COVID-19 Can be Deadly for the Nervous System
By: Sai Srihaas Potu
The coronavirus (COVID-19) outbreak in Wuhan, China has spread rapidly and now there have been over 2 million confirmed cases in the world. An increasing number of cases are known to have been caused by human to human interaction, but researchers still have many unanswered questions such as the source of the virus and the specific details behind its ability to spread between individuals. As of now, symptoms of COVID-19 include fever, dry cough, and fatigue. However, some physicians in affected areas have found that some patients diagnosed with COVID-19 have not shown typical respiratory symptoms, such as fever and coughing, at the time of diagnosis; rather, some infected patients have exhibited only neurological symptoms as the initial symptoms, such as the following: headache, languidness, unstable walking, and malaise. According to recent research, patients affected by COVID-19 can get a cerebral hemorrhage, cerebral infarction, and other deadly neurological diseases if primary symptoms worsen.
In a recent study of 214 patients with COVID-19, 78 (36.4%) patients had neurological manifestations, such as headache, dizziness, acute cerebrovascular diseases, and impaired consciousness. Of these 214 patients, 40 (18.7%) patients required intensive care unit (ICU) interventions for their severe neurological involvement. Currently, although there have been many cases of patients with COVID-19 complicated by cerebral hemorrhages, relevant studies on this association are lacking. Hence, the physiological relationship between COVID-19 and the incidence of cerebral hemorrhage remains unclear.
Based on several lines of evidence, it has been hypothesized that COVID-19 may involve cranial hemorrhage. First, recent studies have shown that this novel severe acute respiratory syndrome (SARS) coronavirus, SARS-CoV-2, invades human respiratory epithelial cells mediated by its S-proteins and angiotensin-converting enzyme 2 (ACE2) receptors on human cell surfaces, as ACE2 is required for SARS-CoV-2 to infect cells. ACE2 signaling lowers blood pressure. Since the expression of ACE2 is reduced in patients with hypertension, the ability of ACE2 to lower blood pressure is concomitantly reduced in these patients. Following SARS-CoV-2 infection, the expression and function of ACE2 proteins are reduced. Since the expression of ACE2 in patients with hypertension is already low, SARS-CoV-2 infection is more likely to induce cerebral hemorrhage in such patients. As a second line of evidence suggesting that SARS-CoV-2 infection may induce cerebral hemorrhage, patients with COVID-19 often suffer from coagulopathy and prolonged prothrombin time, both of which are also contributing factors to secondary cerebral hemorrhage. Hence, we speculate that COVID-19 also has the potential to induce cerebral venous and/or arterial infarctions. Finally, few studies have reported any cases of neurological damage associated with COVID-19. However, a previous study has shown that RNA sequences of the novel human-infectious coronavirus, HCoV-OC43, were detected in the cerebrospinal fluid of a 15-year-old child with acute demyelinating encephalomyelitis. SARS-CoV has also been detected in the sera and cerebrospinal fluids of two patients with persistent epilepsy and SARS. With the outbreak of COVID-19, people need to realize the severity of the disease to protect themselves and the people around them as well.
Without clear clinical symptoms in the patients mentioned above, the diagnosis of COVID-19 is starting to become even more challenging. Also, due to the absence of traditional respiratory symptoms, such patients with COVID-19 may ignore or be unaware of their illness until it becomes fatal. These patients with atypical presentations represent an important hidden source of the spread of the virus. Hence, protective measures need to be taken to ensure the safety of the public and stop the spread of COVID-19.
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