Clinical Letter Use of Nimodipine in a Neonate With Cerebral Vasospasm With Delayed Ischemia From Subarachnoid Hemorrhage in the Posterior Fossa Bridget McGowan, MD a, * , Gurpreet Khaira, MD a, * , Meghan A. Coghlan, MD b , Ali Shaibani, MD c, d , Tord D. Alden, MD d , Andrea C. Pardo, MD a, * a Division of Neurology, Department of Pediatrics, Ann & Robert H. Lurie Children's Hospital of Chicago, Northwestern University Feinberg School of Medicine, Chicago, Illinois b Division of Neonatology, Department of Pediatrics, Ann & Robert H. Lurie Children's Hospital of Chicago, Northwestern University Feinberg School of Medicine, Chicago, Illinois c Department of Neurological Surgery, Ann & Robert H. Lurie Children's Hospital of Chicago, Northwestern University Feinberg School of Medicine, Chicago, Illinois d Department of Radiology, Ann & Robert H. Lurie Children's Hospital of Chicago, Northwestern University Feinberg School of Medicine, Chicago, Illinois article info Article history: Received 21 April 2020 Accepted 27 June 2020 Available online 3 July 2020 Keywords: Neonatal Subarachnoid hemorrhage Nimodipine Vasospasm Background Subarachnoid hemorrhage (SAH) causing cerebral vasospasm and delayed cerebral ischemia is a significant source of morbidity and mortality in adults. 1 Oral nimodipine is the standard of care for preventing delayed cerebral ischemia (DCI) in those with aneu- rysmal SAH. 1,2 Although use of nimodipine has been described in older children, 3 its use in the neonatal population has not yet been reported. We describe the use of nimodipine in a neonate with SAH resulting in vasospasm and DCI. Patient Description This neonate was born at 39 weeks' gestation to a 44-year-old primigravida mother with no significant past medical history. He was delivered via Caesarean section due to failed labor progression. Apgar scores were 8 and 9 at one and five minutes, respectively, and routine postnatal care was provided. At six hours of life, he devel- oped respiratory distress, hypotonia, and lethargy requiring intu- bation and admission to the neonatal intensive care unit. Magnetic resonance imaging (MRI) showed a large extra-axial hematoma in the posterior fossa with severe mass effect on the cerebellum and brainstem with restricted diffusion (Fig 1). Neuroprotective mea- sures were initiated immediately. Initial electroencephalography did not show seizures. Repeat MRI at six days of life (DOL) showed extensive SAH (of unknown etiology, although there was suspicion of ruptured Conflicts of interest: The authors declare no conflict of interest. Funding: This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors. Financial disclosure: The authors have indicated they have no financial re- lationships relevant to this article to disclose. * Communications should be addressed to: Dr. Pardo; Division of Neurology; Department of Pediatrics; Ann & Robert H. Lurie Children's Hospital of Chicago; Northwestern University Feinberg School of Medicine; 225 E. Chicago Ave, Box 51; Chicago, IL 60611. E-mail address: apardo@luriechildrens.org (A.C. Pardo). * Equally responsible for the work described in this article. Contents lists available at ScienceDirect Pediatric Neurology journal homepage: www.elsevier.com/locate/pnu https://doi.org/10.1016/j.pediatrneurol.2020.06.018 0887-8994/© 2020 Elsevier Inc. All rights reserved. Pediatric Neurology 111 (2020) 44e45