Ictal and Post-Ictal Brainstem Posturing Is Associated with Generalized Convulsive Seizures (GCS) Severity Markers and Breathing Compromise
Abstract number :
1.126
Submission category :
3. Neurophysiology / 3A. Video EEG Epilepsy-Monitoring
Year :
2019
Submission ID :
2421121
Source :
www.aesnet.org
Presentation date :
12/7/2019 6:00:00 PM
Published date :
Nov 25, 2019, 12:14 PM
Authors :
Laura Vilella Bertran, UT Health Science Center at Houston; Nuria Lacuey, UT Health Science Center at Houston; Johnson P. Hampson, UT Health Science Center at Houston; Liang Zhu, UT Health Science Center at Houston; Shirin Omidi, UT Health Science Center
Rationale: Sudden Unexpected Death in Epilepsy (SUDEP) is the leading category of death in patients with refractory epilepsy. Post-ictal generalized EEG suppression (PGES) along with breathing dysfunction were noted in all monitored SUDEP cases in MORTEMUS. Moreover, PGES duration >50 seconds is associated with higher risk of SUDEP. Tonic phase semiology of Generalized Convulsive Seizures (GCS) is strongly linked to incidence of PGES, particularly when characterized by bilateral symmetric tonic arm extension posturing. We set out to analyze ictal and post-ictal tonic GCS semiology and their possible association with PGES and peri-ictal breathing dysfunction, postulated as seizure severity biomarkers. Methods: This is a multicentric retrospective analysis of GCS in adult Epilepsy Monitoring Units. Tonic phase semiology was classified as 1) Ictal decerebration: bilateral symmetric tonic extension of both arms, 2) Ictal decortication: bilateral symmetric tonic flexion of both arms without progression to decerebration, 3) Ictal hemi-decerebration: tonic extension of one arm with contralateral flexion and 4) absence of ictal tonic phase. In addition, presence of post-ictal posturing (decerebration or decortication) was assessed. PGES was determined by a validated automated EEG suppression detection tool. Breathing was monitored using thoraco-abdominal belts, video and SpO2, two minutes before and 3 minutes after GCS. Results: 295 seizures in 180 patients (90 female) were analyzed. Mean age was 36.7±13.3 years. Ictal decerebration was observed in 122/295 (41.4%) seizures, ictal decortication in 47/295 (15.9%) seizures and ictal hemi-decerebration in 28/295 (9.5%) seizures. No tonic phase was noted in the remaining 98/295 (33.2%) seizures. Postictal posturing was present in 18/295 (6.1%) seizures (16 with decortication and 2 with decerebration). PGES occurred in 197/293 (67%) seizures with a duration of 36.5±21.4 seconds (s); Ictal central apnea (ICA) was observed in 83/205 (40.4%) seizures and, post-convulsive central apnea (PCCA) in 45/285 (15.8%) seizures; Total hypoxemia duration (n=127) was 142.6 ± 65.5s. SpO2 recovery to 90% after GCS (n=120) was 43.2 ± 34.2s. After multivariate regression analysis, risk of PGES increased with ictal decerebration [RR 2.776, 95% CI (1.318-5.844), p=0.007], decortication [RR 2.846, 95% CI (1.288-6.290), p=0.010] or hemi-decerebration [RR 3.198, 95% CI 1.542-6.631, p=0.002] when compared to absence of tonic phase. Moreover, PGES duration was significantly longer in those seizures with ictal decerebration [Est 20.447, 95% CI (4.742-36.153), p=0.011], but not in seizures with other semiologies (p>0.05). Table 1. Finally, hypoxemia duration was longer in seizures with ictal decerebration (Est 21.106, 95% CI (0.170-42.042), p=0.048) but not in those with other semiology types. Regarding post-ictal posturing, it conferred increased risk of PCCA [RR 3.148, 95% CI (1.604-6.176), p=0.001] and longer times of SpO2 recovery [Est 27.837, 95% CI (1.983-53.690), p=0.035].Table 2. Conclusions: Ictal decerebration, decortication and hemi-decerebration during GCS increase the risk of PGES. Moreover, ictal decerebration is associated with longer PGES and hypoxemia durations. Post-ictal posturing is associated with a threefold increased risk of PCCA and longer SpO2 recovery. Therefore, peri-ictal brainstem semiology, including decerebration and post-ictal posturing, could be surrogates for GCS severity biomarkers. Funding: NIH/NINDS U01-NS090405, NIH/NINDS U01-NS090407, NIH/NINDS U01-NS090414.
Neurophysiology