I think that your suggestion that hypnotic analgesia involves frontal control of thalamocortical is very interesting and promising. The frontal activation that you first reported in your 133-xe study in 1993 is replicated in our data showing massive frontal increase in rCBF associated with suggestions for pain modulation.
However, there is one important result in your brain imaging study that seems difficult to reconcile with the rest of the litterature on SERP and with your and our more recent brain imaging results. In your 133-xe study, you found an INCREASE in somatosensory cortex activity during hypnotic analgesia using an ischemic model. If I remember correctly, this increase was modulated by the hypnotic susceptibilty of subjects, right? In contrast, pain-evoked activity in other studies is found to decrease with hypnotic analgesia, and activity in pain-related regions (S1, S2, Insula and Anterior cingulate) has been found to correlate positively with pain perception. In your early study, activity in S1 appears to be inversely related to pain perception. Did I get this right? If so, what could be the difference between that study and the more recent ones that might explain this discrepancy?
There is ongoing controversy concerning the involvement of S1 in pain processing and early brain imaging studies of pain-evoked changes showed both increases and decreases in S1. Part of the answer might rely in the dynamic of activation in S1 with possibly an early activation at stimulus onset and a late de-activation (e.g. see an early study by Apkarian). Presumably, your study have been more sensitive to the late part of the stimulation. However, I am not sure how this dynamic effect could be integrated in your model. Do you have any insight on how these results might reconcile with your model of thalamocortical inhibitory processes?