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Advanced Neurology Neurological complications of COVID-19

(GBS) are also increasingly well-recognized as one of the 19 patients , most likely due to the insufficient viral load
[72]
complications of COVID-19. Recently, a study described in the CSF or the fact that the virus does not enter the CSF.
the development of GBS in COVID-19 patients, who first The COVID-19-related neurological complications are
developed weakness in the lower limbs and then progressive mainly observed in the central nervous system (CNS), the
quadriplegia on the 5–10 days after the onset of COVID-19 peripheral nervous system (PNS), and the musculoskeletal
symptoms . However, no SARS-CoV-2 was detected in system. Possibly, different mechanisms, such as neuronal
[69]
the CSF of these patients, and the CSF protein levels were retrograde dissemination and systemic hematogenous
normal in 40% of infected patients. However, another study spread, are in place to allow viral entry and damage to
reported the isolation of conalbumin from CSF in COVID- the nervous system. Although the exact mechanism of
19 patients with GBS, and CSF analysis showed normal white SARS-CoV-2 invasion remains unclear, multiple lines of
blood cell counts and elevated protein levels . In general, evidence showed that the virus can destroy the neurons by
[70]
GBS responds well to intravenous immunoglobulin therapy, either of the two mechanisms . In addition to destroying
[73]
which brings about significant improvement in nervous the blood-brain barrier and causing central neuron death
system, suggesting that neuropathy is immune-mediated , through viremia, SARS-CoV-2 can also infect olfactory
[71]
but the long-term outcomes are still unclear. bulb (OB) and subsequent transport to neurons .
[74]
3. Mechanisms underlying the neurologic SARS-CoV-2 could cause viremia to destroy neurons
complications of COVID-19 by binding to ACE2. ACE2 receptors are widely
expressed in the CNS systems, including neurons,
In this section, we summarize the underlying mechanisms astrocytes, oligodendrocytes, and OB . Binding of the
[17]
of how COVID-19 affects the nervous system (Figure 1). transmembrane protease serine 2 to the ACE2 receptor
Early in the outbreak of COVID, researchers had attempted results in protein cleavage and activation of the spike
to detect the SARS-CoV-2 RNA in the CSF of infected protein, therefore allowing the virus to enter the host cell .
[75]
patients with neurological symptoms . However, the virus Thus, SARS-CoV-2 has the potential to infect neurons and
[65]
has never been successfully detected in most COVID- glial cells throughout the CNS.

Figure 1. Mechanisms underlying the damages to the central nervous system mediated by SARS-CoV-2. The binding of SARS-CoV-2 to the ACE2 receptor
leads to neuronal apoptosis or death. In addition, SARS-CoV-2 not only disrupts the blood-brain barrier by triggering cytokine storm, but also spreads
retrograde through neurons by infecting the olfactory bulb, thus disrupting the normal function of the central nervous system. The schematic is illustrated
with Figdraw (www.figdraw.com).

Volume 1 Issue 2 (2022) 5 https://doi.org/10.36922/an.v1i2.83