[Quantitative hyperpnea in EEG (author's transl)].
After summarizing the phenomena of respiratory physiology involved in the hyperpnea test, the author studies the quantitative relation between the drop in PECO2 (pressure of CO2 in expired air) and changes in the EEG during hyperpnea. Normal subjects are divided into two groups of a hundred (6 to 19 1/2 years of age; 20 to 59 1/2 years of age). The PECO2 at rest is higher among the young subjects than among the adults, and its decline during hyperpnea is sharper. Thus, children show discrete respiratory acidosis in comparison with adults. The EEG of normal adults is practically unchanged during hyperpnea whereas, in the young group, moderate changes in the profile were observed in 45 out of 100 cases (classified empirically as normal). The PECO2 reaches a lower level in subjects showing EEG changes than in those showing none. All the reported differences are statistically significant (p less than 0.01). The probability of hyperpnea modifying the EEG profile becomes progressively less with age, and may be related to the reduced production of CO2 in older subjects. Epileptic subjects (primary generalized epilepsy) produce more CO2 than normal subjects during the hyperpnea test. The statistical data reported in the study show the importance of the size of the drop in ventilatory CO2 in the determination of EEG changes. The rest of hyperpnea in EEG can therefore be validly interpreted only if capnographic variations are measured. A standard quantitative hyperpnea test of this type should be devised, with specification of the hypocapnia level to be achieved.
[Quantitative hyperpnea in EEG (author's transl)]. After summarizing the phenomena of respiratory physiology involved in the hyperpnea test, the author studies the quantitative relation between the drop in PECO2 (pressure of CO2 in expired air) and changes in the EEG during hyperpnea. Normal subjects are divided into two groups of a hundred (6 to 19 1/2 years of age; 20 to 59 1/2 years of age). The PECO2 at rest is higher among the young subjects than among the adults, and its decline during hyperpnea is sharper. Thus, children show discrete respiratory acidosis in comparison with adults. The EEG of normal adults is practically unchanged during hyperpnea whereas, in the young group, moderate changes in the profile were observed in 45 out of 100 cases (classified empirically as normal). The PECO2 reaches a lower level in subjects showing EEG changes than in those showing none. All the reported differences are statistically significant (p less than 0.01). The probability of hyperpnea modifying the EEG profile becomes progressively less with age, and may be related to the reduced production of CO2 in older subjects. Epileptic subjects (primary generalized epilepsy) produce more CO2 than normal subjects during the hyperpnea test. The statistical data reported in the study show the importance of the size of the drop in ventilatory CO2 in the determination of EEG changes. The rest of hyperpnea in EEG can therefore be validly interpreted only if capnographic variations are measured. A standard quantitative hyperpnea test of this type should be devised, with specification of the hypocapnia level to be achieved.