Goal: The goal of this study was to determine the neuroinvasive pathways of SARS-CoV-2 and discuss the neurosympomology of the virus through a comprehensive literature review.

Results:

• The viral presence of SARS-CoV-1 has been established in the CNS through autopsy analysis
• Studies using mice have shown that SARS-CoV-1 has reached the brain possibly through the olfactory nerves and spread to thalamus and brainstem.
• Covid-19 neurological symptoms include dizziness, loss of smell and taste, headache, and loss of consciousness
• Research on the type of symptoms that occur in mild vs severe patients - suggest that an early stage of viral transmission can cause direct injury to nasal nerves
• Analysis of incidents of Guillain-Barré syndrome in Covid-19 patients suggests that whether GBS is caused by a direct attack on the myelin sheath, or through blood brain barrier permeability due to the increased inflammation of the cytokine storm in the CNS
• Incidents of Encephalitis have been established in Covid-19 patients across the world.
• The widespread ACE2 receptor might be the reason for such a variety of symptoms and might explain how the virus makes its way through the olfactory epithelium (OE). The virus might attach to ACE2 receptors and invade the olfactory epithelium, then the olfactory ensheathing cells surrounding the olfactory neurons. Evidence for this route includes that non-neural cells in the OE have the SARS-Cov-2 entry genes. Further, olfactory nerves in autopsy analyses have shown tissue damage.
• Another potential pathways for Covid-19 reaches neurological systems include direct invasion to the nasal cavity, with evidence that this is what causes headaches.
• Another includes direct invasion into the bloodstream via epithelial erosion, which could allow the virus to cross the BBB, with evidence showing this from postmortem analysis.
• Further, it is possible that the cytokine storm that occurs as an immune response to covid can compromise the blood brain barrier, reduces circulating AE2 and increases angiotensin II, which predisposes patients to stroke and clotting.