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Pediatric MOGAD in the Intensive Care Unit: A Case Series
Alyssa D Runco1,2, Daniel Davila-Williams1, Karen K Moeller3
1Division of Neurology and Developmental Neuroscience, Department of Pediatrics, Baylor College of Medicine and Texas Children's Hospital, 6701 Fannin Street, Ste 1250, Houston, TX, 77030, USA.
Background:
Myelin oligodendrocyte glycoprotein antibody disease (MOGAD) is an antibody mediated demyelinating disorder of the central nervous system with a spectrum of clinical presentations and severity, including a subgroup of patients requiring admission to an intensive care unit (ICU) due to severity of their disease. While there is a growing body of literature on MOGAD, there are limited reports focusing on patients requiring admission to an ICU. The aim of this study was to better characterize a population of pediatric patients with MOGAD with critical illness, focusing on patients requiring ICU admission.
Methods:
A retrospective chart review was performed on pediatric patients with MOGAD between January 2017 and December 2024 at a large pediatric tertiary care center. Clinical, laboratory, and imaging data were collected for all patients with MOGAD. Magnetic resonance neuroimaging was reviewed by a board-certified pediatric neuroradiologist.
Results:
Of the 124 pediatric patients with MOGAD identified, 37 required ICU admission for either altered mental status, seizures, and/or rapid onset of weakness. Of those requiring ICU admission, 16 were intubated due to altered mental status or seizures for a median duration of 3 days (IQR 2-10.8 days). Fever was common, present in 24 of the patients in the ICU. Seven patients received intracranial pressure (ICP)-directed hyperosmolar therapy, and two patients had an ICP monitoring device placed. In total, 12 patients had neuroimaging evidence of increased ICP, with 4 of these having evidence of herniation or cerebral shift. Seizures were present in 18 patients, and 11 patients had status epilepticus. There were 27 patients who had continuous electroencephalography (cEEG) monitoring with a heterogeneity of background patterns observed.
Conclusions:
Severe presentations of MOGAD are increasingly recognized, including patients with a clinical course complicated by status epilepticus or increased ICP. Anticipating and addressing these complications may prevent secondary cerebral injury. No specific EEG biomarkers for MOGAD were observed in our cohort.
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