One of the standard functional tests that reveal hidden pathological activity in the EEG is hyperventilation. With deep breathing , a spasm of arterioles occurs in the blood as a result of CO reduction and cerebral blood flow decreases. At the initial stage hypoxia leads to short-term hyperpolarization of neuronal membranes, which is replaced by their depolarization. The depolarization shift of the membrane potential causes an increase in the excitability of neurons with which the change in the EEG is mainly connected. An additional factor in increasing the excitability of neurons is alkalosis, which develops at the initial stage of hyperventilation as a result of a decrease in the CO content. In a hyperventilation test, the duration of which is usually 3 minutes, in healthy adult subjects there is no significant change in EEG, except for a slight increase in the amplitude of the main rhythm, as well as a slight increase in slow-wave activity, while in people with epilepsy or other diseases of the central nervous system the EEG increases or appeared abnormal activity .
We found that with hyperventilation in healthy people, SCP in all monopolar leads, as well as the averaged SCP, gradually increase . Shifts of UPP during hyperventilation are due to the transition to anaerobic metabolism and the acidification of blood flowing from the brain, which is caused by a spasm of arterioles. The origin of these changes was discussed in more detail in the section “The Effect of Hyperventilation on the Indicators of the Energy Exchange of the Brain”.
When hyperventilation in healthy people, EEG changes were mild. There was a slight, albeit significant, increase in the relative spectral power of the delta activity in most parts of the brain with the exception of the left temporal region. There was a decrease in the relative potency of beta1 activity in the right temporal region. Changes in the relative spectral power of other EEG frequency ranges were not statistically significant .
The positive correlation between the relative spectral power of the alpha rhythm in the occipital region and the UPP in the same brain region during hyperventilation persisted in the state of calm wakefulness ( r = 0.55; p = 0.035).
There was no association of beta activity parameters with UPP during hyperventilation, however, changes in beta1 activity in the central region correlated with shifts in local UPP in the same brain region ( r = 0.56; p = 0.031).
The negative correlation between the UPP in the occipital region and the spectral power of the delta and theta activity in the same region remained ( r = -0.52; p = 0.047 for theta; r = -0.59; p = 0.021 for the delta ranges ).
Thus, with hyperventilation in healthy subjects, the correlation dependence between SCP and EEG was essentially the same as in rest. However, the relationship between these parameters became less close, which may indicate the appearance of additional factors that alter the dependence existing in the background. The most important of these factors is the difference in the mechanisms that cause a shift in the cerebral pH to the acidic side, at rest and during hyperventilation. At rest, high SCP values reflect a decrease in cerebral pH, associated with a high intensity of aerobic energy exchange. During hyperventilation, brain acidification is largely
caused by the transition to an energetically unfavorable anaerobic metabolism. AT
In this case, the relationship between EEG and SCP becomes more complex, and the linear correlation between these characteristics decreases.