Acute worsening of CADASIL in a patient with COVID-19 infection: illustrative case.

Autor:	Rosenblum JS; 1Neuro-Oncology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland., Tunacao JM; 2Department of Radiology, Stony Brook University Medical Center, Stony Brook, New York., Nazari MA; 3Internal Medicine and Pediatrics, Georgetown Hospital, Washington, District of Columbia., Ronk H; 1Neuro-Oncology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland., Dang DD; 1Neuro-Oncology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland.; 4Department of Neurosurgery, Inova Fairfax Medical Campus, Inova Health System, Falls Church, Virginia., Downing C; 2Department of Radiology, Stony Brook University Medical Center, Stony Brook, New York., Zhuang Z; 1Neuro-Oncology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland., Heiss JD; 5Surgical Neurology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland., Smirniotopoulos JG; 6Department of Radiology, George Washington University, Washington, District of Columbia.; 7MedPix® National Library of Medicine, Bethesda, Maryland; and., Bluestone A; 2Department of Radiology, Stony Brook University Medical Center, Stony Brook, New York., Badia J; 2Department of Radiology, Stony Brook University Medical Center, Stony Brook, New York., White J; 8Department of Family Medicine, Mather Hospital, Northwell Health System, Port Jefferson, New York.
Jazyk:	angličtina
Zdroj:	Journal of neurosurgery. Case lessons [J Neurosurg Case Lessons] 2022 Dec 26; Vol. 4 (26). Date of Electronic Publication: 2022 Dec 26 (Print Publication: 2022).
DOI:	10.3171/CASE22413
Abstrakt:	Background: Reports of cerebrovascular ischemia and stroke occurring as predominant neurological sequelae of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, which causes coronavirus disease 2019 (COVID-19), are increasingly evident within the literature. While various pathophysiological mechanisms have been postulated, including hypercoagulability, endothelial invasion, and systemic inflammation, discrete mechanisms for viral neurotropism remain unclear and controversial. Observations: The authors present a unique case study of a 64-year-old male with acute COVID-19 infection and acute worsening of previously stable cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL), a rare heritable arteriopathy due to mutation in the Notch3 gene, which is critical for vascular development and tone. Delayed cranial neuropathies, brainstem fluid-attenuated inversion recovery signal, and enhancement of olfactory and vagus nerves on magnetic resonance neurography in this patient further support viral neurotropism via cranial nerves in addition to cerebral vasculature. Lessons: To the authors' knowledge, this is the first case in the literature that not only demonstrates the consequences of COVID-19 infection in a patient with altered cerebrovascular autoregulation such as CADASIL but also highlights the tropism of SARS-CoV-2 for (1) cranial nerves as a mode of entry to the central nervous system and (2) vessels as a cause of cerebrovascular ischemia.
Databáze:	MEDLINE
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