Clinical usefulness of the muscle contracture test: time to reevaluate?

and Chamberlin. Indeed, we provided evidence that propofol anesthesia desynchronized the circadian rhythms of rest-activity and body temperature in rodents in the experimental condition of either alternation of light/dark or constant darkness. By citing the study of Sessler et al. of 1991, they create the impression that anesthetic exposure does not affect the circadian rhythms in humans. It must be pointed out that this first study was unable to demonstrate any effect in five human volunteers. Sessler et al. acknowledged that such data did not exclude an effect that could be missed. Indeed, the shifts in acrophase were 1.2, 2.1, 0.7, 1.6, and 0.7 h in the five subjects. Drs. Eikermann and Chamberlin have once again overlooked our previous study (cited in the article) that demonstrated a desynchronization of the circadian rest-activity rhythm after propofol anesthesia in patients. When dealing with clinical studies, as we clearly state in the discussion of our article, one has to be cautious in drawing conclusion from merely one or two studies. Further studies are necessary to specify the magnitude of anesthetic effects on human circadian rhythms. In contrast to the concerns of Drs. Eikermann and Chamberlin, we find that data in this field support the concept that either the “gears” and/or the “hands” of the clock might be influenced by propofol administration. It is premature to eliminate the importance of the concept of gears or hands at this early stage, as they suggest. However, we agree with them that a more profound understanding of the mechanism is an important question. Future studies should rigorously examine the effects of anesthesia on the complex pathways involved in the regulation of the clock. To this end, we are currently pursuing further experiments on the effect of anesthesia on some of these pathways (i.e., the expression of clock genes within the suprachiasmatic nucleus, the melatonin release by the pineal gland).