Arun Murugesan1, M R Sandhya Rani2, Laura Vilella1, Nuria Lacuey1, Johnson P Hampson1, Carl L Faingold1, Daniel Friedman1, Orrin Devinsky1, Rup K Sainju1, Stephan Schuele1, Beate Diehl1, Maromi Nei1, Ronald M Harper1, Lisa M Bateman1, George Richerson1, Samden D Lhatoo1. 1. From the Department of Neurology (A.M.), Case Western Reserve University; Department of Neurology (M.R.S.R., L.V., N.L., J.P.H., S.D.L.), McGovern Medical School, University of Texas Health Science Center at Houston; Department of Pharmacology and Neurology (C.L.F.), Southern Illinois University School of Medicine, Springfield; Department of Neurology (D.F., O.D.), New York University School of Medicine, New York; Department of Neurology (R.K.S., G.R.), University of Iowa Carver College of Medicine, Iowa City; Department of Neurology (S.S.), Northwestern University Feinberg School of Medicine, Chicago, IL; Institute of Neurology (B.D.), University College London, UK; Department of Neurology (M.N.), Sidney Kimmel Medical College at Thomas Jefferson University, Philadelphia, PA; Department of Neurobiology (R.M.H.), David Geffen School of Medicine at UCLA, Los Angeles, CA; Department of Neurology (L.M.B.), Columbia University Medical Center, New York, NY; and Center for SUDEP Research (M.R.S.R., L.V., N.L., D.F., O.D., R.K.S., S.S., B.D., M.N., R.M.H., L.M.B., G.R., S.D.L.), National Institute for Neurological Disorders and Stroke, Bethesda, MD. 2. From the Department of Neurology (A.M.), Case Western Reserve University; Department of Neurology (M.R.S.R., L.V., N.L., J.P.H., S.D.L.), McGovern Medical School, University of Texas Health Science Center at Houston; Department of Pharmacology and Neurology (C.L.F.), Southern Illinois University School of Medicine, Springfield; Department of Neurology (D.F., O.D.), New York University School of Medicine, New York; Department of Neurology (R.K.S., G.R.), University of Iowa Carver College of Medicine, Iowa City; Department of Neurology (S.S.), Northwestern University Feinberg School of Medicine, Chicago, IL; Institute of Neurology (B.D.), University College London, UK; Department of Neurology (M.N.), Sidney Kimmel Medical College at Thomas Jefferson University, Philadelphia, PA; Department of Neurobiology (R.M.H.), David Geffen School of Medicine at UCLA, Los Angeles, CA; Department of Neurology (L.M.B.), Columbia University Medical Center, New York, NY; and Center for SUDEP Research (M.R.S.R., L.V., N.L., D.F., O.D., R.K.S., S.S., B.D., M.N., R.M.H., L.M.B., G.R., S.D.L.), National Institute for Neurological Disorders and Stroke, Bethesda, MD. M.R.Sandhya.Rani@uth.tmc.edu.
Abstract
OBJECTIVE: To determine the relationship between serum serotonin (5-HT) levels, ictal central apnea (ICA), and postconvulsive central apnea (PCCA) in epileptic seizures. METHODS: We prospectively evaluated video EEG, plethysmography, capillary oxygen saturation (SpO2), and ECG for 49 patients (49 seizures) enrolled in a multicenter study of sudden unexpected death in epilepsy (SUDEP). Postictal and interictal venous blood samples were collected after a clinical seizure for measurement of serum 5-HT levels. Seizures were classified according to the International League Against Epilepsy 2017 seizure classification. We analyzed seizures with and without ICA (n = 49) and generalized convulsive seizures (GCS) with and without PCCA (n = 27). RESULTS: Postictal serum 5-HT levels were increased over interictal levels for seizures without ICA (p = 0.01), compared to seizures with ICA (p = 0.21). In patients with GCS without PCCA, serum 5-HT levels were increased postictally compared to interictal levels (p < 0.001), but not in patients with seizures with PCCA (p = 0.22). Postictal minus interictal 5-HT levels also differed between the 2 groups with and without PCCA (p = 0.03). Increased heart rate was accompanied by increased serum 5-HT levels (postictal minus interictal) after seizures without PCCA (p = 0.03) compared to those with PCCA (p = 0.42). CONCLUSIONS: The data suggest that significant seizure-related increases in serum 5-HT levels are associated with a lower incidence of seizure-related breathing dysfunction, and may reflect physiologic changes that confer a protective effect against deleterious phenomena leading to SUDEP. These results need to be confirmed with a larger sample size study.
OBJECTIVE: To determine the relationship between serum serotonin (5-HT) levels, ictal central apnea (ICA), and postconvulsive central apnea (PCCA) in epilepticseizures. METHODS: We prospectively evaluated video EEG, plethysmography, capillary oxygen saturation (SpO2), and ECG for 49 patients (49 seizures) enrolled in a multicenter study of sudden unexpected death in epilepsy (SUDEP). Postictal and interictal venous blood samples were collected after a clinical seizure for measurement of serum 5-HT levels. Seizures were classified according to the International League Against Epilepsy 2017 seizure classification. We analyzed seizures with and without ICA (n = 49) and generalized convulsive seizures (GCS) with and without PCCA (n = 27). RESULTS: Postictal serum 5-HT levels were increased over interictal levels for seizures without ICA (p = 0.01), compared to seizures with ICA (p = 0.21). In patients with GCS without PCCA, serum 5-HT levels were increased postictally compared to interictal levels (p < 0.001), but not in patients with seizures with PCCA (p = 0.22). Postictal minus interictal 5-HT levels also differed between the 2 groups with and without PCCA (p = 0.03). Increased heart rate was accompanied by increased serum 5-HT levels (postictal minus interictal) after seizures without PCCA (p = 0.03) compared to those with PCCA (p = 0.42). CONCLUSIONS: The data suggest that significant seizure-related increases in serum 5-HT levels are associated with a lower incidence of seizure-related breathing dysfunction, and may reflect physiologic changes that confer a protective effect against deleterious phenomena leading to SUDEP. These results need to be confirmed with a larger sample size study.
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