A small study carried out by NIH researchers suggests that severe COVID-19 can damage the brain via the excessive inflammatory response seen in severe cases of the disease.

MRI scans showed damage to small blood vessels in the brain, but no signs of viral RNA were found in tissue samples, leading to the theory that the severe immune reaction seen in patients hospitalized with COVID-19 is likely to blame for this damage.

“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 Avindra Nath, M.D., clinical director at the NIH’s National Institute of Neurological Disorders and Stroke in Bethesda, who was one of the lead researchers behind the study.

Although infection with SARS-CoV-2 is thought of as a respiratory illness and does indeed have a serious impact on the lungs, it also has a neurological impact on the body. For example, a range of symptoms from headaches to cognitive dysfunction to delirium, as well as the well-publicized loss of taste and smell have been reported in patents with COVID-19.

Nath and colleagues aimed to assess in more detail what impact infection with SARS-CoV-2 has on the brain of patients with severe COVID-19.

In a collaboration between NIH researchers based in New York, Maryland, Michigan, and Iowa, tissue samples were taken from 19 patients who were infected with the virus when they died – 16 from New York City and 3 from Iowa City. The people who died had a confirmed infection with SARS-CoV-2 when they died and ranged in age from 5 to 73 years, most also had comorbidities of some sort.

As reported in a correspondence article in the New England Journal of Medicine, the researchers carried out high powered MRI scans on the brains of 13 of the people included in the study and found signs of damage in 10 of them. On further examination of the areas of damage, it showed up as abnormalities in the small blood vessels in the brain, which also showed signs of fluid leakage.

However, additional investigation looking at postmortem tissue samples from these patients did not pick-up signs of viral infection in the brain cells. These results suggest the damage was caused by the excessive immune reaction experienced by most patients that die from COVID-19, which has also been shown to cause tissue damage in many organs around the body.

“Originally, we expected to see 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.

“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… 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.”