The proportions were pooled by the random-effects model (DerSimonian–Laird) estimated using the Stuart–Ord (inverse double arcsine square root) method. An individual patient is considered as the unit of analysis. For continuous variables, we have used central tendency (mean or median) and dispersion measures (standard error, standard deviation). For the categorical variables, we used frequencies and proportions. The primary outcomes measured were neurological problems in COVID-19 patients and their prevalence. Thus, in the present study, meta-analysis was conducted on pooled data of individual studies reporting neurological manifestations in COVID-19 patients. Since the neurological complications in COVID-19 patients are increasingly being reported and the exact association between COVID-19 infection and neurological problems remain unclear there is a need for pooled analysis of individual studies across the globe to make a better clinical decision. (16,17) However, these articles included limited studies. (15) Few initial systematic reviews reported neurological complications such as headache, myalgia, dizziness, nausea, vomiting, confusion, smell and taste dysfunction, cerebrovascular disorders, and altered mental status in COVID-19 patients. (14) Thus, it is not clear whether SARS-CoV-2 penetrate the brain or not due to difficulty in accessing brain tissue and CSF samples in COVID-19 patients. (13) However, in another study, RT-PCR assays of CSF samples of 07 COVID-19 patients with neurological problems were found negative. (11,12) The first evidence of direct neuroinvasion of SARS-CoV-2 was reported in a 56-year-old patient gene sequencing of cerebrospinal fluid (CSF) sample confirmed the presence of SARS-CoV-2 in the brain.
(8,9) Since endothelial cells of blood–brain barrier express angiotensin-converting enzyme 2 (ACE2) similar to lung epithelial cells, direct viral entry into the brain is possible. (8) These systemic consequences along with lung alveolar damage cause severe hypoxia, which leads to cerebrovascular vasodilation, cerebral edema, and ischemia. (6−10) Additionally, global inflammatory markers such as interleukin (IL)-6, IL-12, IL-15, and tumor necrosis factor α (TNF-α) can activate glial cells and produce inflammatory responses. The COVID-19 related neurological manifestations are hypothesized to be caused by multiple factors such as damage to specific receptors, secondary hypoxia, cytokine-related injury, and retrograde travel along the olfactory nerve and bulb. Various neurological manifestations related to the central nervous system (CNS) and peripheral nervous system (PNS) are associated with COVID-19 patients. However, the heterogeneity among studies was found to be high. The Stats Direct (version 3) was used for the analysis. We have searched for electronic databases with MeSH terms, and the studies for analysis were selected based on inclusion and exclusion criteria and quality assessment. Thus, we have conducted a meta-analysis of clinical studies associated with neurological problems in COVID-19 patients.
However, the exact association of the nervous system with COVID-19 infection is still unclear. in COVID-19 patients have indicated the involvement of the nervous system. Common symptoms such as dizziness, headache, olfactory dysfunction, nausea, vomiting, etc.