How hyperventilation alters the electroencephalogram: a review of controversial viewpoints emphasizing neurophysiological mechanisms.
This paper reviews the literature on the EEG effects of hyperventilation, with particular emphasis on the literature concerning the mechanism of EEG slowing with hyperventilation. We suggest that there is no definite evidence to support the theory that the EEG slowing and "activation" are caused by hypoxia secondary to cerebral vasoconstriction induced by hypocapnia during voluntary hyperventilation. Since it is known that hypocapnia produces decreased activity in the mesencephalic reticular formation and that lesions of the thalamus abolish the hyperventilation response, we propose a strong, albeit speculative, analogy between awake-sleep transitory states and the mechanism of EEG "activation" by hyperventilation. Furthermore, it is proposed that both the EEG changes and the associated clinical symptomatology (as well as changes in level of anesthesia, which vary with arterial PCO2) may be explained by altered arousal, and that the vasoconstriction observed during hyperventilation is a central neurogenic response to hypocapnia at a brainstem level.