One hundred eighty-seven seizures were captured in 33 patients (13 female). The mean age was 36.4 ± 13.3 years (35, 18–66) [mean ± SD (median, range)]. The body mass index (BMI) was 27.3 ± 5 (25.6, 20.5–37.6). One hundred sixty seizures were of temporal onset, 16 of frontal onset, 1 of central onset, and in 10 seizures the onset was undetermined. Seizure lateralization was left in 100, right in 74, undetermined in 9, and had a near simultaneous bilateral onset in 4. Additional clinical details are provided in Table S1. One patient was studied twice, initially with noninvasive scalp monitoring and several months later again with intracranial electrodes.
Five patients were on AED monotherapy; the remaining patients were on two or more AEDs prior to reductions of AEDs. Forty-one of the 187 seizures progressed to generalized convulsions. Ictal/postictal ETCO2 peak values were available for 94 seizures. SaO2 nadir values were available for 163 seizures, including 36 seizures that progressed to generalized convulsions.
For all 187 seizures the seizure duration was 111 ± 95 s (84, 17–724). The time to contralateral spread of seizure was 36 ± 52 s (19, 0–375). The time to secondarily generalized convulsion was 64 ± 47 s (45, 13–240).
The baseline ETCO2 was 35 ± 6 mm Hg (37, 19–47). The patient with the baseline ETCO2 of 19 mm Hg had been hyperventilating to provoke a seizure. The peak ictal/postictal ETCO2 was 49 ± 11 mm Hg (47, 30–94). The ictal/postictal ETCO2 increase from baseline was 14 ± 11 mm Hg (11, −1 to 50). For the 94 seizures in which ETCO2 information was available, peak ETCO2 increases to 50 mm Hg or above occurred with 35 seizures with or without secondarily generalized convulsions. ETCO2 was at or above 60 mm Hg and 70 mm Hg with 15 and 5 seizures, respectively (Fig. S1A). Eleven of the 33 patients had seizures with ETCO2 elevation above 50 mm Hg. Of these 11 patients, in 6 the ETCO2 was above 60 mm Hg and in 2 above 70 mm Hg for at least one seizure. The ETCO2 peak occurred 175 ± 118 s (158, 10–660) after seizure onset and 56 ± 111 s (27, −318 to 552) after seizure termination. The ETCO2 peak occurred 45 ± 86 s (32, −224 to 271) after the SAO2 nadir. The duration of the ictal/postictal ETCO2 increase was 424 ± 807 s (154, 4 to 6225) (Fig. S1B).
The baseline SaO2 on room air was 97 ± 2% (98, 92–100). The SaO2 nadir on room air for seizures that did not progress to generalized convulsions was 88 ± 11% (92, 43–100). With secondary generalized convulsions the SaO2 nadir on room air was 74 ± 11% (75, 50–91). The time from seizure onset to onset of desaturation below 90% was 81 ± 62 s (67, −2 to 431). The time from seizure onset to SaO2 nadir was 111 ± 70 s (96, 22−469). The duration of desaturation (<90% to ≥90%) was 80 ± 89 s (59, 4–712). The time from onset of desaturation below 90% to return of saturation to within 2% of baseline SaO2 was 176 ± 281 s (103, 13 to 2036).
Following partial seizures that did not evolve into generalized convulsions, peak ETCO2 values declined rapidly over 500 s, followed by a more gradual decline over the next 1000 s. The ETCO2 values remained at least 3 mm Hg above preictal levels for 1,500 s. A similar decline from peak ETCO2 values occurred following secondarily generalized convulsions (Fig. 1).
Figure 1. Locally weighted scatterplot smoothing (LOESS) plots for the change in end-tidal CO2 (ETCO2) values relative to preictal baseline. The tracings show the postictal decline in ETCO2 values starting with the greatest ETCO2 change recorded in the ictal/postictal period. The fitted curve (red) and 95% confidence intervals (blue) are shown. (A) shows the decay from peak ETCO2 change with partial onset seizures that progressed to generalized convulsions. (B) shows the decay from peak ETCO2 change with partial seizures that did not progress to generalized convulsions.
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The duration of apnea was 49 ± 46 s (31, 6–222). There were 67 central, 8 obstructive, and 9 mixed apneas (apneas with both central and obstructive components). There was inadequate information to characterize the apnea in six seizures, as abdominal movement information was not available. There were three hypopneas. Both airflow and abdominal movement information was unavailable with 58 seizures. No apnea was detected with the remaining seizures.
The RR in the preictal baseline was 18.6 ± 5.2 breaths per minute (18, 8–36) and increased to 25.7 ± 10.0 breaths per minute (24, 12–60) in the immediate postictal period. The increase in RR was statistically significant (p < 0.001). The square root transformed amplitude of the peak to peak airflow signal at baseline was 3.2 ± 2.6 (2.7, 0.04–7.6) and in the immediate postictal period was 11.7 ± 7.7 (13.0, 0.36–28). The postictal airflow amplitude was significantly higher than the amplitude during preictal baseline (two-sided Wilcoxon signed-rank test, p = 0.001) (Fig. S2).
The preictal heart rate was 85 ± 19 bpm (84, 54–192). The peak ictal heart rate was 131 ± 27 bpm (126, 72–210). The ictal heart rate change was 45 ± 27 bpm (42, −12 to 120). The duration of ictal tachycardia was 329 ± 737 s (80, 10−4,251).
Relationship of seizure duration and change in ETCO2 and SaO2
For all seizures, the peak ictal/postictal increase in ETCO2 did not correlate with seizure duration (p = 0.074). The peak change in ETCO2 did not correlate with the duration of secondarily generalized seizures (p = 0.138). The duration of ETCO2 increase above baseline did not correlate with seizure duration in seizures that did not progress to generalized convulsions (p = 0.103). The duration of oxygen desaturation was significantly associated with seizure duration (p = 0.005).
There was no correlation between seizure duration and apnea duration (p = 0.137, Spearman rank correlation coefficient 0.203). No association was demonstrated between apnea duration and contralateral spread of seizures (p = 0.515, two-sided Wilcoxon rank-sum test). An association was demonstrated between seizure duration and contralateral spread of seizures (p = 0, two-sided Wilcoxon rank-sum test). Contralateral spread of seizures and seizure duration that had p < 0.3 from univariate analysis were used as candidate variables and included in the multivariable robust linear regression model. Multivariable analysis showed the p-values of contralateral spread of seizures and seizure duration of p ≤ 0.0001 and p = 0.006, respectively, indicating that the contralateral spread of seizures and seizure duration are jointly associated with ETCO2 change.