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The Surprising Neuroscience of COVID-19

Effects on the central nervous system might contribute to respiratory failure.

A recent bulletin from physicians in the U.K. described the loss of smell and taste in COVID-19 patients, suggesting that the virus might affect parts of the central nervous system in addition to its well-known affinity for the respiratory system.

Indeed, in an earlier outbreak of coronavirus in China, Hong Kong researcher Dr. K.K. Lau and co-workers found that some patients exhibited convulsions, delirium, and restlessness, while Dr. Jun Xu, of the Guangzhou Institute of Respiratory Diseases, estimated that 4-5 percent of all SARS coronavirus patients displayed central nervous system symptoms. Some SARS coronavirus patients have even exhibited marked brain damage on CAT scans.

In the latest outbreak of coronavirus, evidence of central nervous system involvement is accumulating, such as a March 21 report by Dr. Asia Filatov of Charles E. Schmidt College of Medicine that a COVID-19 patient exhibited encephalopathy (brain disease). And recent data from Wuhan, described in the March 12 edition of Neurology Today, indicate that neurological symptoms, such as "altered consciousness," occur in up to one-third of COVID-19 cases.

But could the central nervous system action of COVID-19 directly contribute to the acute respiratory distress associated with the disease?

The answer might be "yes" according to recent collaborative research from Drs. Yan-Chao Li, Wan-Zhu Bai, and Tsutomu Hashikawa.

Writing in the February 27 edition of the Journal of Medical Virology, Li and colleagues cite research on the coronavirus showing that sometimes SARS-Cov infects the brainstem centers that control respiration, making it difficult for infected patients to breathe spontaneously.

Li et al. go on to say that if COVID-19 behaves the same way that its close relative, SARS-Cov, does, COVID-19 could spread from the lungs to the brain through neuronal fibers (axons) that connect lung chemoreceptor neurons (which monitor oxygen levels in the blood) and mechanoreceptors (which monitor lung expansion and contraction in order to regulate respiration) to neurons in the medulla oblongata that control both heart rate and respiration rate. Li et al. suggest when the virus travels from the lung to the medulla, then crosses synapses to cardiorespiratory neurons in the brain, those infected cardiorespiratory neurons may cease to function properly, inhibiting spontaneous breathing.

The researchers conclude that a deeper understanding of the way that COVID-19 infection of the brain might contribute to respiratory collapse could lead to better methods of preventing and treating the acute respiratory failure associated with the disease.


Li YC1, Bai WZ2, Hashikawa, The neuroinvasive potential of SARS-CoV2 may play a role in the respiratory failure of COVID-19 patients. T3. J Med Virol. 2020 Feb 27. doi: 10.1002/jmv.25728. [Epub ahead of print]