Early evidence of pronounced brain involvement in fatal COVID-19 outcomes

Pulmonary and heart failure are considered the primary causes of COVID-19-associated death, but the precise pathology of disease progression is unknown. [...]recent reports describe irregularities in coagulation for a subset of patients.1 Here we report the findings of autopsies of six patients (four men and two women, aged 58–82 years) who died from COVID-19 in April, 2020. Abundant experimental and animal model evidence of a neurogenic pathway for SARS CoV-2 via olfactory (CN I), trigeminal nerves (CN V), and the brainstem nuclei led us to look for evidence of localised brainstem alterations.4 In all brains examined, we observed localised perivascular and interstitial encephalitis with neuronal cell loss and axon degeneration in the dorsal motor nuclei of the vagus nerve, CN V, nucleus tractus solitarii, dorsal raphe nuclei, and fasciculus longitudinalis medialis, but no territorial infarctions (appendix). The most prominent changes were those of a diffuse alveolar damage with virus-induced epithelial changes, capillaritis, and organising pneumonia without interstitial collagen deposition.3,5,6 Intranuclear inclusion bodies were not observed.