COVID-19-associated acute disseminated encephalomyelitis (ADEM)
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LETTER TO THE EDITORS
COVID‑19‑associated acute disseminated encephalomyelitis (ADEM) Timothy Parsons1,2 · Sarah Banks1,2 · Chay Bae2 · Joel Gelber1 · Hussein Alahmadi1 · Matthew Tichauer1,2 Received: 6 May 2020 / Revised: 21 May 2020 / Accepted: 25 May 2020 © Springer-Verlag GmbH Germany, part of Springer Nature 2020
Abstract A 51-year-old woman with COVID-19 infection developed coma and an impaired oculocephalic response to one side. MRI of the brain demonstrated acute multifocal demyelinating lesions, and CSF testing did not identify a direct cerebral infection. High-dose steroids followed by a course of IVIG was administered, and the patient regained consciousness over the course of several weeks. As more patients reach the weeks after initial infection with COVID-19, acute disseminated encephalomyelitis should be considered a potentially treatable cause of profound encephalopathy or multifocal neurological deficits. Keywords ADEM · Post-infectious · COVID-19 · Coronavirus · Demyelinating disease Dear Editor, Neurological symptoms with SARS-CoV-2 infection (COVID-19) have been commonly encountered, but specific syndromes are only beginning to be described. Here, we report a patient with coma, an impaired unilateral oculocephalic response, and left hemiparesis. MRI, CSF, and her clinical course were consistent with acute disseminated encephalomyelitis (ADEM). A 51-year-old woman presented to a local hospital with dyspnea, fever, and vomiting. She had no pertinent neurological history. She was febrile, tachycardic, and hypoxic. Chest X-ray revealed extensive patchy airspace opacification. SARS-CoV-2 PCR from a nasopharyngeal swab was positive. She was intubated, and was maintained on sedative drips. On hospital day 18, she was transferred to our facility due to persistent fever and failure to progress clinically. Sedatives were held on arrival. Neurological exam was notable for unresponsiveness (GCS 3). Pupils were equal and reactive to light, corneal responses were intact, and the oculocephalic response to the left was impaired. Muscle tone was flaccid throughout, and the extremities did not move
* Timothy Parsons [email protected] 1
The Hospital of Central Connecticut, Hartford Healthcare, 100 Grand St., New Britain, CT 06052, USA
University of Connecticut School of Medicine, Farmington, CT, USA
2
spontaneously or to noxious stimuli. Deep tendon reflexes were depressed, and plantar responses were mute. An MRI of the brain done with and without gadolinium contrast on hospital day 24 showed scattered hyperintense lesions on FLAIR imaging in deep hemispheric and juxtacortical white matter. These lesions were hyperintense on diffusion weighted imaging (DWI), and a minority showed subtle restricted diffusion on the apparent diffusion coefficient (ADC), indicating acuity, but not consistent with infarction (Figs. 1, 2). A FLAIR hyperintensity in the left frontal juxtacortical white matter showed mild enhancement with gadolinium contrast (Fig. 3). There was a small amount of intraventricula
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