I thank Dr. Plourde for his interest in my article, although I disagree with his characterization of my arguments. First, the relation of gamma oscillations and cognitive binding was only one of several potential mechanisms addressed, rather than the singular foundation on which my theory was based. Furthermore, it was not merely gamma activity, but the coherence of gamma activity that was discussed in this context, and it was made explicit that there are data contradicting such coherence as the sole mechanism of information synthesis. Finally, my proposal of general anesthesia as cognitive unbinding was based on evidence of anesthetic effects seen at several different levels of neural processing (i.e. , convergence, assembly, synchrony). For these reasons, the syllogism formulated by Dr. Plourde is flawed.

In terms of the relevance of gamma oscillations, I am unable to reconcile Dr. Plourde’s assertion that they are “not necessarily related to higher cognitive processes” and yet ultimately reflect “a physiologic condition almost certainly required for consciousness.” The coordinated depolarization of thalamic and cortical neurons could be the foreground rather than the background activity of cognitive neural processes. Indeed, one of the references that Dr. Plourde cites for the “background activity hypothesis” in fact seems to support the alternative by stating that “the short-scale, discrete synchronization of fast oscillations during waking correlates well with the characteristics of conscious processes in this behavioral state.”1 

As for Dr. Plourde’s assertion that my arguments are undermined by a post hoc ergo propter hoc  fallacy, I have stated no strict causal relation but rather have offered associated observations. I believe the pursuit of a general theory of anesthesia will necessarily progress from correlation (e.g. , general anesthesia is correlated with unbinding) to causation (e.g. , general anesthesia causes unbinding) to identity (e.g. , general anesthesia is unbinding). Both in the study of anesthesia and consciousness, we are still at the stage of searching for neural correlates, in the hope that they will lead us to a more substantive causal understanding.

There is a wealth of literature on the electroencephalographic changes associated with anesthesia, and there were no doubt numerous omissions in my relatively limited article. I very much appreciate those that Dr. Plourde has brought to my attention.

Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts. gmashour@partners.org

Steriade M: Corticothalamic resonance, states of vigilance and mentation. Neuroscience 2000; 101:243–76