COVID-19 Can Cause Brain Damage Without Infiltrating Tissue

COVID-19 is known to cause neurological complications in patients who test positive for the virus, but new research from the National Institutes of Health (NIH) has revealed that SARS-CoV-2 does not always find its way into the brains of infected patients.

Based on findings from high-powered MRI scans, researches from the NIH determined that these neurological responses are a result of the body’s inflammatory response to the virus rather than the virus actually making its way into the brain. They published their findings recently in the New England Journal of Medicine.

Instead of detecting evidence of SARS-CoV-2 in the brains of 19 patients who died shortly after contracting the virus, the investigators repeatedly identified damage from thinning and leaky brain blood vessels. These findings indicate the neurological damage was not caused by a direct viral attack on the brain.

“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,” said senior study author Avindra Nath, M.D., clinical director for the NIH National Institute of Neurological Disorders and Strokes (NINDS). “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.”

Even though COVID-19 is primarily respiratory in nature, it frequently leads to neurological problems, as well, including headaches, cognitive dysfunction, dizziness, and loss of smell. In more severe cases, viral infection has been associated with stroke, as well as inflammation and blood vessel damage.

Nath’s team used MRI scanners that were four-to-10 times more sensitive than standard MRI scanners to try to figure out how the COVID-19 virus affects the brain. To do so, they took brain tissue samples from 19 patients between the ages of 5 and 73 who died after testing positive for the virus between March 2020 and July 2020. These individuals died within a few hours to two months of first reporting symptoms, and many had one or more risk factors, such as diabetes, obesity, and cardiovascular disease. Sixteen patients came from New York City, and three were from Iowa.

The team concentrated on tissue from the olfactory bulb and brain stems because they are believed to be two areas that are highly susceptible to the virus. While they anticipated seeing damage caused by lack of oxygen, they were, instead, surprised. Not only did they find no evidence of genetic material or protein from SARS-CoV-2, but they also unearthed damage that usually accompanies a stroke or other neuroinflammatory disease, Nath said.

Based on the MRI scans, they saw both regions had a high number of hyperintensities, indicating inflammation, as well as hypointensities, revealing bleeding. A more in-depth look with a microscope revealed thinner-than-normal blood vessels that were leaking blood proteins, such as fibrinogen, into the brain, potentially triggering an immune reaction. These hyperintensities were also surrounded by T cells from the patient’s blood and microglia. Hypointensities contained clotted and leaky blood vessels without any immune response, the team said.

While unexpected, the team said, these findings can help inform how investigators examine this virus going forward.

“So far, our results suggest that the damage we saw may not have been caused by the SARS-CoV-2 virus directly infecting the brain,” Nath said. “In the future, we plan to study how COVID-19 harms the brain’s blood vessels and whether that produces some of the short- and long-term symptoms we see in patients.”

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