-
.
- Ελληνικά
For two years, since the outbreak of the COVID-19 pandemic, clinical data have been collected showing an association of SARS-CoV-2 infection with neurological side effects such as "anosmia" or "agueusia" (loss of smell or taste) and neuroimmunological syndromes.
In April 2021, a study was published in the prestigious Lancet journal in which the comparative and statistical history of 236 thousand people who had contracted COVID-19 and had been treated was studied. The study showed that one in three of these people experienced a neurological or psychiatric problem six months after becoming ill, one in fifty had a stroke and one in eleven developed severe brain disorders.
How are these neurological effects related to a viral disease that until then the medical world had mainly treated as a respiratory infection that caused lung and immune problems? Is this association documented by the data so far and, if so, is the new coronavirus or our immune system responsible, which reacts to the "invasion" and causes a devastating inflammation which, among other things, also affects the brain?
What do we know so far?
Before SARS-CoV-2, six coronaviruses were known to affect humans. Four of them cause mild respiratory infections, while two, MERS-CoV in 2012 and SARS-CoV in 2002-03 have caused pandemics and deaths. Using experimental models it has been found that these two coronaviruses (MERS-CoV and SARS-CoV) can invade the nervous system and cause a variety of neurological problems in both the central (CNS) and peripheral (PNS) systems.
The mechanism of coronavirus entry into the host cell
The virus, through its spike of glycoprotein S, binds to the angiotensin converting enzyme receptor 2 (ACE2). The ACE2 enzyme is detected in many organs and systems of the body: in the nose, lungs, kidneys, liver, blood vessels, immune system and brain vessels (but not in the brain). At this stage of the attack patients have hyposmia, anosmia and agueusia which are reversible.
After binding ACE2 first to respiratory epithelial cells and then to blood vessel epithelial cells, the virus triggers a "cytokine storm", with a marked increase in levels of interleukin-1, interleukin-6 and tumour necrosis factor. High levels of these cytokines increase vascular permeability, swelling and cause extensive inflammatory changes and hypercoagulability of the blood resulting in small and large blood clots. This combination of extensive inflammation, vascular damage and hypercoagulability leads to acute respiratory distress syndrome (ARDS), renal failure, liver damage, heart failure, myocardial infarction, vascular stroke with multiple neurological sequelae.
Subsequently, it causes a prolonged neuroinflammatory reaction leading to disruption of the brain barriers (blood-brain, meningeal) and direct entry of SARS-CoV-2 and various blood components into the central nervous system, possibly resulting in seizures, encephalopathy, vascular strokes, coma.
Ways of central nervous system attack by coronavirus
Possible ways of CNS attack by coronavirus include:
-Hematogenous dissemination via virus particles or via single-cell macrophages-Neurogenic dissemination via brain conjugates such as the olfactory, trigeminal and vagus nerves.
Pandemic and neurological effects
The effects of coronavirus infection of the central and peripheral nervous system that have been documented include: neurological symptoms, neurological disorders and late neurological manifestations.
The most common neurological symptoms are: dizziness (9%), headache (6-13%), catabolism, hypoencephaly - agueusia (5-30%), hyposmia - anosmia (5-70%), myalgia (14.9%).
The most frequent neurological disorders are: vascular episodes (ischaemic, haemorrhagic), venous sinus thrombosis, encephalopathy, pyrexia, haemorrhagic necrotizing encephalitis (Weston's syndrome), ADEM, myelitis myasthenia myasthenia pyrexia, Miller-Fisher syndrome, Guillain-Barre syndrome, cranial polyneuritis.
The most frequent late neurological manifestations are: Alzheimer's disease, Parkinson's disease, motor neurone disease, neuromuscular disorders with respiratory distress, autoimmune diseases, multiple sclerosis, optic neuromyelitis, myasthenia, Guillain-Barre syndrome, autoimmune neuropathies.
Uncertainties and conclusions
Although the neurobiological mechanism of the action of coronaviruses on the brain is beginning to be understood, we still do not know which of the above-mentioned assessed neurological disorders can be attributed exclusively to the invasion of the coronavirus into the body and which to pre-existing underlying factors such as genetic predisposition, excessive stress, psychosomatic exhaustion and even the constant fear of disease.
In conclusion, however, and with the assistance of several clinical studies and meta-analyses that either preceded or followed the research published in the Lancet, we could take the following as data:
-The SARS-CoV-2 virus causes an intense inflammatory reaction with a "cytokine storm", coagulation disorders and multiorgan failure.
-The nervous system is affected by the virus by haematogenous or neurogenic dissemination and the direct effect on the nervous parenchyma has not been fully documented.
-There is evidence of both immediate and long-term impairment of natural and acquired immunity with induction of immune inflammatory and degenerative diseases of the nervous system.
The COVID-19 pandemic is ongoing and information is being gathered daily at both clinical and laboratory levels.
Physicians should be prepared for the occurrence of neurological complications in patients with COVID-19 disease both during the pandemic and later, in order to understand the natural history of SARS-CoV-2 infection and its impact on the central and peripheral nervous system.
Having said that, it seems that the "post-COVID" era will probably be accompanied by a "new pandemic" of search, knowledge, and perhaps more radical treatment of neurological diseases
Source.gr
Contents of this article including associated images are belongs Cyprus Times
Views & opinions expressed are those of the author and/or Cyprus Times
Source
