EEG and end-tidal carbon dioxide concentration in the hyperventilation syndrome

The hyperventilation syndrome (HVS) is a functional disorder with repeated involuntary hyperventilation attacks together with symptoms of respiratory alkalosis. We have studied the EEG and end-tibial pCO2 in the resting state and during hyperventilation activation in 12 HVS patients in order to find out whether there is a greater susceptibility to cerebral vasoconstriction in HVS patients than in controls, as indicated by slowing of the EEG. A surprisingly high proportion (58%) of abnormal resting EEGs was found in HVS patients, although the patients were neurologically normal. More theta and beta background activity was usually revealed in a quantitative computer analysis, especially frontally. Although the hyperventilation activation caused the same degree of hypocapnia in HVS patients and in controls, peripheral symptoms like tingling and numbness of fingers, as well as carpopedal spasms, occurred much more often in HVS patients. However, the EEG changes due to hyperventilation were similar in both HVS patients and normal controls, and it thus seems that the reason for cerebral symptoms in HVS patients is not a greater susceptibility to cerebral vasoconstriction.