COVID-19 neurological damage (SARS-CoV-2)

The scientific community, in these days, begins to question himself more intensely about the neurological damage resulting from infection with COVID-19 (SARS-CoV-2).
There is growing evidence that the nervous system is frequently involved in hospitalized and non-hospitalized patients with Covid-19. This is not surprising, because neurological manifestations have also been described for a long time in infections with other respiratory viruses, including other coronaviruses. However, in the neurological field, the manifestations of Covid-19 are common and disabling enough to have attracted widespread attention in the scientific field and create concern for their short and long-term impact on the health of the population.

Neurological damage COVID-19 solutions

What COVID-19 neurological damage is and where does it come from?

Covid-19 often manifests with very varied neurological and neuropsychiatric symptoms including encephalitis, dizziness, sleep disorders, cognitive deficits, delirium, hallucinations and depression.
Simile a SARS-CoV-1, SARS-CoV-2 uses ACE2 as the main attack receptor of the "proteina Spike” (fig.1) for cellular entry. ACE2 protein was observed in the vascular system, but to a lesser extent in the lining of the cerebral vessels. However, RNA sequencing has demonstrated its presence, albeit modest in the human brain. The considerations of the prof. Paolo Calabresi, Full Professor of Neurology and Director of the Neurology of the Gemelli Polyclinic in Rome, drawn from a article by “inSalute news”:
Studies in transgenic mice have shown that SARS-CoV-2 can infect neurons and cause neuronal death using a mechanism that depends on the ACE2 protein., the same used in other organs. Clinico-pathological studies that have shown the presence of the virus in the brain or cerebrospinal fluid have not always been unique. Indeed, while some studies have shown SARS-CoV-2 RNA in the brain or CSF in patients with encephalopathy in Covid-19 patients, other studies have not replicated these results.

How SARS-CoV-2 works in the brain?

The action of SARS-CoV-2 As prof. Calabresi in above mentioned article:
“An important scientific question is to establish which are the ways of penetration of the virus into the brain. A first hypothesis is that of the olfactory pathway. Indeed, loss of smell is a frequent neurological manifestation in Covid-19. Furthermore, MRI studies have shown an increase in the signal in the olfactory cortex that could be associated with infection. Therefore the virus could be internalized in the nerve terminals of the olfactory mucosa and thus spread to other regions of the brain., as described for other coronaviruses.

Alterations of the blood-brain barrier (a natural barrier that protects the brain from the rest of the body) could facilitate the entry of the virus into the brain. Indeed, during the "cytokine storm" unleashed by SARS-CoV-2, some of these cytokines could alter this protective barrier and favor the entry of the virus.

Neurological damage COVID-19 pexels

The correlation between virus entry and brain damage

The virus's aggression mechanism seems to be strengthened with its advancement within the nervous system, indeed, always explains prof. Calabresi:
There is another brain damage mechanism linked to global brain ischemia caused by respiratory failure. Ischemic brain damage is also from thromboembolic strokes related to an increase in intravascular coagulation. Often such cerebral strokes appear to have different characteristics from those commonly seen in patients not affected by Covid-19 and affect a younger population.
Hypercoagulability related to Covid-19 which increases susceptibility to cerebrovascular. Autopsy findings have shown widespread microthrombi also in the brain. Patients with Covid-19 may also be at risk of cardioembolic stroke due to the acute heart injury and arrhythmias reported in approximately the 10% of hospitalized for Covid-19.

Regarding the manifestations of the central nervous system, we observed a higher frequency of headache in SARS-CoV-2 positive patients, hyposmia and encephalopathy always related to systemic conditions (fever or hypoxia). Furthermore, muscle involvement was more frequent in SARS-CoV-2 infection.

The Air Log clinical solution 6

A limitation of the cytokine storm can certainly contain the neuro-invasion responsible for retrograde axonal damage.
As highlighted in a document on Molecular Pathologies, previously published by CH.I.S.S. srl, the formulato Air Log 6 strong of its molecule with specific retroviral inhibition functions FAST VIREX is a valid tool for the reduction of copies of Sars-CoV-2 genomes present in the air responsible for the rapid spread of the pandemic first identified by research carried out by a team of Arpa Piemonte
In conclusion, the neurological manifestations of Covid-19 constitute one of the main challenges for public health not only for the acute effects on the brain, but also for the long-term damage to brain health that could result. These delayed manifestations may also be present in patients who have not shown neurological symptoms in the acute phase. This possibility requires careful epidemiological surveillance now and in the future.