John Murphy, The COVID 19 Long-haul Foundation
Abstract
SARS-CoV-2 has demonstrated a remarkable capacity for multisystem involvement, extending beyond its primary respiratory tropism to affect neurological, vascular, and otologic domains. Among the less recognized but clinically significant manifestations are middle-ear damage and vestibular dysfunction, including vertigo and sensorineural hearing loss. Intriguingly, similar symptoms have emerged following COVID-19 vaccination, prompting investigation into shared immunopathogenic mechanisms. This review synthesizes current evidence on the etiology of COVID-related otologic and vestibular symptoms, compares post-infectious and post-vaccination presentations, and explores implications for diagnosis, management, and future research.
Introduction
Since its emergence in late 2019, SARS-CoV-2 has challenged conventional paradigms of viral pathophysiology. While respiratory symptoms dominate the clinical picture, a growing body of literature reveals that the virus can affect the auditory and vestibular systems through direct invasion, immune-mediated inflammation, and vascular compromise. Reports of vertigo, tinnitus, and hearing loss—both during acute infection and following vaccination—suggest that otologic symptoms may be underrecognized components of COVID-19’s systemic impact.
This article aims to:
- Characterize the mechanisms by which SARS-CoV-2 damages middle-ear and vestibular structures
- Examine the parallels between infection-induced and vaccine-induced otologic symptoms
- Provide a framework for clinical recognition and future investigation
Otologic Manifestations of SARS-CoV-2 Infection
Middle-Ear Pathology
Middle-ear involvement in COVID-19 is often secondary to upper respiratory inflammation. Eustachian tube dysfunction, mucosal edema, and serous effusion can result in conductive hearing loss and otalgia. Studies have identified ACE2 and TMPRSS2 receptor expression in middle-ear tissues, suggesting a plausible route for direct viral invasion (Jeong et al., 2021).
Inner Ear and Vestibular Dysfunction
Sensorineural hearing loss (SNHL), vestibular neuritis, and acute vertigo have been documented in COVID-19 patients (Mustafa, 2020; Degen et al., 2021). These symptoms may arise from viral neurotropism, cytokine-induced inflammation, or ischemic injury to the cochlea and vestibular apparatus. The labyrinthine artery, a terminal vessel with no collateral supply, is particularly vulnerable to microvascular insults.
Mechanisms of Injury
Viral Neurotropism
SARS-CoV-2 has demonstrated affinity for neural tissues, including cranial nerves and glial cells. The virus’s entry via ACE2 and TMPRSS2 receptors in cochlear and vestibular structures may lead to direct cytopathic effects (Jeong et al., 2021).
Immune-Mediated Inflammation
Systemic inflammation and cytokine release—hallmarks of severe COVID-19—can disrupt endolymphatic homeostasis and damage hair cells. Elevated levels of IL-6, TNF-α, and other pro-inflammatory mediators have been implicated in auditory dysfunction (Cure et al., 2020).
Vascular Compromise
COVID-19 is associated with endothelial dysfunction, hypercoagulability, and microthrombi formation. These vascular insults can impair perfusion of the inner ear, leading to ischemia and subsequent hearing loss or vertigo (Goss et al., 2021).
Post-Vaccination Otologic Symptoms
Clinical Observations
Following administration of mRNA and adenoviral vector vaccines, some individuals have reported transient otologic symptoms, including tinnitus, dizziness, and hearing changes. While most cases are self-limiting, rare instances of persistent SNHL and vestibular dysfunction have been documented (Formeister et al., 2021; Zaynab et al., 2022).
Immunopathogenic Hypotheses
Unlike infection, vaccines do not introduce live virus into the body. However, the spike protein—expressed post-vaccination—may trigger immune responses that mimic those seen in natural infection. Proposed mechanisms include:
- Molecular mimicry leading to autoimmune activation (Vojdani et al., 2021)
- Endothelial activation and microvascular changes (Goss et al., 2021)
- Inflammatory cytokine release affecting cochlear and vestibular tissues
Comparative Pathophysiology
| Mechanism | SARS-CoV-2 Infection | COVID-19 Vaccination |
|---|---|---|
| Direct viral invasion | Confirmed | Absent |
| Immune-mediated damage | Prominent | Possible |
| Vascular compromise | Frequent | Rare |
| Autoimmune activation | Suspected | Suspected |
| Symptom duration | Variable | Typically transient |
While the mechanisms differ in origin—viral replication vs. antigenic stimulation—the downstream effects may converge on similar pathways of inflammation and vascular stress.
Clinical Implications
Otologic symptoms should be considered part of the differential diagnosis in both post-COVID and post-vaccine presentations. Audiologic and vestibular testing may be warranted in patients with persistent symptoms. Clinicians should maintain a high index of suspicion, particularly in individuals with pre-existing otologic conditions or autoimmune predisposition.
Future Directions
Further research is needed to:
- Elucidate the molecular pathways linking spike protein expression to otologic symptoms
- Determine the prevalence and risk factors for vaccine-related auditory and vestibular effects
- Develop targeted therapies to mitigate inflammation and restore function in affected patients
Longitudinal studies and controlled trials will be essential to distinguish causality from coincidence and to guide evidence-based management.
