It was first detected in Wuhan, China, in December 2019, and by March 2021, the World Health Organization (WHO) declared it a global pandemic.
As of November 2, 2022, there have been over 628 million confirmed cases of COVID-19 worldwide, with more than 6.57 million deaths. Despite the availability of vaccines, COVID-19 continues to be a significant public health concern.
SARS-CoV-2 has been found to disrupt the immune system, leading to the production of various autoantibodies. This immune dysregulation can result in central nervous system (CNS) damage, either through direct infection of the CNS or as a result of an autoimmune response to the virus.
Studies have shown that SARS-CoV-2 can cross the blood-brain barrier and cause CNS demyelination. Consequently, there have been reports linking SARS-CoV-2 infection to CNS autoimmune demyelinating disorders such as transverse myelitis (TM), acute demyelinating encephalomyelitis (ADEM), multiple sclerosis (MS), and neuromyelitis optica spectrum disorder (NMOSD).
NMOSD is a chronic, relapsing autoimmune disorder characterized by severe CNS demyelination attacks, often affecting the spinal cord, optic nerves, brainstem, and area postrema.
The underlying mechanisms that lead to NMOSD are not fully understood, but evidence suggests that environmental factors, including viral infections and vaccinations, in combination with genetic susceptibility, contribute to CNS inflammation.
Given the ongoing prevalence of COVID-19, it is crucial to investigate the association between SARS-CoV-2 infection and neuroinflammatory conditions such as NMOSD.
This systematic review aims to assess the link between SARS-CoV-2 infection, post-infectious manifestations of NMOSD, and the potential association between COVID-19 vaccination and the development or relapse of NMOSD.
The literature review included 41 cases of NMOSD associated with SARS-CoV-2 infection or COVID-19 vaccination. The analysis revealed that these cases met standardized diagnostic criteria, with most patients developing neurological symptoms within two weeks of exposure.
The majority of cases responded well to standard immune therapies, and the overall neurological morbidity was moderate, with a mortality rate of 7%.
Previous case series and reports have demonstrated an association between NMOSD and various viral infections, such as Epstein-Barr virus, influenza virus, human immunodeficiency viruses (HIV), and varicella-zoster virus. SARS-CoV-2 infection has now been added to the list of potential risk factors for CNS demyelinating diseases, including NMOSD. Additionally, case reports have shown a connection between COVID-19 vaccinations and the onset of ADEM, TM, and MS.
The pathological mechanisms underlying the development of NMOSD after COVID-19 vaccination or SARS-CoV-2 infection are not fully understood. It is hypothesized that a combination of viral and vaccine-related factors, along with individual susceptibility, contributes to NMOSD pathogenesis.
SARS-CoV-2 can infect not only the respiratory system but also the central and peripheral nervous systems. Once the virus or vaccine enters the nervous system, various mechanisms, including molecular mimicry, immune-mediated injury, and blood-brain barrier permeability, may lead to NMOSD development.
Cytotoxic lesions of the corpus callosum (CLOCCs) have also been associated with COVID-19 vaccinations. The underlying pathogenic mechanism between vaccine-induced NMOSD and CLOCC.
The underlying pathogenic mechanism between vaccine-induced NMOSD and cytotoxic lesions of the corpus callosum (CLOCCs) is not yet fully understood. However, it is believed that an immune-mediated response triggered by the vaccine may play a role. The presence of autoantibodies, such as anti-MOG (myelin oligodendrocyte glycoprotein) antibodies, has been detected in some cases of NMOSD and CLOCCs following COVID-19 vaccination.
These autoantibodies may target specific components of the myelin sheath in the central nervous system, leading to demyelination and the characteristic neurological symptoms associated with NMOSD.
It is important to note that the occurrence of NMOSD or CLOCCs following SARS-CoV-2 infection or COVID-19 vaccination appears to be rare. The vast majority of individuals who receive the vaccine or contract the virus do not develop these neuroinflammatory conditions. The benefits of COVID-19 vaccination in preventing severe illness, hospitalization, and death from COVID-19 far outweigh the potential risks of these rare neurological complications.
Further research is needed to better understand the association between SARS-CoV-2 infection, COVID-19 vaccination, and the development or relapse of NMOSD and CLOCCs. Long-term surveillance and monitoring of vaccinated individuals, as well as continued investigation into the immunological and molecular mechanisms involved, will provide valuable insights into the relationship between COVID-19 and neuroinflammatory disorders.
If you or someone you know experiences neurological symptoms after receiving a COVID-19 vaccine or contracting SARS-CoV-2, it is important to seek medical attention promptly. Healthcare professionals can evaluate the symptoms, conduct appropriate diagnostic tests, and provide the necessary treatment and support.
Neuromyelitis optica spectrum disorder (NMOSD) is a rare autoimmune condition that affects the central nervous system, mainly the optic nerves and the spinal cord. NMOSD causes inflammation and damage to the protective covering of nerve fibers, called myelin, resulting in vision loss, muscle weakness, paralysis, pain, and bladder and bowel problems.
NMOSD can occur in people of any age, gender, or ethnicity, but it is more common in women and people of Asian or African descent. NMOSD is often misdiagnosed as multiple sclerosis (MS), because they share some similar symptoms and signs. However, NMOSD and MS have different causes, treatments, and outcomes.
Therefore, it is important to distinguish between them using specific blood tests and imaging techniques. NMOSD is caused by the presence of antibodies that target a protein called aquaporin-4 (AQP4), which is found on the surface of astrocytes, a type of brain cell that supports nerve cells.
These antibodies trigger an immune attack on the astrocytes and the surrounding myelin, leading to inflammation and damage. The exact reason why some people develop these antibodies is unknown, but genetic and environmental factors may play a role. NMOSD has no cure, but treatments are available to reduce the frequency and severity of attacks, prevent complications, and improve quality of life.
These treatments include immunosuppressive drugs that suppress the immune system and prevent further damage, plasma exchange that removes harmful antibodies from the blood, and symptomatic therapies that address specific problems such as pain, spasticity, or bladder dysfunction.
NMOSD is a serious and potentially life-threatening condition that requires prompt diagnosis and treatment. People with NMOSD should be monitored regularly by a neurologist who specializes in this disorder and follow a comprehensive care plan that includes medication adherence, rehabilitation, and supportive care.
reference link :https://www.frontiersin.org/articles/10.3389/fneur.2023.1099758/full