Stephen A Thompson1, Stephen Hantus. 1. *Department of Neurology, University of Texas Health Science Center, Houston, Texas, U.S.A.; and†Epilepsy Center, Neurological Institute, Cleveland Clinic, Cleveland, Ohio, U.S.A.
Abstract
PURPOSE: Pharmacologic sedation is often used to induce burst suppression in cases of refractory status epilepticus, but there is little evidence to guide the weaning of sedation. Similarly, the morphologic feature of bursts is of unknown clinical relevance. Recently, the standardized American Clinical Neurophysiology Society terminology of critical care EEG introduced the term highly epileptiform bursts (HEBs). Knowing the association of HEBs with seizure may direct the therapy for refractory status epilepticus. METHODS: Consecutive adult patients classified as having burst suppression were identified in our EEG database. Those of an anoxic etiology were excluded. Available EEG records were reviewed, both visually and quantitatively, for the presence of burst suppression. Using the American Clinical Neurophysiology Society terminology, burst suppression was dichotomized into HEBs or nonepileptiform bursts. Periods of transition out of burst suppression were identified, and whether burst suppression was followed by seizure or a continuous slow EEG within 24 hours was determined. RESULTS: Twenty-four patients were identified with a burst suppression pattern followed by either seizure or a continuous slow EEG within 24 hours, with some patients having multiple (maximal 5) transitions out of burst suppression, for a total of 33 examples of burst suppression. HEBs were associated with subsequent seizure (P = 0.0001), independent of medication exposure. CONCLUSIONS: Whether or not HEBs are indeed predictive of recurrent seizure or may be used to direct the therapy for status epilepticus, specifically the weaning of anesthetic medications, requires further prospective study in a larger cohort of patients.
PURPOSE: Pharmacologic sedation is often used to induce burst suppression in cases of refractory status epilepticus, but there is little evidence to guide the weaning of sedation. Similarly, the morphologic feature of bursts is of unknown clinical relevance. Recently, the standardized American Clinical Neurophysiology Society terminology of critical care EEG introduced the term highly epileptiform bursts (HEBs). Knowing the association of HEBs with seizure may direct the therapy for refractory status epilepticus. METHODS: Consecutive adult patients classified as having burst suppression were identified in our EEG database. Those of an anoxic etiology were excluded. Available EEG records were reviewed, both visually and quantitatively, for the presence of burst suppression. Using the American Clinical Neurophysiology Society terminology, burst suppression was dichotomized into HEBs or nonepileptiform bursts. Periods of transition out of burst suppression were identified, and whether burst suppression was followed by seizure or a continuous slow EEG within 24 hours was determined. RESULTS: Twenty-four patients were identified with a burst suppression pattern followed by either seizure or a continuous slow EEG within 24 hours, with some patients having multiple (maximal 5) transitions out of burst suppression, for a total of 33 examples of burst suppression. HEBs were associated with subsequent seizure (P = 0.0001), independent of medication exposure. CONCLUSIONS: Whether or not HEBs are indeed predictive of recurrent seizure or may be used to direct the therapy for status epilepticus, specifically the weaning of anesthetic medications, requires further prospective study in a larger cohort of patients.
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