical allodynia in neuronal hyperexcitability in spinal cord injured rats. See J Neurosci Res. 2007 Jun 4
Interestingly, although the rats spinal cords were only HALF cut, ie. hemisected on ONE side of the cord, the hyperexcitability of the wide dynamic range neurons responsible for mechanical allodynia (touch alloydynia) were hyperexcitable on BOTH sides of the cord. In case you are interested the drug used to block AMPA receptors was NQBX, applied topically.
It is no surprise and you will note that we have assumed as much in prior articles. Still, it is nice to see someone take the time and trouble to test this one out. It is important to distinguish slow from fast pain in CP because if we wish to treat patients rationally, we must know not only what type of central pain we are treating, but also whether we are going after the slow or the fast pain. We hope this imposes a requirement on future researchers to test BOTH spontaneous and evoked burning when reporting on therapeutic benefit or on imaging techniques for pain.