• Annals of neurology · Aug 2016

    Clinically distinct electroencephalographic phenotypes of early myoclonus after cardiac arrest.

    • Jonathan Elmer, Jon C Rittenberger, John Faro, Bradley J Molyneaux, Alexandra Popescu, Clifton W Callaway, Maria Baldwin, and Pittsburgh Post-Cardiac Arrest Service.
    • Department of Emergency Medicine, University of Pittsburgh, Pittsburgh, PA.
    • Ann. Neurol. 2016 Aug 1; 80 (2): 175-84.

    ObjectiveWe tested the hypothesis that there are readily classifiable electroencephalographic (EEG) phenotypes of early postanoxic multifocal myoclonus (PAMM) that develop after cardiac arrest.MethodsWe studied a cohort of consecutive comatose patients treated after cardiac arrest from January 2012 to February 2015. For patients with clinically evident myoclonus before awakening, 2 expert physicians reviewed and classified all EEG recordings. Major categories included: Pattern 1, suppression-burst background with high-amplitude polyspikes in lockstep with myoclonic jerks; and Pattern 2, continuous background with narrow, vertex spike-wave discharges in lockstep with myoclonic jerks. Other patterns were subcortical myoclonus and unclassifiable. We compared population characteristics and outcomes across these EEG subtypes.ResultsOverall, 401 patients were included, of whom 69 (16%) had early myoclonus. Among these patients, Pattern 1 was the most common, occurring in 48 patients (74%), whereas Pattern 2 occurred in 8 patients (12%). The remaining patients had subcortical myoclonus (n = 2, 3%) or other patterns (n = 7, 11%). No patients with Pattern 1, subcortical myoclonus, or other patterns survived with favorable outcome. By contrast, 4 of 8 patients (50%) with Pattern 2 on EEG survived, and 4 of 4 (100%) survivors had favorable outcomes despite remaining comatose for 1 to 2 weeks postarrest.InterpretationEarly PAMM is common after cardiac arrest. We describe 2 distinct patterns with distinct prognostic significances. For patients with Pattern 1 EEGs, it may be appropriate to abandon our current clinical standard of aggressive therapy with conventional antiepileptic therapy in favor of early limitation of care or novel neuroprotective strategies. Ann Neurol 2016;80:175-184.© 2016 American Neurological Association.

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