https://www.medscape.com/viewarticle/928424?src=soc_fb_200411_mscpedt_news_mdscp_neuro&faf=1&fbclid=IwAR0c9ubahCR0XtVio8hi2KVDJ2fmVzU0mkuT4HLLb3qDQRH1BpvgxNJIq3c You can see this information as well.
-Previous viral phylogenetic studies, experimental research in mice and viral receptor analysis in humans suggest that SARS-CoV2 is potentially neurotrophic.
- From the experiences of previous epidemics with SARS-CoV and MERS-CoV, it is estimated that neurological clinical manifestations may be immediate or long-term.
- Clinical studies in patients hospitalized with COVID-19 reveal neurological manifestations in approximately 40% of cases.
- Loss of olfaction and taste appear early in 60% of cases and may be associated with direct neuroinvasion.
- Some authors associate severe respiratory failures with viral neuroinvasion of the brain stem, although acute involvement of peripheral nerves and respiratory muscles may still increase such failures.
- COVID-19 positive cases have developed severe neurological diseases such as stroke, viral encephalitis, meningitis, Guillain Barré (GBS) and necrotizing hemorrhagic encephalopathy.
- The viral genome has been detected in the CSF of recovered patients which generates the alert for possible latent state of the virus in the CNS.
- Due to the affections of the immune response caused by the virus and its latency in the CNS, it is possible that COVID-19 is associated in the long term with autoimmune neurological diseases such as multiple sclerosis, GBS and schizophrenia.
I would like to say "Thank you" for this discussion thread, which certainly demonstrates startling new information about "Neurology and COVID-19" that probes into the complexities about both subjects, providing in-depth scientific and medical insight.
I appreciate very much your answer to this discussion, as follows:
📷Roberto Rodríguez-Labrada added a reply 2 days ago
"Previous viral phylogenetic studies, experimental research in mice and viral receptor analysis in humans suggest that SARS-CoV2 is potentially neurotrophic.
- From the experiences of previous epidemics with SARS-CoV and MERS-CoV, it is estimated that neurological clinical manifestations may be immediate or long-term.
- Clinical studies in patients hospitalized with COVID-19 reveal neurological manifestations in approximately 40% of cases.
- Loss of olfaction and taste appear early in 60% of cases and may be associated with direct neuro-invasion.- Some authors associate severe respiratory failures with viral neuro-invasion of the brain stem, although acute involvement of peripheral nerves and respiratory muscles may still increase such failures.
- COVID-19 positive cases have developed severe neurological diseases such as stroke, viral encephalitis, meningitis, Guillain Barré (GBS) and necrotizing hemorrhagic encephalopathy.
- The viral genome has been detected in the CSF of recovered patients which generates the alert for possible latent state of the virus in the CNS.
- Due to the affections of the immune response caused by the virus and its latency in the CNS, it is possible that COVID-19 is associated in the long term with autoimmune neurological diseases such as multiple sclerosis, GBS and schizophrenia.
The Spectrum of Neurologic Disease in the Severe Acute Respiratory Syndrome Coronavirus 2 Pandemic Infection Neurologists Move to the Frontlines Samuel J. Pleasure,MD, PhD; Ari J. Green, MD; S. Andrew Josephson, MD
JAMA Neurology Published online April 10, 2020 Editorial of related article:
Mao L, Jin H,Wang M, et al. Neurologic manifestations of hospitalized patients with coronavirus disease 2019 inWuhan, China. JAMA Neurol. Published online April 10, 2020. doi:10.1001/jamaneurol.2020.1127
I found the following two references to be interesting:
Wu Y, Xu X, Chen Z, Duan J, Hashimoto K, Yang L, et al. Nervous system involvement after infection with covid-19 and other coronaviruses. Brain, Behavior, and Immunity. 2020
Mao L, Wang M, Chen S, He Q, Chang J, Hong C, et al. Neurological manifestations of hospitalized patients with covid-19 in wuhan, china: A retrospective case series study. 2020
Lu L, Xiong W, Liu D, et al. New-onset acute symptomatic seizure and risk factors in Corona Virus Disease 2019: A Retrospective Multicenter Study [published online ahead of print, 2020 Apr 18]. Epilepsia. 2020;10.1111/epi.16524. doi:10.1111/epi.16524
Guidon AC, Amato AA. COVID-19 and neuromuscular disorders [published online ahead of print, 2020 Apr 13]. Neurology. 2020;10.1212/WNL.0000000000009566. doi:10.1212/WNL.0000000000009566
Here they are some reviews and discussion based on the latest evidence about How Covid-19 affects the brain https://www.medscape.com/viewarticle/928903
also, Neurologic Symptoms and COVID-19: What's Known, What Isn't. https://www.medscape.com/viewarticle/928157
As the number of Corona virus cases and reports and publications increasing, we are starting to see an increasing number of reports of neurological symptoms, perhaps in over a third of patients. Many of these symptoms were mild and include things like headaches or dizziness that could be caused by a robust immune response. Other more specific and severe symptoms were also seen and include loss of smell or taste, muscle weakness, stroke, seizure, and hallucinations.
