key: cord-1046024-1q4p76hp
authors: Radmanesh, Alireza; Derman, Anna; Ishida, Koto
title: COVID-19-associated delayed posthypoxic leukoencephalopathy
date: 2020-05-27
journal: J Neurol Sci
DOI: 10.1016/j.jns.2020.116945
sha: 0caf58a81b47f13580717955fcfc3be33609cc80
doc_id: 1046024
cord_uid: 1q4p76hp

nan

A 50 year-old man with controlled hypertension and type II diabetes presented after one week of dyspnea and cough with a blood O2 saturation of 90%. A Reverse Transcriptase-Polymerase Chain Reaction assay on a nasopharyngeal swab specimen confirmed severe acute respiratory syndrome coronavirus 2, and a diagnosis of coronavirus disease 2019 (COVID-19) pneumonia. On initial neurologic examination, the patient was alert and fully oriented with fluent speech and no focal deficits. On the second hospital day and while on 2L of supplemental O2 through nasal cannula, blood O2 saturation dropped to 70% and he was intubated. His Unlike acute hypoxic-ischemic brain injury, which is related to glutamate excitotoxicity and predominantly involves the deep and cortical gray matter, DPHL is thought to result from necrosis of vulnerable oligodendrocytes in arterial border zones during a hypoxic insult and failed myelin turnover, leading to widespread demyelination with axonal sparing, without myelin vacuolization 2 . Relative respiratory status, DPHL and brain imaging evaluation should be considered 4 .

Treatment is mainly supportive, and prognosis is highly variable but usually poor with permanent disability 2 . For our patient, plan of care discussions with the family are ongoing. 

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