Due to its new origin and quick evolution, the 2019 coronavirus, also known as COVID-19, has presented several difficulties for medical professionals. Recent research has identified COVID-19’s clinical presentation of vertigo or dizziness. Numerous studies from around the world are being published daily, and they have identified COVID-19’s primary clinical symptom of dizziness. It is not shocking because viral infections have long been linked to nausea and vomiting.
The most frequent neurological symptom of COVID-19, according to a previous study from China, is dizziness. 1 It has been suggested that the COVID-19 virus, which causes SARS-CoV-2 or severe acute respiratory syndrome coronavirus 2, might produce dizziness due to its neuroinvasive potential. According to Baig et al.’s hypothesis, the virus attaches to angiotensin-converting enzyme receptors in the capillary endothelium before entering the brain tissue from the bloodstream. 2 Hypoxia, hypercoagulopathy, direct invasion, and immune-mediated injury were among the hypothesised mechanisms of neuroinvasion causing vertigo.
Table of Contents
More Information – Covid Dizziness
To pinpoint dizziness as a clinical symptom of COVID-19, a literature review was conducted using publications published in PubMed on August 1, 2020. The following keywords were used in the article search: COVID-19, SARS-CoV 2, Coronavirus illness, wooziness, vertigo, and dizziness.
Three case reports and 11 studies were among the 14 papers we found (Table 1). From this review, 141 cases in total were pooled. Vertigo or dizziness was a presenting symptom for every patient in our study. In 3/141 individuals (2.13%), dizziness was the first sign of COVID-19; in 2 of these patients, dizziness was subsequently accompanied by respiratory symptoms. 9,13 Most research describing lightheadedness as a clinical symptom is from China (11/14), the origin of the pandemic. Only two of the 14 studies that were included particularly examined and treated dizziness. Dizziness was not adequately researched and characterised since it was not the main focus of most studies (9, 11). Additionally, just one research by Malayala et al.11 indicated the result of dizziness, and in that study, the patient’s vestibular rehabilitation was effective.
Even though it is a nonspecific COVID-19 symptom, dizziness needs to be thoroughly investigated to identify its primary cause, which may be acute labyrinthitis, vestibular neuritis, acute otitis media, or a stroke due to COVID-19.
We want to highlight that dizziness should not be taken casually as it has been proven to be a famous clinical manifestation among COVID-19 patients. Parallel to that, association with other audiovestibular images, such as hearing loss and tinnitus ought to be determined. Persistent dizziness posttreatment from COVID-19 requires referral to the Otorhinolaryngology Department for thorough examination and investigation. Additionally, we recommend vestibular rehabilitation therapy, which has revealed promising results, to be carried out for stable COVID-19 patients with dizziness. Lastly, it is imperative that attending physicians remain vigilant, especially when managing nonspecific symptoms such as dizziness, as they can be easily overlooked.
Since SARS-CoV-2 neurotropism may cause a wide range of neuropathic consequences, it is not unexpected that COVID-19 clinical manifestations include vertigo and wooziness sensations. Given the broad nature of central and peripheral audiovestibular pathways, there may be some potential pathogenic processes. The substantial proportion of COVID-19 patients who report having vertigo and dizzy symptoms may be due to the cytokine storm, CNS viral invasion through ACE 2 receptors, and other systemic causes. We thoroughly analyse clinical trials that found dizziness and vertigo to be COVID-19 clinical symptoms in this research and talk about their etiopathogenesis.
Following the past severe outbreaks of the Middle East Respiratory Syndrome Coronavirus (MERS-CoV) and SARS-CoV, the World Health Organization (WHO) proclaimed the coronavirus disease 2019 (COVID-2019) to be a pandemic on March 11, 2020. In a couple of weeks, the pandemic’s epicentre swiftly migrated from China to Europe to the United States to back to Europe.
Although the respiratory system is most impacted by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, neurological consequences have also been widely documented . The angiotensin-converting enzyme 2 (ACE 2) receptor is expressed in numerous tissues, including the neurological parenchyma. Like SARS-CoV, the COVID-19 virus enters the Central Nervous System (CNS) through this receptor.
The incidence of dizziness and vertigo symptoms as a symptom of COVID-19 illness is reviewed in this publication, and we also examine the probable neurotropic processes of SARS-CoV-2.
The Neurotropism of COVID-19 Disease
Encephalitis, meningitis, demyelination, and Guillain-Barre Syndrome are included in the range of neurologic disorders that COVID-19 is known to produce. SARS-CoV-2 in the cerebrospinal fluid (CSF) of COVID-19 patients was verified by genome sequencing as a direct viral invasion of the brain resulting in symptomatic encephalitis.
The absence of lymphatic drainage and the existence of a functional hemato-labyrinthine barrier make the inner ear a favourable immune location. To maintain the ionic grade and the endocochlear potential for the operational procedures of mechanical-electrical transduction of the internal and external hair cells. The hemato-labyrinthine fence in the stria vascularis is a highly specialised network that regulates ion exchanges among the blood and the interstitial space in the cochlea (and, seemingly, also the vestibule). The endolymphatic sac, the primary antigen-processing site, controls local immunity, and its loss lowers the immunological response in the inner ear.
Final Verdict –
The CNS is hypothesised to get involved in COVID-19 infection through a hematogenous route and retrograde axonal trafficking. Through the expression of ACE 2 receptors in the capillary endothelium, the general circulation of the COVID-19 virus enhances CNS invasion. The COVID-19 virus may also enter the brain through the cribriform plate near the olfactory bulb through the respiratory pathway, which may then move to the brainstem and thalamus.