Infectious Disease

Controlling irritation may very well be important in neurological issues from COVID-19

January 08, 2021

2 min read

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Nath does not report any relevant financial information. In the study you will find all relevant financial information from all other authors.

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Post-mortem testing in a convenience sample of patients who had died from COVID-19 showed multifocal microvascular injury to the brain and olfactory bulbs with no evidence of viral infection.

The results of the correspondence, published in the New England Journal of Medicine, “could influence the interpretation of the changes observed on MRI from punctiform hyperintensities and linear hypointensities in patients with COVID-19,” the researchers said. However, due to the limited clinical information available, the researchers also noted that “no conclusions” could be drawn regarding the neurological characteristics of COVID-19.

Healio Neurology spoke with Avindra Nath, MD, Head of the Division of Nervous System Infections and Clinical Director of the National Institute of Neurological Disorders and Stroke at the NIH to learn more about the results.

Q: What prompted this research?

A: Most patients with COVID-19 have neurological manifestations; However, the mechanisms by which they occur are largely unknown. We tried to determine the underlying pathology in the brain to look for clues, specifically to determine the extent to which the virus might be present in brain cells, to determine the integrity of the brain cells and blood vessels in the brain, and if there is any evidence of inflammation in the brain.

Q: what did? The results show?

A: Patients with COVID-19 often have neuropathological findings that may have been asymptomatic at the time of acute infection. Some patients may die suddenly from the infection without warning. For example, in our study, some patients died in their sleep, one was found dead on the New York subway, and another patient who was lifting his sister fell down and died.

Patients often have multifocal brain disease that can easily be missed on pathological examination. However, we used high resolution postmortem MRI scans which pinpointed exactly where the lesions were. This enabled us to return to the regions of the brain to study by histological examination.

We found that there were many foci of small blood vessel damage from which blood products leaked into the brain tissue. The reason for this was not clear, but it is most likely due to damage by the immune cells or lymphocytes. We found some lymphocytes attached to the endothelial cells in the blood vessels and in the perivascular regions. The inflammatory response is key to the neuropathogenesis of this syndrome as we were unable to find a virus in the brain.

The study may have important implications for the long-term damage to several structures in the brain, particularly the olfactory bulb and brain stem.

Q: How could these results be used in clinical practice?

A: The important practical implication is that controlling inflammation could be key to managing the neurological complications of COVID-19.

Q: What are the next steps in this research?

A: We further characterize the inflammation in these patients’ brains to determine what triggered it and to determine the types of inflammatory molecules that are produced. We are recruiting a cohort of so-called COVID-19 long-distance drivers to see if microvascular injuries and inflammation could trigger their illness.

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