A new study by the National Institutes of Health researchers spotted hallmarks of damage caused by thinning and leaky brain blood vessels in tissue samples from patients who died shortly after contracting Covid-19.

However, they saw no signs of SARS-CoV-2 in the tissue samples, suggesting the damage was not caused by a direct viral attack on the brain.

Avindra Nath, MD, clinical director at the NIH's National Institute of Neurological Disorders and Stroke (NINDS) and the senior author of the study said: “We found that the brains of patients who contract infection from SARS-CoV-2 may be susceptible to microvascular blood vessel damage.”

“Our results suggest that this may be caused by the body's inflammatory response to the virus. We hope these results will help doctors understand the full spectrum of problems patients may suffer so that we can come up with better treatments,” he added.

Neurological implications

Earlier studies have shown that Covid-19 also has neurological implications. These include headaches, delirium, cognitive dysfunction, dizziness, fatigue and loss of the sense of smell.

Several studies have revealed that the disease can cause inflammation and blood vessel damage.

For the new study, the researchers conducted an in-depth analysis of brain tissue samples from 19 patients who had died after experiencing Covid-19 between March and July 2020. The patients died at a wide range of ages, from 5 to 73 years old. They died within a few hours to two months after reporting symptoms.

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The researchers employed a special, high-powered magnetic resonance imaging (MRI) scanner that is 4 to 10 times more sensitive than most MRI scanners, to examine samples of the olfactory bulbs and brainstems from each patient.

The scans revealed that both regions had an abundance of bright spots, called hyperintensities, that often indicate inflammation, and dark spots, called hypointensities, that represent bleeding.

They found that the bright spots contained blood vessels that were thinner than normal and sometimes leaking blood proteins, like fibrinogen, into the brain. This appeared to trigger an immune reaction.

The spots were surrounded by T cells from the blood and the brain's own immune cells called microglia. In contrast, the dark spots contained both clotted and leaky blood vessels but no immune response, the study noted.

"We were completely surprised. Originally, we expected to see the damage that is caused by a lack of oxygen. Instead, we saw multifocal areas of damage that is usually associated with strokes and neuroinflammatory diseases," said Nath.

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Finally, the researchers saw no signs of infection in the brain tissue samples even though they used several methods for detecting genetic material or proteins from SARS-CoV-2.

“So far, our results suggest that the damage we saw may not have been not caused by the SARS-CoV-2 virus directly infecting the brain,” said Dr Nath.

The findings of the study were published in the New England Journal of Medicine.