Multifactorial White Matter Damage in the Acute Phase and Pre-Existing Conditions May Drive Cognitive Dysfunction after SARS-CoV-2 Infection: Neuropathology-Based Evidence

There is an urgent need to better understand the mechanisms underlying acute and long-term neurological symptoms after COVID-19. Neuropathological studies can contribute to a better understanding of some of these mechanisms. We conducted a detailed postmortem neuropathological analysis of 32 patient...

Full description

Saved in:

Bibliographic Details
Published in:	Viruses Vol. 15; no. 4; p. 908
Main Authors:	Gelpi, Ellen, Klotz, Sigrid, Beyerle, Miriam, Wischnewski, Sven, Harter, Verena, Kirschner, Harald, Stolz, Katharina, Reisinger, Christoph, Lindeck-Pozza, Elisabeth, Zoufaly, Alexander, Leoni, Marlene, Gorkiewicz, Gregor, Zacharias, Martin, Haberler, Christine, Hainfellner, Johannes, Woehrer, Adelheid, Hametner, Simon, Roetzer, Thomas, Voigtländer, Till, Ricken, Gerda, Endmayr, Verena, Haider, Carmen, Ludwig, Judith, Polt, Andrea, Wilk, Gloria, Schmid, Susanne, Erben, Irene, Nguyen, Anita, Lang, Susanna, Simonitsch-Klupp, Ingrid, Kornauth, Christoph, Nackenhorst, Maja, Kläger, Johannes, Kain, Renate, Chott, Andreas, Wasicky, Richard, Krause, Robert, Weiss, Günter, Löffler-Rag, Judith, Berger, Thomas, Moser, Patrizia, Soleiman, Afshin, Asslaber, Martin, Sedivy, Roland, Klupp, Nikolaus, Klimpfinger, Martin, Risser, Daniele, Budka, Herbert, Schirmer, Lucas, Pröbstel, Anne-Katrin, Höftberger, Romana
Format:	Journal Article
Language:	English
Published:	Switzerland MDPI AG 31-03-2023 MDPI
Subjects:	Age Aged Autopsies Autopsy Brain Brain injury Brain stem Cognition disorders Cognitive ability Cognitive Dysfunction - etiology Coronaviruses COVID-19 COVID-19 - complications Cranial nerves Encephalitis Forensic medicine Guillain-Barre syndrome Hemorrhage Herpes simplex Humans Hypoxia Infections Inflammation Intensive care Ischemia Leukoencephalopathy Lewy bodies Medical research Medicine, Experimental Morphology Musculoskeletal system Nervous System Diseases - pathology Neuritis Neuronal-glial interactions Neuropathology Pandemics Patients Pre-existing conditions Preexisting Condition Coverage Risk factors SARS-CoV-2 Severe acute respiratory syndrome coronavirus 2 Spinal cord Substantia alba Tau protein Thrombosis white matter White Matter - pathology Austria COVID-19 leukoencephalopathy white matter SARS-CoV-2 neuropathology
Online Access:	Get full text
Tags:	Add Tag No Tags, Be the first to tag this record!

Description
Summary:	There is an urgent need to better understand the mechanisms underlying acute and long-term neurological symptoms after COVID-19. Neuropathological studies can contribute to a better understanding of some of these mechanisms. We conducted a detailed postmortem neuropathological analysis of 32 patients who died due to COVID-19 during 2020 and 2021 in Austria. All cases showed diffuse white matter damage with a diffuse microglial activation of a variable severity, including one case of hemorrhagic leukoencephalopathy. Some cases revealed mild inflammatory changes, including olfactory neuritis (25%), nodular brainstem encephalitis (31%), and cranial nerve neuritis (6%), which were similar to those observed in non-COVID-19 severely ill patients. One previously immunosuppressed patient developed acute herpes simplex encephalitis. Acute vascular pathologies (acute infarcts 22%, vascular thrombosis 12%, diffuse hypoxic-ischemic brain damage 40%) and pre-existing small vessel diseases (34%) were frequent findings. Moreover, silent neurodegenerative pathologies in elderly persons were common (AD neuropathologic changes 32%, age-related neuronal and glial tau pathologies 22%, Lewy bodies 9%, argyrophilic grain disease 12.5%, TDP43 pathology 6%). Our results support some previous neuropathological findings of apparently multifactorial and most likely indirect brain damage in the context of SARS-CoV-2 infection rather than virus-specific damage, and they are in line with the recent experimental data on SARS-CoV-2-related diffuse white matter damage, microglial activation, and cytokine release.
Bibliography:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23
ISSN:	1999-4915 1999-4915
DOI:	10.3390/v15040908