Published in final edit form as of 2020 April 4.
Young Scientists Journal
Abstract: Coronaviruses, first identified in the mid-1960s, are characterized by the club-like projections on their surface, an unusually large RNA genome, and a distinctive replication strategy. A variety of diseases in both mammals, including potentially lethal human respiratory infections, and birds are directly caused by this viral domain. Society has exhibited the fatal nature of a number of species branching from the larger group of coronaviruses in the past, as evident by the SARS-CoV and MERS-CoV outbreaks of 2002 and 2012, respectively. These and the novel 2019-nCoV are types that evolve from animal to human infection. The current and increasing death toll, largely inclusive of those of old age or victim to underlying diseases, is indicative of the virus’s pathogenicity. With dry cough, difficulty breathing, and fatigue being a selected few of the common symptoms of COVID-19, it is apparent that those carrying asthma, diabetes, or heart disease stand with greater vulnerability in combating the virus. Illness branching from the nervous system and/or brain, however, is often unaccounted for amid the global panic and emotional toll associated with the surge of patients in healthcare facilities. The neuroinvasive potential of SARS-CoV2 has proven to be substantial with an increasing number of patients developing signs of brain ailments.
Key Terms: CT scans, Cytokine storm, dementia, MERS-CoV, 2019-nCoV, MRI scans, necrotizing encephalopathy neuroinvasive, Parkinson’s disease, pathogenicity, SARS-CoV, SARS-CoV2, stroke
Commentary: While the typical symptoms of COVID-19 include fever, respiratory difficulties, a subset of the COVID-19 patients are developing serious impairments of the brain. Conditions that are more so triggered by viral infections such as influenza A, influenza B, and human herpesvirus 6 have developed with linkage to COVID-19. CT scans have revealed causal relations between COVID-19 and confusion, lethargy, and disorientation. As in the case of a recent patient, symmetrical tissue damage in the thalamus -- a structure serves as a relay center through which sensory nerves transmit signals from the spinal cord and brainstem in direction of the cerebral cortex -- of the brain progressed to signs of hemorrhage, or bleeding from a rupture vessel. Additional MRI scans hinted at the possibility of coma, liver dysfunctionality, and neurological deficits. The patient was, thus, diagnosed with necrotizing encephalopathy, which is characterized by multiple bilateral brain lesions, mainly involving the thalami. Diagnosis, however, also shows involvement of putamina (one of the nuclei that make up the basal ganglia; aids in movement of the limbs), internal (white matter structure that is located in the inferomedial part of each cerebral hemisphere of the brain) and external capsules (series of white matter fiber tracts in the brain), cerebral white matter (tissue in the brain that is composed of nerve fibers), and the brainstem tegmentum (an area of the brainstem) as major components of the brain. A cytokine storm (a severe immune reaction in which the body releases too many cytokines in the body in relative unison, potentially resulting in hyperinflammation and multiple organ failure) have further complicated the patient’s situation. With the mortality rate being 70% and the precise etiology being unknown, death is largely patent, despite supportive treatment.
It is necessary to grasp a fundamental yet necessary understanding of the cardiovascular implications of the virus in treating those who may be carrying a history of stroke, sensory loss, and necrotizing encephalopathy, etc. SARS-CoV2 enters human cells by means of a ACE2, a receptor that is expressed by many human cell types, including kidney, lung, heart, intestine, and brain tissue. The virus may circulate in the blood and attack ACE2 receptors in the endothelia (a single layer of cells lining various organs and cavities of the body) of blood capillaries in the brain, crossing the blood-brain barrier. In this way, the virus may cause the brain to swell and the brainstem to compress as a result of the invasion of the central nervous system. A weakened sense of smell, as reported by a number of COVID-19 patients, leads to the following notion associated with routes to the brain: if the virus has the potential to infect the nose, then the possibility of accessing the brain’s frontal lobes by means of the olfactory bulb is relatively sound, despite the fact that proof of neural infection via the nasal tract has only been found upon experimentation with mice. Through the nasal cavity, the virus can manage to travel to the olfactory mucosa, which consists of epithelium cells, blood vessels, and the axons of olfactory neurons. This region is connected to the olfactory bulb via small openings called the cribriform plate. This plate is situated at the base of the brain’s frontal lobes; this proximity endangers the tissue located deeper in the brain. With progression, infection of the brainstem, particularly of the medulla (helps regulate breathing, heart and blood vessel function, digestion, sneezing, and swallowing), may result in damaged cardiorespiratory functioning.
The elderly are particularly vulnerable at the onset of crisis. With the aggressive spread of SARS-CoV2, those who carry neurological disorders, such as Parkinson’s and Alzheimer’s (also referred to as senile dementia), are living with great concern. Low blood pressure, respiratory issues, and the heightened likelihood of developing pneumonia and infections accompany Parkinson’s. Social distancing and stay-home protocol must be followed to maintain safety. The individual must reside in a facility with around-the-clock care and facilities. Those with dementia, on the other hand, may have difficulty remembering safety recommendations, such as washing hands often, or in understanding the public health information issued to them. Lacking sufficient self-quarantine measures and ignoring warnings could increase the chances of infection among this population.
Neurological symptoms (e.g. loss of taste or smell, seizures, twitching), in accordance with the discussion thus far, are significant pieces of data in determining treatment methods for patients. Reports of such can allow for efficient triaging of patients. Postmortem examinations, infact, suggest the significance of understanding the role of nerve damage in the progression of COVID-19. The brain, in many cases, may be the source of complication, but is often overlooked amid the heightened emphasis on the respiratory tract, as indicated by the minimal neural data derived from autopsies.
Work Cited:
“Acute Necrotizing Encephalopathy.” Genetic and Rare Diseases Information Center. U.S. Department of Health and Human Services. Accessed April 5, 2020. https://rarediseases.info.nih.gov/diseases/13233/acute-necrotizing-encephalopathy.
“Coronavirus.” Centers for Disease Control and Prevention. Centers for Disease Control and Prevention, February 15, 2020. https://www.cdc.gov/coronavirus/types.html.
“Coronavirus: What You Need to Know.” Alzheimer's San Diego, March 24, 2020. https://www.alzsd.org/coronavirus-what-you-need-to-know/.
“Coronaviruses.” National Institute of Allergy and Infectious Diseases. U.S. Department of Health and Human Services. Accessed April 5, 2020. https://www.niaid.nih.gov/diseases-conditions/coronaviruses.
Fehr, Anthony R, and Stanley Perlman. “Coronaviruses: an Overview of Their Replication and Pathogenesis.” Methods in molecular biology (Clifton, N.J.). U.S. National Library of Medicine, 2015. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4369385/.
St-Amant, Maxime. “Acute Necrotizing Encephalopathy: Radiology Reference Article.” Radiopaedia Blog RSS. Accessed April 5, 2020. https://radiopaedia.org/articles/acute-necrotising-encephalopathy?lang=us.
“Top Questions and Answers on COVID-19 and Parkinson's Disease.” Parkinson's Foundation. Accessed April 5, 2020. https://www.parkinson.org/blog/COVID-19-questions.
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