Multifactorial White Matter Damage in the Acute Phase and Pre-Existing Conditions May Drive Cognitive Dysfunction after SARS-CoV-2 Infection: Neuropathology-Based Evidence.
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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
Аннотация
METHODS: We conducted a detailed postmortem neuropathological analysis of 32 patients who died due to COVID-19 during 2020 and 2021 in Austria.
RESULTS: 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%).
CONCLUSIONS: 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.