Conclusion
SARS-CoV-2 infection and COVID-19 vaccination can both affect the auditory and vestibular systems through overlapping immunological and vascular mechanisms. While most symptoms are mild and reversible, their presence underscores the need for comprehensive evaluation and continued research. Recognizing these manifestations is critical for improving patient care and understanding the full spectrum of COVID-19’s systemic impact.
References
- Jeong M et al. JAMA Otolaryngol Head Neck Surg. 2021.
- Degen C et al. Front Neurol. 2021.
- Mustafa M. Am J Otolaryngol. 2020.
- Cure E et al. Med Hypotheses. 2020.
- Fidan V. Am J Otolaryngol. 2020.
- Formeister EJ et al. JAMA Otolaryngol. 2021.
- Zaynab M et al. Clin Otolaryngol. 2022.
- Vojdani A et al. J Autoimmun. 2021.
- Watad A et al. Rheumatology. 2021.
- Goss AL et al. Circulation. 2021.
- Lechien JR et al. Eur Arch Otorhinolaryngol. 2020.
- VAERS database, CDC.
- Biology Insights. 2023.
- Ada Health. 2023.
- GoodRx Health. 2023.
SARS-CoV-2 and Otologic Pathophysiology: Etiology of Middle-Ear Damage and Vertigo in Infection and Post-Vaccination Syndromes
Abstract Emerging evidence suggests that SARS-CoV-2 infection can induce otologic and vestibular symptoms, including middle-ear damage, tinnitus, and vertigo. These manifestations are increasingly recognized as part of the virus’s neurotropic and vasculopathic profile. Notably, similar symptoms have been reported following COVID-19 vaccination, raising questions about shared immunopathogenic mechanisms. This article reviews the current literature on the etiology of COVID-related ear damage and vertigo, and explores parallels in post-vaccination presentations.
1. Introduction
COVID-19, caused by the SARS-CoV-2 virus, is primarily a respiratory illness, but its systemic effects include neurological, vascular, and immunological sequelae. Otologic symptoms—once considered peripheral—are now recognized as part of the broader clinical spectrum. Vertigo and middle-ear dysfunction have been documented both during acute infection and following vaccination, suggesting overlapping mechanisms.
2. Otologic Manifestations of COVID-19
2.1 Middle-Ear Involvement
- Eustachian tube dysfunction due to upper respiratory inflammation can lead to middle-ear effusion and conductive hearing loss.
- Direct viral invasion of middle-ear mucosa has been proposed, supported by ACE2 receptor expression in ear tissues.
- Secondary bacterial infections may exacerbate middle-ear pathology, especially in immunocompromised patients.
2.2 Inner Ear and Vestibular Damage
- Sensorineural hearing loss (SNHL) and vestibular neuritis have been reported, likely due to viral neurotropism and vascular compromise2.
- Vertigo and dizziness may result from inflammation of the vestibular nerve or ischemia in the labyrinthine artery.
3. Mechanisms of Injury
3.1 Viral Neurotropism
SARS-CoV-2 can infect Schwann cells and cochlear hair cells via ACE2 and TMPRSS2 receptors, leading to direct cytopathic effects.
3.2 Immune-Mediated Inflammation
Cytokine storms and systemic inflammation may damage inner ear structures, disrupt endolymphatic homeostasis, and impair vestibular function.
3.3 Vascular Insults
Microthrombi and endothelial dysfunction have been implicated in cochlear ischemia and vestibular hypoperfusion.
4. Post-Vaccination Otologic Symptoms
4.1 Clinical Reports
- Case series and VAERS data have documented tinnitus, vertigo, and temporary hearing loss following mRNA and adenoviral vector vaccines.
- Most symptoms are transient, but rare cases of persistent SNHL and vestibular dysfunction have been reported.
4.2 Proposed Mechanisms
- Molecular mimicry and autoimmune activation may trigger inflammation in auditory and vestibular pathways.
- Spike protein expression may induce endothelial activation and microvascular changes similar to those seen in infection.
5. Comparative Pathophysiology: Infection vs. Vaccination
| Mechanism | SARS-CoV-2 Infection | COVID-19 Vaccination |
|---|---|---|
| Direct viral invasion | Yes | No |
| Immune-mediated damage | Yes | Yes |
| Vascular compromise | Yes | Rare |
| Autoimmune activation | Possible | Possible |
| Symptom duration | Variable | Usually transient |
6. Clinical Implications
- Otologic symptoms should be considered in differential diagnosis of post-COVID and post-vaccine syndromes.
- Audiologic and vestibular testing may be warranted in persistent cases.
- Further research is needed to clarify long-term outcomes and mechanisms.
7. Conclusion
COVID-19 and its vaccines can both affect the auditory and vestibular systems through overlapping immunological and vascular pathways. While most cases are mild and self-limiting, clinicians should remain vigilant for persistent or progressive symptoms. Understanding these mechanisms is essential for developing targeted therapies and improving patient outcomes.