Although SARS-CoV-2 is unlikely to infect the brain, it can significantly damage it, according to a new study of autopsies from 41 COVID-19 patients.
Researchers at Columbia University said they found no signs of virus in the patients ‘brain cells, but that they saw many brain disorders that could explain the confusion and delirium that was present in some patients with severe coronavirus and the persistent’ brain fog. ‘seen in those with a mild illness.
The study, which the authors call the largest COVID-19 brain autopsy report to date, covers the analysis of samples of autopsies conducted from March to June 2020 and was conducted late last week in Brain. According to them, the findings suggest that the inflammation caused by the coronavirus in other parts of the body or in the blood vessels of the brain could have caused the neurological abnormalities in the autopsies.
Lack of oxygen, cell death
The brain damage consisted of areas starving for oxygen, many of which were hemorrhagic, which the researchers said was probably caused by blood clots that temporarily blocked the flow of oxygen. Many activated microglia, or immune cells in the brain that can be activated by pathogens, have also been identified.
“We have found clusters of microglia that attack neurons, a process called ‘neuronophagy,'” co-senior author Peter Canoll, MD, PhD, said in a Columbia University press release.
Because no virus was observed in the brain, he said the microglia may have been activated by inflammatory cytokines, which have been linked to coronavirus infection. ‘At the same time, hypoxia [reduced oxygen from COVID-19] may cause the expression of ‘eat me’ signals on the surface of neurons, making hypoxic neurons more vulnerable to activated microglia. ‘
Most activated microglia are found in the lower brainstem, which is responsible for heart and breathing rhythms and levels of consciousness, and in the hippocampus, which is involved in mood and memory.
“We know that microglia activity will lead to loss of neurons, and that the loss is permanent,” co-senior author James Goldman, MD, PhD, said in the release. “Is there enough loss of neurons in the hippocampus to cause memory problems? Or in other parts of the brain that help draw our attention? It’s possible, but we really do not know at this stage.”
Implications for survivors
Of the 41 patients, 59% required intensive care, and about half required intubation. Hospital-related complications were common, including deep vein thrombosis or pulmonary embolism (20%), acute renal injury requiring dialysis (17%), and bacteremia (24%). About 20% of patients died within 24 hours of hospitalization, while 27% died 4 or more weeks after admission.
All the patients, who were on average 74 years old, had signs of virus-related lung damage. Sixty-six percent of the patients were male and 83% were Hispanic / Latino.
The authors said that future studies should be aimed at determining whether some COVID-19 survivors have any of these neurological disorders and whether they lead to chronic neurological deficits.
“In view of the brainstem and hippocampal distribution of microglial activation, the latter of which has been linked to cognitive deficits by viruses, it is noteworthy that some COVID-19 survivors develop neuropsychiatric symptoms, including memory disorders, drowsiness, fatigue and insomnia, and that insomnia. symptoms are reported in both the acute and recovery phases, ‘they wrote.
“This study included only patients who were seriously ill and died. These changes may not be seen in patients with a mild illness.”