Re-evaluation of the hypoxia theory as the mechanism of hyperventilation-induced EEG slowing.

To determine whether the well-accepted hypoxia theory accounts for hyperventilation-induced electroencephalogram (EEG) slowing, the authors monitored changes in cerebral oxygenation and end-tidal concentrations of carbon dioxide in 67 patients with epilepsy (age range = 5-12 years) during the hyperventilation activation test in a routine EEG examination. Relative concentration changes in cerebral oxygenated, deoxygenated, total hemoglobin, and oxidized cytochrome oxidase were measured by near-infrared spectroscopy in the frontal region. In all patients, except one who demonstrated EEG slowing, total and oxygenated hemoglobin decreased, and cytochrome oxidase was not reduced. EEG slowing occurred intermittently in 22 patients and was not synchronous with changes in either the cerebral oxygenation or end-tidal concentration of carbon dioxide. The degree of EEG slowing was diminished or the slow waves disappeared abruptly within 1 second after the cessation of hyperventilation in 22 patients when both the cerebral oxygenation and end-tidal concentration of carbon dioxide were still at low levels. The findings during the recovery periods do not confirm the hypoxia theory. It is thus supposed that more subtle mechanisms are the cause of EEG slowing.