Effects of COVID-19 on the nervous system

New papers published in journals JAMA Neurology In May 2020, I will explain the symptoms and complications of COVID-19 related to the nervous system.

The COVID-19 pandemic causes hundreds of thousands of cases of severe pneumonia and dyspnea in 188 countries and regions around the world. The causative agent, SARS-CoV-2, is a new coronavirus with well-known lung complications. However, there is growing evidence that the virus affects other organs such as the nervous system and heart.

Coronavirus: A glimpse

of Coronavirus A large group of enveloped RNA viruses that infect both animals and humans. Human infections are caused by seven coronaviruses, namely human coronavirus (HCoV) –229E, HCoV-NL63, HCoV-HKU1, HCoV-OC43, MERS-CoV, SARS-CoV-1, and SARS-CoV-. It is known to be triggered. 2.

Of these, the last three are known to cause serious human illness. HCoV is more associated with respiratory symptoms, but HCoV-229E, HCoV-OC43, and SARS-CoV-1 are known to infect neurons.

The current research aims to contribute to the knowledge of SARS-CoV-2 neurotropic and post-infection neurological complications. The virus infects humans through ACE2 receptors on a variety of tissues, including airway epithelium, kidney cells, small intestine, appropriate lung tissue, and endothelial cells.

This provides a potential route for CoV to localize in the brain, as the endothelium is located inside systemic blood vessels. In addition, recent reports indicate that ACE2 is also found in brain neurons, astrocytes, and oligodendrocytes, especially in several areas such as the substantia nigra, ventricle, temporal lobe, and olfactory bulb.

Interestingly, ACE2 in neural tissue is expressed not only on the surface but also in the cytoplasm. These findings may suggest that SARS-CoV-2 can infect neurons and glial cells in all parts of the central nervous system.

How does SARS-CoV-2 cause nerve invasion?

Current knowledge points to possible viral entry into nerve cells by several mechanisms. These include virus migration across the synapses of infected cells, olfactory nerve-mediated entry into the brain, infection of the vascular endothelium, and migration of infected leukocytes across the blood-brain barrier (BBB).

Coronaviruses have been shown in several small animal studies to enter the brain from peripheral nerve endings along nerves and throughout synapses. It is facilitated by the presence of endocytic or exocytic pathways between neurons in the motor cortex and another secretory vesicle pathway between neurons and satellite cells.

Fast axonal transport occurs by using axonal microtubules, which allow the virus to reach the neuronal cell body by a retrograde version of this mechanism.

The potential expansion of the olfactory pathway is demonstrated by isolated anosmia and age-related development. In these cases, the virus can cross the lamina cribrosa and enter the central nervous system (CNS) nasally. However, new unpublished studies suggest that olfactory neurons lack ACE2, whereas cells in the olfactory epithelium lack it. This could mean that viral damage to the olfactory epithelium, but not to the olfactory neurons, is responsible for anorexia, but further research is needed to confirm this.

Cross the BBB

The virus can also cross the BBB via two distinct mechanisms. In the first case, infected vascular endothelial cells may transport the virus across the blood vessels to neurons. Once there, the virus begins to sprout and infect more cells.

The second mechanism is that infected white blood cells cross the BBB. This is the so-called Trojan horse mechanism, well known for its role in HIV. The inflamed BBB allows immune cells, cytokines, and even viral particles to enter the brain. However, T lymphocytes can be infected, but the virus cannot replicate.

COVID-19 neurological features

Limited data on the neurological symptoms associated with COVID-19 make it clear that headache, anorexia, and aging are among the most common symptoms. However, other findings include stroke and abnormal consciousness.

Headaches occur in up to one-third of the confirmed cases, but anosmia or aging has a much more variable prevalence. In Italy, about one-fifth of cases have these symptoms, but almost 90% of German patients have such symptoms.

“Given the reports of anosmia that manifest as an initial symptom of COVID-19, researchers may find that a dedicated test for anosmia may offer the potential for early detection of COVID-19 infection.”

Due to various mechanisms such as direct brain infection and damage, toxic metabolic encephalopathy and demyelinating diseases, disturbance of consciousness can occur in up to 37% of patients. Encephalitis has not been recorded as a result of COVID-19.

Toxic and metabolic encephalopathy can result from many disorders in metabolic and endocrine function. These include electrolyte and mineral imbalances, renal dysfunction, cytokine storms, hypoglycemia or hyperglycemia, and liver dysfunction. Patients who are elderly, ill, or who already have symptoms of dementia or are malnourished are at increased risk of this condition.

Less common neurological complications include Guillain-Barre syndrome, a postviral acute inflammatory demyelinating disease, and cerebrovascular events including stroke.

Is COVID-19 Therapy Associated With Neurological Symptoms?

Many different drugs are currently used to treat this condition.

For example, chloroquine and hydroxychloroquine can cause psychosis, peripheral neuropathy, and the latter can exacerbate the symptoms of myasthenia gravis. Tocilizumab, an IL-6 blocker, aims to reduce the excessive release of cytokines that occur in severe inflammation. Although it has limited access to the CNS, it can cause headaches and dizziness.

Precautions for COVID-19 patients with neurological conditions

If the patient already has a neurological condition that requires special care, the risk of COVID-19 may be high due to the coexistence of lung, heart, or liver conditions. , Or immunosuppressive drugs. You are also likely to be in a nursing home where serious outbreaks have been reported in many countries.

The summary of this study is: “Clinicians must continue to carefully monitor patients for neurological disorders. Early detection of neuropathy can lead to improved clinical outcomes and improved treatment algorithms.”