Sylvain Rheims1, Blanca Mercedes Alvarez2, Veriano Alexandre2, Jonathan Curot2, Louis Maillard2, Fabrice Bartolomei2, Philippe Derambure2, Edouard Hirsch2, Véronique Michel2, Francine Chassoux2, Didier Tourniaire2, Arielle Crespel2, Arnaud Biraben2, Vincent Navarro2, Philippe Kahane2, Bertrand De Toffol2, Pierre Thomas2, Sarah Rosenberg2, Luc Valton2, Laurent Bezin2, Philippe Ryvlin2. 1. From the Department of Functional Neurology and Epileptology (S.R., B.M.A., V.A.), Hospices Civils de Lyon and University of Lyon; Lyon's Neuroscience Research Center (S.R., B.M.A., V.A., L.B., P.R.), INSERM U1028/CNRS UMR 5292, France; Hospital of Clinics of Ribeirão Preto (V.A.), University of São Paulo, Brazil; Department of Neurology (J.C., L.V.), University Hospital of Toulouse; Neurology Department (L.M.), University Hospital of Nancy; Clinical Neurophysiology and Epileptology Department (F.B.), Timone Hospital, Marseille; Department of Clinical Neurophysiology (P.D.), Lille University Medical Center, EA 1046, University of Lille2; Department of Neurology (E.H.), University Hospital of Strasbourg; Department of Neurology (V.M.), Hôpital Pellegrin, Bordeaux; Epilepsy Unit, Department of Neurosurgery (F.C.), Centre Hospitalier Sainte-Anne, University Paris Descartes; La Teppe Epilepsy Center (D.T.), Tain l'Hermitage,; Epilepsy Unit (A.C.), Montpellier; Department of Neurology (A.B.), University Hospital of Rennes; Epileptology Unit (V.N.), Assistance Publique-Hôpitaux de Paris, Groupe Hospitalier Pitié-Salpêtrière and Brain and Spine Institute (ICM; INSERM UMRS1127, CNRS UMR7225, UPMC University Paris 06); Department of Neurology (P.K.), Grenoble-Alpes University Hospital, GIN, INSERM U1216, and Grenoble Alpes University; Department of Clinical Neurophysiology (B.D.T.), INSERM U930, University Hospital of Tours; Department of Neurology (P.T.), University Hospital of Nice; Department of Neurology (S.R.), University Hospital of Clermont-Ferrand, France; Department of Clinical Neurosciences (S.R., P.R.), Centre Hospitalo-Universitaire Vaudois, Lausanne, Switzerland; and Epilepsy Institute (E.H., L.B., P.R.), Lyon, France. sylvain.rheims@univ-lyon1.fr. 2. From the Department of Functional Neurology and Epileptology (S.R., B.M.A., V.A.), Hospices Civils de Lyon and University of Lyon; Lyon's Neuroscience Research Center (S.R., B.M.A., V.A., L.B., P.R.), INSERM U1028/CNRS UMR 5292, France; Hospital of Clinics of Ribeirão Preto (V.A.), University of São Paulo, Brazil; Department of Neurology (J.C., L.V.), University Hospital of Toulouse; Neurology Department (L.M.), University Hospital of Nancy; Clinical Neurophysiology and Epileptology Department (F.B.), Timone Hospital, Marseille; Department of Clinical Neurophysiology (P.D.), Lille University Medical Center, EA 1046, University of Lille2; Department of Neurology (E.H.), University Hospital of Strasbourg; Department of Neurology (V.M.), Hôpital Pellegrin, Bordeaux; Epilepsy Unit, Department of Neurosurgery (F.C.), Centre Hospitalier Sainte-Anne, University Paris Descartes; La Teppe Epilepsy Center (D.T.), Tain l'Hermitage,; Epilepsy Unit (A.C.), Montpellier; Department of Neurology (A.B.), University Hospital of Rennes; Epileptology Unit (V.N.), Assistance Publique-Hôpitaux de Paris, Groupe Hospitalier Pitié-Salpêtrière and Brain and Spine Institute (ICM; INSERM UMRS1127, CNRS UMR7225, UPMC University Paris 06); Department of Neurology (P.K.), Grenoble-Alpes University Hospital, GIN, INSERM U1216, and Grenoble Alpes University; Department of Clinical Neurophysiology (B.D.T.), INSERM U930, University Hospital of Tours; Department of Neurology (P.T.), University Hospital of Nice; Department of Neurology (S.R.), University Hospital of Clermont-Ferrand, France; Department of Clinical Neurosciences (S.R., P.R.), Centre Hospitalo-Universitaire Vaudois, Lausanne, Switzerland; and Epilepsy Institute (E.H., L.B., P.R.), Lyon, France.
