Plasma Catecholamine Levels and Cardiovascular Modifications After Generalized Convulsive Seizures
Abstract number :
3.141
Submission category :
3. Neurophysiology / 3C. Other Clinical EEG
Year :
2021
Submission ID :
1826671
Source :
www.aesnet.org
Presentation date :
12/6/2021 12:00:00 PM
Published date :
Nov 22, 2021, 06:55 AM
Authors :
M R Sandhya Rani, PhD - University of Texas Health Science Center; Mojtaba Dayyani - Neurology - University of Texas Health Science Center; Nuria Lacuey - University of Texas Health Science Center; Arun Murugesan - North-East Ohio Medical University; Laura Vilella - University of Texas Health Science Center; Johnson Hampson - University of Texas Health Science Center; Samden Lhatoo - University of Texas Health Science Center
Rationale: Excess of circulating peripheral catecholamines can potentially increase blood pressure (BP) and heart rate (HR) to very high levels resulting in deleterious effects. Catecholamine levels have been shown to increase after generalized convulsive seizures (GCS). Simultaneous data on cardiovascular indices captured during GCS along with the levels of catecholamines at seizure end is non-existent. Herein, we present two subjects for whom we recorded continuous BP, measured catecholamines after a GCS, and correlated our findings with electroclinical seizure features, markers of seizure severity and SUDEP risk.
Methods: We recorded continuous BP, electrocardiogram (ECG), plethysmography and capillary oxygen saturation (SpO2) in two patients with intractable epilepsy undergoing video EEG monitoring in the Epilepsy Monitoring Unit. Post-ictal venous blood samples were collected after a video-recorded GCS and interictal (baseline) sample was collected after at least 12 hours of seizure-free period and levels of plasma epinephrine and norepinephrine were measured. Using the LabChart Pro 8 and the recorded BP signal, we calculated and assessed modifications of cardiac output (CO), stroke volume (SV), total peripheral resistance (TPR), and baroreflex sensitivity (BRS).
Results: In the post-ictal phase, subject one showed a wide pulse pressure (MAP=86.1, SBP=193.1, DBP=32.6) at seizure end, while the second subject revealed post-ictal hypotension (MAP=62.7). The epinephrine to norepinephrine ratio (E/N) was four in the first subject with wide pulse pressure and remarkable increment of HR, decrement of TPR (HR≈140, TPR=0.35) and a notable rise of CO≈14.0 L/min at seizure end. In contrast, the second subject showed E/N of two with a lower HR≈78 and much lower CO and an increased TPR (CO≈3.1 L/min, TPR=1.51). Both subjects demonstrated a reduced BRS value in the post-ictal phase. Some markers of seizure severity presented by both subjects, included long duration of epilepsy ( >10 years), post-ictal generalized encephalographic suppression (PGES) and severe hypoxemia (oxygen saturation < 75%).
Neurophysiology