**4.5 Neurological symptoms are classified into three categories**


Similarly, clinical manifestations such as stroke, acute necrotizing hemorrhagic encephalopathy, acute Guillain–Barré syndrome, and meningitis usually accompany the neurological effects of COVID-19. But they are frequent in individuals who are critically ill, adults who are old, and people who have suffered from previous infections of embolism or cardiovascular diseases [20, 65, 66].

### **5. Possible therapies for COVID-19**

Numerous probable therapies for COVID-19 are being studied and tested, but, fortuitously, some medications have been approved by the FDA and made available for infected individuals [6]. Some pharmaceutical medications are being evaluated as possible therapies with different degrees of success [67]. Hydroxychloroquine, an antimalarial and anti-inflammatory drug, was first suggested to have potential against COVID-19 [6], but was later shown to be ineffective [68]; Ribavirin inhibits viral fusion and entry into host cells [6]. The use of Remdesivir for COVID-19 treatment prevented SARS-CoV-2 replication, while tocilizumab, an antagonist drug, also prevents the virus entry into the host cells [6].

ATN-161 has been shown to affect as an anti-cancer and ischemic stroke agent and has successfully completed phase I clinical trial for cancer showing to be well-tolerated without any toxicity. In an ischemic stroke study, increased expression of α5β1 integrin in post-stroke brain endothelial cells was linked to BB breakdown and then increased neuroinflammation and edema. These conditions can be inhibited by ATN-161 [71]. ATN-161 has been shown to be a potential antiviral therapy following a study that reported ATN-161 blocking viral replication of the beta-coronavirus porcine hemagglutinating encephalomyelitis virus (PHEV) in mice through the α5β1-FAK signaling mechanism [69]. In the study, it was found that SARS-CoV-2 spike protein was attached to α5β1 and α5β1/hACE2 which was inhibited by ATN-161 in VeroE6 cells in vitro. This study, therefore, recommends further studies on the ATN-161 as a possible COVID-19 therapy against COVID-19 related neurological disorders. The last possibility for a possible treatment is convalescent plasma, in which the infected individual receives plasma from a recovered COVID-19 individual. This was done in optimisms that the antibodies in the plasma of the improved individuals could help fight the virus in infected ones [67].

Managing prior neurological diseases such as stroke might remain similar to the pre-COVID-19 era. Continuing immunomodulation should continue as well as constant for drug-related adverse effects observation, since withdrawal may initiate a reversion [70]. Individuals involved must consciously observe hand hygiene and social distancing to avoid being infected with SARS CoV-2 [71, 72].

### **6. Conclusion**

The COVID-19 pandemic has impacted our lives beyond health. Today, we have learned new ways of dealing with a pandemic and our understanding of viruses has expanded to newer dimensions. In this chapter, we reviewed the specific effects of COVID-19 on the neurological system and the various symptoms in the CNS, PNS, and skeletomuscular systems. Studies done so far emphasize the need for further research to ascertain the level of damage SARS-CoV-2 can cause in neurological systems as the exact mechanism of invasion remains unclear. Once clearly defined, existing drugs can be repurposed, new pharmacological interventions can be developed, and combination therapies can be designed to relieve neurological symptoms and the effects of SARS-CoV-2 on neurological systems.

### **Conflict of interest**

The authors declare no conflict of interest.
