PHYSIOLOGIC AND PATHOPHYSIOLOGIC RELATIONSHIP BETWEEN THE ELECTROENCEPHALOGRAM AND THE REGIONAL CEREBRAL BLOOD FLOW

Abstract

The relationship between the electroencephalogram (EEG) and the regional cerebral blood flow (rCBF) has been reviewed with special emphasis on physiologic and pathophysiologic mechanisms. Hyperventilation results in slowing of the EEG and decreased rCBF. It is concluded that decreased cerebral Po₂ caused by decreased rCBF is the main factor responsible for EEG slowing and that increased cerebral pH only is of less importance in the EEG changes. This does not mean that the EEG slowing is caused by “classic hypoxia” since EEG slowing can occur without loss of consciousness and without changes in the aerobic‐anaerobic cerebral glucose metabolism. Other mechanisms influenced by the cerebral Po₂ also seem to be involved. The “cerebral activity” and the cerebral metabolic rate of oxygen (CMRo₂) normally are related and result primarily in an EEG‐CMRo₂ coupling that is reflected in an EEG‐rCBF coupling; when such coupling exists there is a positive correlation between EEG frequency, CMRo₂, and rCBF. These couplings are illustrated by the changes in the EEG and in the CMRo₂ or rCBF occurring during pharmacologic activation or depression of the central nervous system, during mental activity, during grand mal seizure, during dementia, and during various cerebral diseases. Several other factors than the CMRo₂ also influence the EEG and the rCBF, as is most clearly illustrated in instances of physiologic and pathophysiologic uncoupling. Physiologic uncoupling occurs during slow wave sleep and during childhood when the EEG shows definite slowing but the rCBF and CMRo₂ are normal or slightly increased. Pathophysiologic uncoupling develops with various acute brain lesions (anoxic lesions, ischemic lesions, etc.). In some instances, as in the phase after an epileptic grand mal seizure, only the EEG and rCBF show uncoupling whereas the EEG and CMRo₂ remain coupled.