I read with interest the article entitled “Consciousness Unbound: Toward a Paradigm of General Anesthesia.”1The proposal rests on three arguments: (1) There is good evidence that gamma oscillations are implicated in perception (cognitive binding problem) and consciousness; (2) concentrations of general anesthetics sufficient to cause unconsciousness interfere with gamma oscillations; and (3) thus, general anesthetics cause unconsciousness by disrupting gamma oscillations and thus preventing cognitive binding. I would like to offer three comments.

The proposal ignores the alternative, more parsimonious view that gamma oscillations are not necessarily related to higher cognitive processes but are rather simply part of the background activity of the brain, reflecting depolarization of thalamic and cortical neurons,2,3a physiologic condition almost certainly required for consciousness. The background activity view is much less controversial than the cognitive binding proposal and can explain just as well why interference with gamma rhythms leads to unconsciousness. Furthermore, the background activity hypothesis is not incompatible with cognitive binding or other high-level functions that are the subject of much current interest.

The proposal also ignores the possibility that unconsciousness and attenuation or disruption of gamma oscillations are functionally independent effects that both arise from anesthetic action on the brain. Consider the following analogy: When there is pouring rain in London, umbrellas pop up in the streets and car windshield wipers start moving. Would anyone suggest that the two observations are functionally linked?

Finally, I was surprised to see no reference to the early evoked-potentials studies that were the first to demonstrate that general anesthetics attenuate gamma rhythms. Sem-Jacobsen et al.  4reported in 1956 that thiopental abolishes the electroencephalographic changes recorded from the posterior sylvian region in response to trains of auditory clicks delivered at rate of approximately 40/s in patients with intracerebral electrodes. Madler and Pöppel5interpreted the anesthetic-induced alteration of the auditory middle latency response as loss of 40-Hz oscillations and suggested that this may explain the disturbance of time perception during general anesthesia. Plourde and Picton6showed that the 40-Hz auditory steady state response provides a reliable measure of anesthetic effect on consciousness. The auditory steady state response may be used to assess the ability of the auditory system to sustain endogenous gamma oscillations.7 

McGill University, Montréal, Québec, Canada. gilles.plourde@staff.mcgill.ca

Mashour GA: Consciousness unbound: Toward a paradigm of general anesthesia. Anesthesiology 2004; 100:428–33
Steriade M, Amzica F, Contreras D: Synchronization of fast (30–40 Hz) spontaneous cortical rhythms during brain activation. J Neurosci 1996; 16:392–417
Steriade M: Corticothalamic resonance, states of vigilance and mentation. Neuroscience 2000; 101:243–76
Sem-Jacobsen CW, Petersen MC, Dodge HWJ, Lazarte JA, Holman CB: Electroencephalographic rhythms from the depths of the parietal, occipital and temporal lobes in man. Electroencephalogr Clin Neurophysiol 1956; 8:263–78
Madler C, Pöppel E: Auditory evoked potentials indicate the loss of neuronal oscillations during general anesthesia. Naturwissenschaften 1987; 74:42–3
Plourde G, Picton TW: Human auditory steady-state response during general anesthesia. Anesth Analg 1990; 71:460–8
Plourde G: The clinical use of the 40 Hz auditory steady-state response. Int Anesthesiol Clin 1993; 31:107–20