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Copyright ©The Author(s) 2022.
World J Methodol. Sep 20, 2022; 12(5): 365-380
Published online Sep 20, 2022. doi: 10.5662/wjm.v12.i5.365
Table 1 Main hypotheses, mechanisms related to development of the neurological manifestations of coronavirus disease 2019 and prevalence/incidence of these repercussions
Neurological repercussion
Hypotheses/mechanisms related to their development
Prevalence/incidence of manifestation
HeadacheComplications of the viral infection, the host immune response, the presence of severe installed disease or even the drug therapy used[41,45]The headache prevalence varies from 8%[56] to 25%[38] and 70.3%[40], according to the study
DizzinessThe direct injury by binding to the ACE2, or even by hypoxia and coagulation disorders may be related[45]For dizziness, the prevalence is estimated to be around 8%[42] to 9%[5]
ODConductive loss due to edema in the olfactory cleft, injury to the respiratory epithelium or lesion in the olfactory bulb[61,62]About 47% of individuals had a self-reported loss of smell. More frequent in women and young patients[59,60]
GDLocal inflammatory reactions and the relationship with cranial nerves VII, IX, and X[66]About 43.93% of the patients[64]. More prevalent in young and female patients[65]
Disturbances of consciousnessPost-inflammatory state, meningoencephalitis, or may just be a sequela after a traumatic event[48]A range of 3.3% to 19.6% in COVID-19 patients[48,49]
Acute cerebrovascular diseaseIntracerebral hemorrhage can be caused by viral interaction with ACE2 receptors and ischemic stroke is related to late complications in the disease severity[50]The incidence of ischemic stroke in patients with COVID-19 was reported to be between 0.9%[76] and 4.6%[77]
GBSThere are hypotheses that relate the development of GBS to the cytokine storm and autoimmune mechanisms by cross-reaction[74,75]A study suggested an up to 2.6-fold increase in the baseline GBS case rate, from 0.93/100000/yr to 2.43/100000/yr