Abstract
OBJECTIVE: To analyze the factors that determine the occurrence or severity of postictal hypoxemia in the immediate aftermath of a generalized convulsive seizure (GCS). METHODS: We reviewed the video-EEG recordings of 1,006 patients with drug-resistant focal epilepsy included in the REPO2MSE study to identify those with ≥1 GCS and pulse oximetry (SpO2) measurement. Factors determining recovery of SpO2 ≥ 90% were investigated using Cox proportional hazards models. Association between SpO2 nadir and person- or seizure-specific variables was analyzed after correction for individual effects and the varying number of seizures. RESULTS: A total of 107 GCS in 73 patients were analyzed. A transient hypoxemia was observed in 92 GCS (86%). Rate of GCS with SpO2 <70% dropped from 40% to 21% when oxygen was administered early (p = 0.046). Early recovery of SpO2 ≥90% was associated with early administration of oxygen (p = 0.004), absence of postictal generalized EEG suppression (PGES) (p = 0.014), and extratemporal lobe epilepsy (p = 0.001). Lack of early administration of O2 (p = 0.003), occurrence of PGES (p = 0.018), and occurrence of ictal hypoxemia during the focal phase (p = 0.022) were associated with lower SpO2 nadir. CONCLUSION: Postictal hypoxemia was observed in the immediate aftermath of nearly all GCS but administration of oxygen had a strong preventive effect. Severity of postictal hypoxemia was greater in temporal lobe epilepsy and when hypoxemia was already observed before the onset of secondary GCS.
OBJECTIVE: To analyze the factors that determine the occurrence or severity of postictal hypoxemia in the immediate aftermath of a generalized convulsive seizure (GCS). METHODS: We reviewed the video-EEG recordings of 1,006 patients with drug-resistant focal epilepsy included in the REPO2MSE study to identify those with ≥1 GCS and pulse oximetry (SpO2) measurement. Factors determining recovery of SpO2 ≥ 90% were investigated using Cox proportional hazards models. Association between SpO2 nadir and person- or seizure-specific variables was analyzed after correction for individual effects and the varying number of seizures. RESULTS: A total of 107 GCS in 73 patients were analyzed. A transient hypoxemia was observed in 92 GCS (86%). Rate of GCS with SpO2 <70% dropped from 40% to 21% when oxygen was administered early (p = 0.046). Early recovery of SpO2 ≥90% was associated with early administration of oxygen (p = 0.004), absence of postictal generalized EEG suppression (PGES) (p = 0.014), and extratemporal lobe epilepsy (p = 0.001). Lack of early administration of O2 (p = 0.003), occurrence of PGES (p = 0.018), and occurrence of ictal hypoxemia during the focal phase (p = 0.022) were associated with lower SpO2 nadir. CONCLUSION:Postictal hypoxemia was observed in the immediate aftermath of nearly all GCS but administration of oxygen had a strong preventive effect. Severity of postictal hypoxemia was greater in temporal lobe epilepsy and when hypoxemia was already observed before the onset of secondary GCS.
Authors: Laura Vilella; Nuria Lacuey; Johnson P Hampson; Liang Zhu; Shirin Omidi; Manuela Ochoa-Urrea; Shiqiang Tao; M R Sandhya Rani; Rup K Sainju; Daniel Friedman; Maromi Nei; Kingman Strohl; Catherine Scott; Luke Allen; Brian K Gehlbach; Norma J Hupp; Jaison S Hampson; Nassim Shafiabadi; Xiuhe Zhao; Victoria Reick-Mitrisin; Stephan Schuele; Jennifer Ogren; Ronald M Harper; Beate Diehl; Lisa M Bateman; Orrin Devinsky; George B Richerson; Philippe Ryvlin; Guo-Qiang Zhang; Samden D Lhatoo Journal: Neurology Date: 2020-12-02 Impact factor: 9.910
Authors: Michael Lucchesi; Joshua B Silverman; Krishnamurthi Sundaram; Richard Kollmar; Mark Stewart Journal: Front Neurol Date: 2021-01-25 Impact factor: 4.003