Neurological complications of COVID-19 are common – in about half of the patients hospitalized. These include protective pain, dizziness, myalgia, changes in consciousness, disturbances in smell and taste, weakness, strokes, and convulsions. In severe patients, the proportion of neurological diseases is higher than in patients with less severe forms. It remains unclear which of the neurological problems are specific to COVID-19.
The coronavirus causes COVID-19 is an RNA virus of the Coronaviridae family. It contains several proteins in its structure: spike protein, or S-protein, envelope or E-protein, membrane or M-protein, and nucleocapsidor N-protein).
The S protein is responsible for attaching to the host cell. Due to the high similarity of the S-protein with angiotensin-converting enzyme 2 (ACE2), the ACE2 receptors become a target for SARS-Cov-2, respectively, coronavirus can enter any cell of the human body that contains the ACE2 receptor. The virus then initiates the assembly of its proteins in the ribosome of the host cell and is released through exocytosis.
The gates of infection in COVID-19 can be epithelial and smooth muscle cells of the respiratory tract, kidneys, esophagus, bladder, ileum, heart, and the central nervous system. By far the fastest and most easily achievable target is type 2 alveolocytes, so the first and typical symptoms of SARS-CoV-2 infection include coughing, shortness of breath, fever, weakness, often as manifestations of viral pneumonia.
COVID-19 can cause long-term damage to the central nervous system several years after infection. Therefore, examine the study whether it can lead to cognitive decline, Alzheimer’s, Parkinson’s, or other forms of dementia.
There is currently no evidence that the coronavirus can actually cause Alzheimer’s in the future. The virus is able to enter the brain – there is already the first evidence that the coronavirus is able to infect neurons in the brain through the mucous membranes after passing through the nose. Previous research also suggests that COVID-19 can cause delirium, stroke, and even paralysis.
All the above, and in addition, the ability of the virus to persist from two to five days on surfaces at a temperature of 18–25 °C, undoubtedly determines its belonging to highly contagious diseases.
Mortality in COVID-19 is not fully understood and is approximately 3-4%. However, the indicators for countries vary from 0.1 to 11%, which can be explained by the specifics of testing the population (from selective testing of severe cases to total screening) and the peculiarities of the sample of sick patients.
So, according to the World Health Organization, mortality in COVID-19 increases with age and is
- 0.4% in patients 40-49 years old
- 1.3% – 50-59 years old
- 3.6% – 60-69 years old
- 8, 1% – 70–79 years
- More than 14.9% of patients over 80 years old.
There is a correlation between concomitant diseases and mortality in COVID-19: the highest mortality was found in comorbid cardiovascular pathology (13.2%), diabetes mellitus (9.2%), arterial hypertension (8.4%), chronic respiratory diseases (8.1%). The relationship between the severity of COVID-19 and concomitant cardiovascular pathology is understandable given the high tropism of this virus to target cells containing ACE2 receptors.
All about pandemic
Based on the current knowledge about the pathogenesis of COVID-19, it can be assumed that damage to the nervous system in this disease can cause not only direct contact with the virus, but also immune inflammation, hypoxia, and hypoxemia against the background of acute respiratory distress syndrome, as well as increased tendency to thrombosis and at the same time the risk of hemorrhage against the background of disseminated intravascular coagulation syndrome.
The scientists analyzed the structure of SARS-CoV-2 proteins and, based on three-dimensional modeling, showed that the ORF8 protein can bind to porphyrin, and the ORF10 protein can attack the 1-beta chain of hemoglobin and bind to heme. Based on the data obtained, the authors suggested that these structural features of the virus can be an additional substrate for hypoxemia, as well as explain the mechanism of viremia in adult patients and a milder course of the disease (given the different structure of hemoglobin) in children. Note that this computationally based study was immediately criticized for lack of experimental evidence.
Thus, the data available to date suggest the possibility of damage in COVID-19 and the central and peripheral nervous systems. The most typical manifestation is ischemic stroke, especially in patients with severe and moderate disease and concomitant cardiovascular pathology. Damage to the nervous system is realized through the direct action of the virus, as well as due to autoimmune damage to the nervous system against the background of a cytokine storm as a result of hypo- and hypercoagulation with an exacerbation of an existing cardiovascular pathology or the development of a new disease (for example, myocarditis). Of course, because of the entire five-month incidence of COVID-19, it is impossible to draw full conclusions about the frequency and prevalence of neurological manifestations of the disease, as well as about delayed complications.
Now, thanks to our article, you have learned all the necessary information about the neurological manifestations of COVID-19.