Article Text

Download PDFPDF
Correspondence
Brain autopsies in fatal COVID-19 and postulated pathophysiology: more puzzling than a Rubik’s cube
  1. Sudhir Mehta1,
  2. Sudhir Bhandari1,
  3. Shaurya Mehta2
  1. 1 Department of Medicine, SMS Medical College (University Medical School), Jaipur, Rajasthan, India
  2. 2 Department of Nephrology, Jaslok Hospital & Research Centre, Mumbai, Maharashtra, India
  1. Correspondence to Professor Sudhir Mehta, Department of Medicine, SMS Medical College (University Medical School), Jaipur, Rajasthan 302004, India; s.smehta{at}hotmail.com

Statistics from Altmetric.com

Request Permissions

If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.

The Editor

A little over century after the 1918 influenza pandemic, the world is witnessing another pandemic of similar magnitude, caused by SARS-CoV-2 and affecting nearly 215 countries. Although SARS-CoV-2 primarily affects the lungs, neurological presentations are being recognised with increasing frequency. Recently, Ellul and colleagues1 have elaborated a spectrum of neurological diseases in 901 patients of COVID-19. Here, we describe three case series of brain autopsies2–4 that have revealed distinctly different pathologies, failing to explain the common pathobiological mechanism of central nervous system (CNS) involvement in severe COVID-19.

Solomon et al 2 reported histopathological changes in autopsies of 18 patients with COVID-19 from a teaching hospital. Gross inspection showed no changes suggestive of acute stroke, herniation or olfactory bulb damage. Microscopic examination revealed changes of acute hypoxia in the cerebrum and cerebellum in 100% of patients with COVID-19, with neuronal loss in various structures like cerebral cortex, hippocampus and cerebellar Purkinje cell layer. There were no findings of thrombosis or vasculitis. Focal …

View Full Text

Footnotes

  • Handling editor Runjan Chetty.

  • Contributors All authors contributed equally to the manuscript.

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Competing interests None declared.

  • Provenance and peer review Not commissioned; internally peer reviewed.