W e thank the editor for the opportunity to respond to the letter by Pressman et al. 1 This is a critique of the article by Cartwright and Guilleminault 2 recently published in the Journal of Clinical Sleep Medicine. We address the salient points their letter raised:
The aim of our article
Was the method appropriate?We based the method for our study on the hypotheses proposed by Espa et al. 4 as the conditions necessary to precipitate an occurrence of a SWS parasomnia. "The occurrence of SWS parasomnia requires not only a SWS pressure increase but also SWS arousal enhancement." This is the push/pull model that Pressman argued was a theory that only Cartwright held in the debate he refers the reader to review. [5][6][7][8] He argued forcefully and repeatedly that SW only occurred with an increase of SWS and that this was the accepted wisdom. In fact the two variable model was stated earlier by Broughton et al. 9 in describing the Ken Parks case. "These typical polysomnographic features of sleepwalkers suggest the coexistence of both pressure for deep sleep (SWS) and of heightened arousal causing inability to sustain such sleep." This opposite pressure model was used in the Pilon et al. 10 study which succeeded in eliciting sleepwalking events in the laboratory by combining increasing pressure for SWS by a prior period of sleep deprivation and increasing arousals from sleep by delivering auditory tones during the recovery sleep. Neither of these manipulations was successful when applied singly. It was this opposite pressure model that we tested in the case study reported in our recent paper.The evidence presented in court supported both pressures were present in the defendant on the night of the event (he had a period of prior sleep deprivation and excessive caffeine intake during the day before the event). Thus the conditions for a SW event were present. Furthermore we pointed out that "the additional history of snoring and a mild breathing disorder validated in the PSG may be a contributing cause of his low SWA, high CAP rate and arousal into non-conscious acts when sleep deprived and over-caffeinated."Pressman et al. 1 raise the question whether a low SWA in the fi rst NREM cycle, measured after the fact (not months or years) but specifi cally in this case eight months after the incident, can be a reliable marker of a predisposition to SW. The authors of the critique point out that the studies showing high reliability within subjects of the profi le of the