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Medline ® Abstract for Reference 104

of 'Convulsive status epilepticus in adults: Treatment and prognosis'

New-onset refractory status epilepticus: Etiology, clinical features, and outcome.
Gaspard N, Foreman BP, Alvarez V, Cabrera Kang C, Probasco JC, Jongeling AC, Meyers E, Espinera A, Haas KF, Schmitt SE, Gerard EE, Gofton T, Kaplan PW, Lee JW, Legros B, Szaflarski JP, Westover BM, LaRoche SM, Hirsch LJ, Critical Care EEG Monitoring Research Consortium (CCEMRC), Critical Care EEG Monitoring Research Consortium CCEMRC
Neurology. 2015 Nov;85(18):1604-13. Epub 2015 Aug 21.
OBJECTIVES: The aims of this study were to determine the etiology, clinical features, and predictors of outcome of new-onset refractory status epilepticus.
METHODS: Retrospective review of patients with refractory status epilepticus without etiology identified within 48 hours of admission between January 1, 2008, and December 31, 2013, in 13 academic medical centers. The primary outcome measure was poor functional outcome at discharge (defined as a score>3 on the modified Rankin Scale).
RESULTS: Of 130 cases, 67 (52%) remained cryptogenic. The most common identified etiologies were autoimmune (19%) and paraneoplastic (18%) encephalitis. Full data were available in 125 cases (62 cryptogenic). Poor outcome occurred in 77 of 125 cases (62%), and 28 (22%) died. Predictors of poor outcome included duration of status epilepticus, use of anesthetics, and medical complications. Among the 63 patients with available follow-up data (median 9 months), functional status improved in 36 (57%); 79% had good or fair outcome at last follow-up, but epilepsy developed in 37% with most survivors (92%) remaining on antiseizure medications. Immune therapies were used less frequently in cryptogenic cases, despite a comparable prevalence of inflammatory CSF changes.
CONCLUSIONS: Autoimmune encephalitis is the most commonly identified cause of new-onset refractory status epilepticus, but half remain cryptogenic. Outcome at discharge is poor but improves during follow-up. Epilepsy develops in most cases. The role of anesthetics and immune therapies warrants further investigation.
From the Yale University School of Medicine (N.G., L.J.H.), Department of Neurology, Division of Epilepsy and Clinical Neurophysiology and Comprehensive Epilepsy Center, New Haven, CT; UniversitéLibre de Bruxelles-Hôpital Erasme (N.G., B.L.), Brussels, Belgium; University of Cincinnati Department of Neurology and Rehabilitation Medicine (B.P.F.), OH; Department of Neurology (V.A.), Hôpital de Sion; Department of Clinical Neurosciences (V.A.), Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland; Department of Neurology (V.A., J.W.L.), Brigham and Women's Hospital, Harvard Medical School, Boston MA; Emory University School of Medicine (C.C.K., S.M.L.), Atlanta, GA; Johns Hopkins Bayview Medical Center (J.C.P., P.W.K.), Department of Neurology, and Johns Hopkins University School of Medicine, Baltimore MD; Department of Neurology (A.C.J., E.M.), Columbia University, New York, NY; Vanderbilt University Medical Center (K.F.H.), Nashville, TN; Hospital of the University of Pennsylvania (S.E.S.), Philadelphia; Feinberg School of Medicine (A.E., E.E.G.), Northwestern University, Chicago, IL; University of Western Ontario (T.G.), Canada; University of Alabama at Birmingham (J.P.S.); and Department of Neurology (B.M.W.), Massachusetts General Hospital, Boston. ngaspard@ulb.ac.be.