Neurological Effects in COVID-19 Patients

Aayushi Gaur, U. I. E. T., Kurukshetra University

Doctors battled to keep patients breathing in the early months of the COVID-19 pandemic, focusing mostly on treating lung and circulatory system damage. However, evidence of neurological consequences was already collecting at the time. Some COVID-19 patients were suffering from delirium, which manifested as confusion, disorientation, and agitation. The first report of someone with COVID-19 who experienced edema and inflammation in brain tissues was reported in April by a group in Japan.

A patient with degradation of myelin, a fatty covering that shields neuron and is irreversibly destroyed in neurodegenerative disorders such as multiple sclerosis, was reported in another report. Alysson Muotri, a neurologist at the University of California, San Diego is of the opinion that the neurological symptoms are becoming all the way more scary.

As a woman claimed Lions and monkeys had been observed at the woman’s home. She was becoming increasingly disoriented and hostile toward others, certain that her spouse was a fraud. She was in her mid-50s, decades older than the average onset of psychosis, and had no prior mental history. COVID-19 was something she did have. Hers was one of the earliest documented examples of a person suffering from psychosis after getting the illness.

Stroke, brain hemorrhage, and memory loss are now on the list. Serious illnesses are known to induce such symptoms, but the size of the COVID-19 pandemic implies that thousands, if not tens of thousands, of individuals, may already be experiencing them, with some having permanent consequences.

Although viruses have the ability to infiltrate and infect the brain, it is unclear whether SARS-CoV-2 does so to a substantial degree. Overstimulation of the immune system might be to blame for the neurological symptoms. It’s critical to figure out since these two circumstances necessitate very different approaches. Benedict Michael, a neurologist at the University of Liverpool, UK, believes that this is the reason why looking into disease mechanisms are so essential.

Patient’s Case Studies

Research published in July stated that it gathered 43 comprehensive case reports of patients who had COVID-19-related neurological problems. Michael Zandi, a neurologist at University College London and one of the study’s primary authors mentions that certain patterns are emerging. Stroke and encephalitis are the most frequent neurological side effects. Acute disseminated encephalomyelitis, in which both the brain and spinal cord are inflamed and neurons lose their myelin coverings, can lead to symptoms similar to multiple sclerosis. Only minor respiratory symptoms were present in several of the worst-affected individuals.

Peripheral nerve injury, which is prevalent in Guillain–Barré syndrome, and “a hodgepodge of things,” such as anxiety and post-traumatic stress disorder, are less common consequences. SARS and Middle East respiratory disease (MERS), both caused by coronaviruses, have exhibited similar symptoms. However, because there were fewer persons sick during earlier epidemics, there are fewer statistics available.

At least 0.04% of patients with SARS and 0.2% of those with MERS had symptoms affecting the central nervous system. Given that COVID-19 has now been verified in 197 million people throughout the world, this might mean that between 10,000 and 50,000 people have had neurological problems. Clinical investigations have usually focused on patients with COVID-19 who were hospitalized, especially those who required acute care, which makes estimating instances difficult. This group may have a higher than 50% prevalence of neurological symptoms.

Neuroscientist’s Say

For many neuroscientists, the most important topic is why the brain is altered at all. Although the pattern of diseases is pretty similar, De Felice adds the underlying processes are yet unknown.

Finding an answer will assist physicians in selecting the most appropriate therapies. These patients should be administered with remdesivir or other antiviral drugs if the viral infection is detected in the central nervous system. If the virus is not detected in the CNS it could mean that the virus has left the body and treatment of anti-inflammation therapeutics will suffice. 

The ability of SARS-CoV-2 to infect neurons has clearly been demonstrated. Muotri’s research specializes in the development of “organoids” which are small clusters of brain tissue that are developed into neurons by coaxing pluripotent human stem cells. SARS-CoV-2 might infect neurons in these organoids, killing some and decreasing the development of connections between them, according to a May preprint. As per the preprint released on the 8th of September work by immunologist Akiko Iwasaki and her colleagues done at Yale University School of Medicine appears to supports the using of human organoids, mouse brains, and certain post-mortem exams. However, the virus’s ability to penetrate people’s brains remains a mystery.

In late May, a team led by Mary Fowkes, a pathologist at Mount Sinai’s Icahn School of Medicine, published a preprint documenting post mortems in 67 persons who had died with COVID-19. “We’ve seen the virus in the brain itself,” adds Fowkes, who used electron microscopes to confirm his suspicions. However, virus levels were modest and not always detectable. As loss of smell is such a frequent complaint, neurologists wondered if the olfactory nerve could be used to get access. Furthermore, if the virus entered the brain via the olfactory nerve, the afflicted brain area should be the first to be impacted, but that was not the case, because Fowkes wasn’t able to see the virus in the olfactory bulb. It can be deduced that the infections in the brain, she claims, are tiny and concentrate around blood arteries.

Conclusion

In comparison to other organs, viruses are difficult to locate in the brain. Despite their great sensitivity, polymerase chain reaction (PCR) tests often fail to identify it there, and numerous investigations have failed to locate virus particles in the cerebrospinal fluid (CSF) that surrounds the brain and spinal cord. One reason might be that the ACE2 receptor, a protein found on human cells that the virus utilizes to enter, is not highly expressed in brain cells. Biomarkers that can effectively discriminate between a viral brain infection and immunological activity will be needed, according to experts. For the time being, this implies additional clinical research, autopsies, and physiological investigations.

Also read: Hirschsprung disease patients show novel gene revelations!

References:

1. Paterson, R. W., Brown, R. L., Benjamin, L., Nortley, R., Wiethoff, S., Bharucha, T., Jayaseelan, D. L., Kumar, G., Raftopoulos, R. E., Zambreanu, L., Vivekanandam, V., Khoo, A., Geraldes, R., Chinthapalli, K., Boyd, E., Tuzlali, H., Price, G., Christofi, G., Morrow, J., … Zandi, M. S. (2020). Emerging spectrum of COVID-19 neurology: clinical, radiological and laboratory findings. Brain, 143(10), 3104-3120. https://doi.org/10.1093/brain/awaa240https://academic.oup.com/brain/article/143/10/3104/5868408 .  
2. Ghannam, M., Alshaer, Q., Al-Chalabi, M., Zakarna, L., Robertson, J., & Manousakis, G. (2020). Neurological involvement of coronavirus disease 2019: a systematic review. Journal of neurology, 267(11), 3135–3153. https://doi.org/10.1007/s00415-020-09990-2.

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