Delayed cerebral ischemia is a major complication after subarachnoid hemorrhage. Our previous study showed that alpha power reduction in continuous quantitative EEG predicts delayed cerebral ischemia. In this prospective cohort, we aimed to determine the prognostic value of alpha power in quantitative EEG for the long-term outcome of patients with subarachnoid hemorrhage.
Adult patients with nontraumatic subarachnoid hemorrhage were included if admitted early enough for EEG to start within 72 hours after symptom onset. Continuous six-channel EEG was applied. Unselected EEG signals underwent automated artifact rejection, power spectral analysis, and detrending. Alpha power decline of ≥40% for ≥5 hours was defined as critical EEG event based on previous findings. Six-month outcome was obtained using the modified Rankin scale.
Twenty-two patients were included (14 male; mean age, 59 years; Hunt and Hess grade I–IV; duration of EEG monitoring, median 14 days). Poor outcome (modified Rankin scale, 2–5) was noted in 11 of 16 patients (69%) with critical EEG events. All six patients (100%) without EEG events achieved an excellent outcome (modified Rankin scale 0, 1) (P = 0.0062; sensitivity 100%, specificity 54.5%). Vasospasm detected with transcranial Doppler/Duplex sonography appeared 1.5 days after EEG events and showed weaker association with outcome (P = 0.035; sensitivity 100%, specificity 45.5%). There was no significant association between EEG events and ischemic lesions on imaging (P = 0.1). Also, no association between ischemic lesions and outcome was seen (P = 0.64).
Stable alpha power in quantitative EEG reflects successful therapy and predicts good functional outcome after subarachnoid hemorrhage. Critical alpha power reduction indicates an increased risk of poor functional outcome.
Departments of *Neurology and
†Neurosurgery, University Hospital Erlangen, Schwabachanlage, Germany.
Address correspondence and reprint requests to Stephanie Gollwitzer, MD, Department of Neurology, Epilepsy Center, University Hospital Erlangen, Schwabachanlage 6, 91054 Erlangen, Germany; e-mail: firstname.lastname@example.org.
H. M. Hamer has served on the scientific advisory board of Cerbomed, Desitin, Eisai, GlaxoSmithKline, Pfizer, and UCB Pharma. He served on the speakers' bureau of or received unrestricted grants from Ad-Tech, Cyberonics, Desitin, Eisai, GlaxoSmithKline, Ingelheim Boehringer, Nihon Kohden, Novartis, Pfizer, and UCB Pharma. S. Gollwitzer has served on the scientific advisory board or on the speaker's bureau or received grants from of Desitin, Eisai, and UCB Pharma. M. D Onugoren received a travel grant from Fresenius Medical Care (Bad Homburg, Germany) and obtained honoraria for a talk from Eisai (Frankfurt, Germany). H. B. Huttner received grants from Novartis, personal fees from Boehringer Ingelheim, grants and personal fees from UCB, and grants and personal fees from Medtronic. The remaining authors have no conflicts of interests to disclose.
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