In a new study, researchers found hallmarks of brain damage caused by thinning and leaky brain blood vessels in tissue samples from COVID-19 patients who died shortly after contracting the disease.
In addition, 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.
The research was conducted by a team at the National Institutes of Health.
Although COVID-19 is primarily a respiratory disease, patients often experience neurological problems including headaches, delirium, cognitive dysfunction, dizziness, fatigue, and loss of sense of smell.
The disease may also cause patients to suffer strokes and other neuropathologies. Several studies have shown that the disease can cause inflammation and blood vessel damage.
In one of these studies, the researchers found evidence of small amounts of SARS-CoV-2 in some patients’ brains.
Nevertheless, scientists are still trying to understand how the disease affects the brain.
In this study, the team conducted an in-depth examination 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.
Many patients had one or more risk factors, including diabetes, obesity, and heart disease.
Eight of the patients were found dead at home or in public settings. Another three patients collapsed and died suddenly.
Initially, the researchers used 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.
These regions are thought to be highly susceptible to COVID-19. Olfactory bulbs control our sense of smell while the brainstem controls our breathing and heart rate.
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.
The researchers then 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.
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.
These results suggest that the damage we saw may not have been not caused by the SARS-CoV-2 virus directly infecting the brain.
In the future, the team plans to study how COVID-19 harms the brain’s blood vessels and whether that produces some of the short- and long-term symptoms.
One author of the study is Avindra Nath, M.D., the clinical director at the NIH’s National Institute of Neurological Disorders and Stroke (NINDS).
The study is published in the New England Journal of Medicine.
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