Olfactory transmucosal SARS-CoV-2 invasion as a port of central nervous system entry in individuals with COVID-19.

The newly identified severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes COVID-19, a pandemic respiratory disease. Moreover, thromboembolic events throughout the body, including in the CNS, have been described. Given the neurological symptoms observed in a large majority of individuals with COVID-19, SARS-CoV-2 penetrance of the CNS is likely. By various means, we demonstrate the presence of SARS-CoV-2 RNA and protein in anatomically distinct regions of the nasopharynx and brain. Furthermore, we describe the morphological changes associated with infection such as thromboembolic ischemic infarction of the CNS and present evidence of SARS-CoV-2 neurotropism. SARS-CoV-2 can enter the nervous system by crossing the neural-mucosal interface in olfactory mucosa, exploiting the close vicinity of olfactory mucosal, endothelial and nervous tissue, including delicate olfactory and sensory nerve endings. Subsequently, SARS-CoV-2 appears to follow neuroanatomical structures, penetrating defined neuroanatomical areas including the primary respiratory and cardiovascular control center in the medulla oblongata.

Superior Canal Dehiscence: A Comparative Postmortem Multislice Computed Tomography Study.

OBJECTIVE: Superior canal dehiscence is defined by missing bony coverage of the superior canal against the middle cranial fossa. The gold standard in diagnosis is high-resolution computed tomography (CT). A false-positive CT scan, identifying a dehiscence when one is not present, could lead to unnecessary surgical therapy. This study aims to compare postmortem CT scans with autopsy findings with regard to superior canal dehiscence. STUDY DESIGN: Postmortem study. SETTING: Tertiary referral center. SUBJECTS AND METHODS: Twenty-two nontraumatic death cases within a 3-month period (January to March 2017) were included with 44 temporal bones. Each body underwent postmortem head CT prior to medicolegal autopsy. The middle fossa floor was exposed, and if present, the superior semicircular canal dehiscence was identified and measured. In each case, 3 comparable photographs were taken during the autopsy (left temporal bone, right temporal bone, overview). RESULTS: Autopsy findings revealed bony dehiscences in 11% of the temporal bones, whereas CT scan revealed bony dehiscences in 16%. The length of the dehiscences were longer when measured by CT imaging. CONCLUSION: The diagnosis of superior canal dehiscence syndrome requires high-resolution CT with clinical symptoms and physiologic evidence of a third mobile window. Our study underlines a mismatch between multislice CT imaging in the coronal plane and the presence of a dehiscence on autopsy.