Ictal hypoxemia in localization-related epilepsy: analysis of incidence, severity and risk factors.

Ictal hypoxemia has been reported in small series of cases and may contribute to sudden unexpected death in epilepsy (SUDEP). We sought to determine the incidence and severity of ictal hypoxemia in patients with localization-related epilepsy undergoing in-patient video-EEG telemetry. We examined whether seizure-associated oxygen desaturation was a consequence of hypoventilation and whether factors such as seizure localization and lateralization, seizure duration, contralateral spread of seizures, patient position at seizure onset and body mass index influenced ictal-related hypoxemia. A total of 304 seizures with accompanying oxygen saturation data were recorded in 56 consecutive patients with intractable localization-related epilepsy; 51 of 304 seizures progressed to generalized convulsions. Pulse oximetry showed oxygen desaturations below 90% in 101 (33.2%) of all seizures with or without secondary generalization, with 31 (10.2%) seizures accompanied by desaturations below 80% and 11 (3.6%) seizures below 70%. The mean duration of desaturation below 90% was 69.2 +/- 65.2 s (47; 6-327). The mean oxygen saturation nadir following secondary generalization was 75.4% +/- 11.4% (77%; 42-100%). Desaturations below 90% were significantly correlated with seizure localization [P = 0.005; odds ratio (OR) of temporal versus extratemporal = 5.202; 95% CI = (1.665, 16.257)], seizure lateralization [P = 0.001; OR of right versus left = 2.098; 95% CI = (1.078, 4.085)], contralateral spread of seizures [P = 0.028; OR of contralateral spread versus no spread = 2.591; 95% CI = (1.112, 6.039)] and gender [P = 0.048; OR of female versus male = 0.422; 95% CI = (0.179, 0.994)]. In the subset of 253 partial seizures without secondary generalized convulsions, 34.8% of seizures had desaturations below 90%, 31.8% had desaturations below 80% and 12.5% had desaturations below 70%. The degree of desaturation was significantly correlated with seizure duration (P = 0.001) and with electrographic evidence of seizure spread to the contralateral hemisphere (P = 0.003). Central apnoeas or hypopnoeas occurred with 50% of 100 seizures. Mixed or obstructive apnoeas occurred with 9% of these seizures. End-tidal carbon dioxide (ETCO2) was recorded in seven patients (19 seizures). The mean increase in ETCO2 from preictal baseline was 18.6 +/- 17.7 mm Hg (13.2; 2.8-77.8). In these 19 seizures, all oxygen desaturations below 85% were accompanied by an increase in ETCO2. Ictal hypoxemia occurs often in patients with localization-related epilepsy and may be pronounced and prolonged; even with seizures that do not progress to generalized convulsions. Oxygen desaturations are accompanied by increases in ETCO2, supporting the assumption that ictal oxygen desaturation is a consequence of hypoventilation. Ictal hypoxemia and hypercapnia may contribute to SUDEP.

[1]  P. Ryvlin,et al.  La chirurgie de l’épilepsie réduit-elle la surmortalité des épilepsies partielles pharmacorésistantes ? , 2008 .

[2]  J. Leiter,et al.  Changes in respiratory-modulated neural activities, consistent with obstructive and central apnea, during fictive seizures in an in situ anaesthetized rat preparation , 2006, Epilepsy Research.

[3]  Srinivasan Tupal,et al.  Evidence Supporting a Role of Serotonin in Modulation of Sudden Death Induced by Seizures in DBA/2 Mice , 2006, Epilepsia.

[4]  J. Stockman Cardiac Arrhythmias in Focal Epilepsy: A Prospective Long-term Study , 2006 .

[5]  Samuel Wiebe,et al.  Sudden unexpected death in epilepsy: Evidence-based analysis of incidence and risk factors , 2005, Epilepsy Research.

[6]  Josemir W Sander,et al.  Case-control study of SUDEP , 2005, Neurology.

[7]  Maromi Nei,et al.  EEG and ECG in Sudden Unexplained Death in Epilepsy , 2004, Epilepsia.

[8]  G. Holstege,et al.  Amygdaloid projections to the mesencephalon, pons and medulla oblongata in the cat , 1978, Experimental Brain Research.

[9]  Evgeni Ponimaskin,et al.  Serotonin receptors: guardians of stable breathing. , 2003, Trends in molecular medicine.

[10]  C. Elger,et al.  Cardiac Asystole in Epilepsy: Clinical and Neurophysiologic Features , 2003, Epilepsia.

[11]  A. Goldberger,et al.  Oxygen Desaturations Triggered by Partial Seizures: Implications for Cardiopulmonary Instability in Epilepsy , 2000, Epilepsia.

[12]  R. Siedenberg,et al.  Central apnea and acute cardiac ischemia in a sheep model of epileptic sudden death , 1997, Annals of neurology.

[13]  S. Boyd,et al.  HYPOXAEMIA AND CARDIORESPIRATORY CHANGES DURING EPILEPTIC SEIZURES IN YOUNG CHILDREN , 1996, Developmental medicine and child neurology.

[14]  B. Lipworth,et al.  Effects of hypercapnia on hemodynamic, inotropic, lusitropic, and electrophysiologic indices in humans. , 1996, Chest.

[15]  Josemir W Sander,et al.  Apnoea and bradycardia during epileptic seizures: relation to sudden death in epilepsy. , 1996, Journal of neurology, neurosurgery, and psychiatry.

[16]  G. Poe,et al.  Hippocampal reflected optical patterns during sleep and waking states in the freely behaving cat , 1994, The Journal of neuroscience : the official journal of the Society for Neuroscience.

[17]  R. Harper,et al.  Cardiac and Respiratory Correlations with Unit Discharge in Epileptic Human Temporal Lobe , 1990, Epilepsia.

[18]  E. Neafsey,et al.  Cardiovascular and respiratory responses to electrical and chemical stimulation of the hippocampus in anesthetized and awake rats , 1988, Brain Research.

[19]  G. Holstege Anatomical evidence for a strong ventral parabrachial projection to nucleus raphe magnus and adjacent tegmental field , 1988, Brain Research.

[20]  L. D. Blumhardt,et al.  ELECTROCARDIOGRAPHIC ACCOMPANIMENTS OF TEMPORAL LOBE EPILEPTIC SEIZURES , 1986, The Lancet.

[21]  S. Zeger,et al.  Longitudinal data analysis using generalized linear models , 1986 .

[22]  A. Bianchi,et al.  Inspiratory onset or termination induced by electrical stimulation of the brain. , 1982, Respiration physiology.

[23]  S. Goldberg,et al.  MEASUREMENT OF ŒSTRIOL EXCRETION IN PREGNANCY , 1971 .

[24]  H. Jasper,et al.  Respiratory responses to stimulation of temporal pole, insula, and hippocampal and limbic gyri in man. , 1952, A.M.A. archives of neurology and psychiatry.

[25]  J. Elliotson St. Thomas's Hospital , 1829, The Medico-chirurgical review.