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Scientists have identified hallmarks of brain damage in a handful of patients after they died of coronavirus complications.
A team from the US National Institute of Neurological Disorders and Stroke (NINDS) analysed brain tissue post-mortem of 19 individuals, aged five to 73, between a few hours and several months after they died.
Scan results suggest the brain regions that control breathing, heart rate and sense of smell showed signs of inflammation and bleeding.
On closer inspection, the scientists found these regions were made up of thinned, clotted and “leaky” blood vessels, which are usually associated with strokes.
This is not the first time an issue like this has been flagged. In July, an expert warned it “remains to be seen” whether the coronavirus causes the same brain damage as Spanish flu.
Watch: How does severe coronavirus affect the brain?
“We found the brains of patients who contract infection from [the coronavirus] may be susceptible to microvascular blood vessel damage,” said NINDS study author Dr Avindra Nath.
“Our results suggest 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.”
The coronavirus was initially considered a respiratory infection, however, it is now known the pathogen can affect virtually any part of the body.
How this occurs is somewhat unclear. It has been suggested the virus may directly invade tissue or trigger an inflammatory response that affects many organs.
To learn more, the NINDS scientists analysed brain tissue samples from 16 patients who died in New York and three from Iowa.
The majority of the patients had an underlying health condition, like diabetes, obesity or heart disease.
A high-powered MRI scan analysed the patients’ olfactory bulbs – which control the sense of smell, and brainstems – which regulate breathing and heart rate.
The results – published in the New England Journal of Medicine – suggest that some patients had an abundance of “bright spots” called hyperintensities in both brain regions, often indicating inflammation.
Some also had dark spots, hypointensities, which imply bleeding.
After looking at these regions more closely, the scientists found nine of the patients’ bright spots were made up of blood vessels that were thinner than normal, sometimes leaking proteins into the brain.
These spots were surrounded by immune cells, suggested the immune system was involved in their onset or progression.
The dark spots – found in 10 patients – were made up of both clotted and leaky blood vessels, but showed no sign of an immune response.
“We were completely surprised,” said Dr Nath.
“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.”
The scientists did not find the coronavirus itself in the patients’ brain tissue, suggesting an inflammatory immune response or other biological pathway may have been to blame.
They stressed, however, the infection may have been cleared by the time of analysis or the virus present at too low numbers to be detected.
Dr Nath said so far, the results suggest the damage may not have been caused by the virus directly infecting the brain.
“In the future, we plan to study how COVID-19 [the disease caused by the coronavirus] harms the brain’s blood vessels and whether that produces some of the short- and long-term symptoms we see in patients,” he added.
How could coronavirus affect the brain?
In July, a small study by University College London (UCL) found a “higher than expected number of people” with the coronavirus showed signs of brain damage, with these patients not necessarily having severe respiratory symptoms.
Out of the 43 patients, 10 had transient encephalopathies, temporary brain dysfunction, alongside delirium or psychosis. Nine made a full recovery with just supportive care.
The UCL scientists also picked up on a dozen cases of brain inflammation, of which nine were acute disseminated encephalomyelitis (ADEM).
ADEM is defined as a “brief but widespread attack of inflammation in the brain and spinal cord”. This damages the fatty protective covering that surrounds nerves and allows electrical impulses to be transmitted.
Viral or bacterial infections are a recognised cause.
The scientists noted they typically see one ADEM case per month. This rose to an incident a week from around early March, the height of the UK’s first coronavirus wave.
Eight cases of stroke and eight other forms of nerve damage were also identified. The latter was mainly Guillain-Barré syndrome, a neurological condition that in severe cases leaves patients struggling to swallow, walk or even breathe.
Six of the eight patients with nerve damage made a “partial and ongoing recovery”.
UCL study author Dr Michael Zandi said at the time: “Whether we will see an epidemic on a large scale of brain damage linked to the pandemic – perhaps similar to the encephalitis lethargica [sleeping sickness] outbreak in the 1920s and 1930s after the 1918 influenza pandemic – remains to be seen.”
The 1918 Spanish flu pandemic left some patients enduring viral encephalitis, brain swelling that can occur if an infection enters the central nervous system.
Some survivors went on to develop viral Parkinsonism, defined as symptoms similar to Parkinson’s disease-like shaking and stiff movements.
Previous UCL research also found a “higher than expected number of [coronavirus] patients with stroke”, which was put down to the infection making blood “stickier”.
Experts have previously said “time will tell” how the coronavirus affects the brain, with some complications being “very likely” but rare.
Watch: Can you catch coronavirus twice?