Several recent studies have identified the presence of neurological symptoms in COVID-19 cases. Some of these studies are case reports where symptoms are observed in individuals. Several reports have described Covid-19 patients suffering from Guillain–Barré syndrome. Guillain–Barré syndrome is a neurological disorder where the immune system responds to an infection and ends up mistakenly attacking nerve cells, resulting in muscle weakness and eventually paralysis.
Other case studies have described severe Covid-19 encephalitis (brain inflammation and swelling) and stroke in healthy young people with otherwise mild Covid-19 symptoms.
Changes in consciousness, such as disorientation, inattention, and movement disorders, were also seen in severe cases and found to persist after recovery.
SARS-CoV-2, the coronavirus that causes Covid-19, may cause neurological disorders by directly infecting the brain or as a result of the strong activation of the immune system.
Recent studies have found the novel coronavirus in the brains of fatal cases of Covid-19. It has also been suggested that infection of olfactory neurons in the nose may enable the virus to spread from the respiratory tract to the brain.
Cells in the human brain express the ACE2 protein on their surface. ACE2 is a protein involved in blood pressure regulation and is the receptor the virus uses to enter and infect cells. ACE2 is also found on endothelial cells that line blood vessels. Infection of endothelial cells may allow the virus to pass from the respiratory tract to the blood and then across the blood-brain barrier into the brain. Once in the brain, replication of the virus may cause neurological disorders.
SARS-CoV-2 infection also results in a very strong response by the immune system. This immune response may directly cause neurological disorders in the form of Guillain–Barré syndrome. But brain inflammation might also indirectly cause neurological damage, such as through brain swelling. And it’s associated with – though doesn’t necessarily cause – neurodegenerative diseases such as Alzheimer’s, Parkinson’s and amyotrophic lateral sclerosis (ALS, motoneuron disease). ALS patients may be particularly vulnerable to Covid-19, as their respiratory neuromotor system is already directly affected and weakened by the disease. Recently an ALS patient in England died soon after diagnosed with Covid-19.
Therefore, effects of SARS-CoV-2 on the brain may be an interactive process with already existing conditions.
During 2002-2003, cases of patients with polyneuropathy, ischemic cerebrovascular disease, and encephalitis associated with the SARS-CoV-1 virus were described, an idea supported by evidence of cerebral edema and meningeal vasodilation in autopsies of patients who died of the infection. Studies in murine models also showed viral particles and SARS-CoV-1 genomic sequences in brain neurons, for which an infection route was proposed through the olfactory epithelium and the olfactory bulb to the brain, a hypothesis that has also been raised for explain the neurological compromise of SARS-CoV-2, since in neurons and glial cells there is a high expression of angiotensin-converting enzyme 2 (ACE-2) receptors.
Lung infections with different human coronaviruses have been observed to cause an increase in alveolar and interstitial inflammatory exudate, which generates a state of hypoxia that induces anaerobic metabolism. Likewise, a severe hyperinflammatory systemic reaction occurs characterized by an excessive release of proinflammatory factors such as interleukin (IL) 6, IL 12, IL 15 and tumor necrosis factor alpha, which is called a cytokine storm that seems to be common to several of the coronaviruses, especially SARS-CoV-2. Furthermore, studies in in vitro cell cultures identified that glial cells, after being infected by different coronaviruses, express an increase in the secretion of these proinflammatory substances. This hyperinflammatory syndrome at the CNS level could cause chronic inflammation and brain damage.
This description, as well as the main neurological manifestations described to date, we detail in our letter to the editor available at the following link.
Article Manifestaciones neurológicas de la infección por SARS-CoV-2
Very interesting article. The hypothesis of direct damage to the vascular endothelium at the systemic level continues to postulate, one way or the other, by one organ or another, the implication of RACE II in the pathophysiology of viral infection.
THE VIRUS ENTRY IN THE HUMAN BODY AND ITS NANO PATHOLOGY. STAGE II FOCUS SHOLD BE ON THE VIRUS SURVIVAL FROM THE SUSTENANCE STAGE TO PROLIFERATION STAGE ; WHERE IT'S GENOME SPLITS AND DUPLICATE THE VIRAL GENOME. WE CAN DEFINITELY CEASE THE STAGE I OF SUSTENANCE AND BE DONE WITH THE VIRUS, NO PROLIFERATION. FINITO.