Abstract

COVID-19 and its vaccines have been associated with vestibular symptoms including vertigo, dizziness, and cognitive impairment (“brain fog”). This article reviews the etiology (viral invasion, immune activation, spike protein effects), physiology (inner ear and central integration pathways), and pathology (neuritis, microvascular injury, neuroinflammation) of vestibular dysfunction. Evidence from case reports, clinical studies, and mechanistic analyses is synthesized to highlight risk factors and therapeutic implications.

Introduction

The vestibular system, comprising the semicircular canals, otolith organs, vestibular nerve, and brainstem integration centers, is essential for balance and spatial orientation. SARS-CoV-2 infection and spike protein exposure via vaccination have been linked to vestibular dysfunction. Clinical manifestations include vertigo, dizziness, imbalance, and cognitive complaints. Understanding the mechanisms is critical for diagnosis, treatment, and public health policy.

Etiology

• Direct viral invasion: ACE2 receptors are expressed in inner ear tissues, allowing SARS-CoV-2 entry.
• Immune-mediated injury: Cytokine storms and autoantibody production can damage vestibular hair cells.
• Microvascular compromise: Endothelial dysfunction and thrombosis impair labyrinthine artery perfusion.
• Spike protein bioactivity: Spike proteins bind ACE2, triggering local inflammation and vascular permeability.
• Vaccination context: mRNA vaccines produce spike proteins that may circulate and interact with vestibular tissues.

Physiology

• Normal vestibular physiology involves hair cell transduction and vestibulo-ocular reflexes.
• Disruption occurs via:
  • Hair cell apoptosis from inflammatory mediators.
  • Neurotransmission imbalance (glutamate excitotoxicity).
  • Vascular hypoperfusion leading to ischemia.
  • Neuroinflammation in vestibular nuclei.

Pathology

• Vertigo: Asymmetric input from damaged vestibular organs.
• Dizziness: Multifactorial—vascular compromise, autonomic dysfunction, central integration failure.
• Brain fog: Neuroinflammation, microglial activation, impaired cerebral perfusion.
• Histopathology: degeneration of vestibular hair cells, demyelination of vestibular nerve fibers, microvascular lesions.
• Comparative pathology: overlap with Long COVID syndromes.

Clinical Observations

• Case reports of vestibular neuritis post-COVID infection.
• Persistent dizziness after infection documented in otology clinics.
• Long COVID cohorts show imbalance and cognitive complaints.
• Vaccine surveillance reports rare but notable vestibular symptoms.

Risk Stratification

• Genetic predisposition (ACE2 polymorphisms, HLA variants).
• Pre-existing vestibular disorders.
• Cardiovascular/metabolic comorbidities.
• Age and sex differences in immune response and vascular integrity.

Therapeutic Implications

• Acute management: corticosteroids, antivirals, vestibular suppressants.
• Long-term rehabilitation: vestibular therapy, cognitive rehabilitation.
• Monitoring: audiovestibular testing, neuroimaging, biomarker assays.
• Future directions: targeted vaccine design, spike protein clearance strategies.

Conclusion

COVID-19 and mRNA vaccination can disrupt vestibular function through viral, immune, vascular, and spike protein mechanisms. Vertigo, dizziness, and brain fog are clinically significant outcomes requiring further study, risk stratification, and therapeutic innovation.

Footnotes / References

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