WILL A CRITICAL-LEVEL OF HYPERVENTILATION-INDUCED HYPOCAPNIA ALWAYS INDUCE AN ABSENCE SEIZURE

We wished to determine if the degree of hypocapnia correlates with inc reased frequency of absence seizures and if there is a critical pCO(2) at which absence seizures are reliably provoked. Twelve untreated chi ldren with newly diagnosed absence epilepsy were continuously monitore d by EEG and end-expiratory CO2 recording during quiet respiration and hyperventilation (to absence seizure or exhaustion) while breathing f our gas mixtures: (a) room air, (b) 100% O-2, (c) 4% CO2 in room air, or (d) 4% CO2 + 96% O-2. In quiet respiration, a reduction in number o f spike and wave bursts and total seconds of spike and wave was noted in children breathing supplemental CO2 (gases c and d vs. gases a and b), p < 0.05. Supplemental O-2 had no effect. Eight subjects had absen ce seizures elicited with each trial of hyperventilation. All subjects had their own critical pCO(2), ranging from 19 to 28 mmHg. Three chil dren had no seizures, two despite hypocapnia to pCO(2) of 19 and 21 an d I who achieved a pCO(2) of only 25. In 1, absence seizures were prov oked in only six of nine hyperventilation trials to pCO(2) of 17-23. I n 67% of subjects, absence seizures were reliably provoked by hypocapn ia. Critical pCO(2) varied among children with absence. Determination of whether variation in sensitivity to hypocapnia may be helpful in de termining response to antiepileptic drugs (AEDs) or remission of seizu res will require further study.