Vestibular neuronitis after COVID-19 vaccination.

A woman in her 50s presented with acute vertigo and vomiting within 72 hours of receiving the Pfizer-BioNTech COVID-19 vaccine. The only neurological deficit was an impaired vestibulo-ocular reflex with horizontal nystagmus. The patient was subsequently diagnosed with vestibular neuronitis. She was managed symptomatically with prochlorperazine and betahistine, and underwent vestibular rehabilitation for 6 weeks. She made a full recovery and experienced no further symptoms. She received the second dose of the vaccine without complications.This case demonstrates a temporal association between COVID-19 vaccination and vestibular neuronitis. Neurological adverse events are rare but recognised side effects of COVID-19 vaccines and healthcare professionals should be aware of them. This ensures timely management of patients with such presentations. Treatment should be the same as for non-vaccine-associated vestibular neuronitis. The nature of the relationship between COVID-19 vaccination and vestibular neuronitis remains unclear and patients therefore require investigations to exclude other recognised causes of vestibular neuronitis.

Case of COVID-19-induced vestibular neuritis in a child.

Since the outbreak of the COVID-19 pandemic, there has been a growing need to fully understand all the possible clinical features of the epidemic, which often presents with unusual manifestations, especially in children. In this report, we describe the case of a child with a COVID-19 infection and suffering exclusively from vertigo and fever. Altogether, considering the clinical manifestation, laboratory tests and imaging, given the patient's positivity to SARS-CoV-2 infection and its neurotropic potential, we assumed that the child had COVID-19-induced vestibular neuritis, which, in consideration of the spontaneous improvement of symptoms, did not require any therapeutic adjustments, apart from the natural compensation of the central nervous system.This case suggests the importance of having an index of suspicion for a COVID-19 infection in patients with paediatrics presenting with vertigo and adds valuable information to the limited literature on COVID-19 presentation and management in children.

Treatment of peripheral vestibular dysfunction using photobiomodulation.

Gentamicin, which is still used in modern medicine, is a known vestibular toxic agent, and various degrees of balance problems have been observed after exposure to this pharmacologic agent. Photobiomodulation is a candidate therapy for vertigo due to its ability to reach deep inner ear organs such as the cochlea. Previous reports have suggested that photobiomodulation can improve hearing and cochlea function. However, few studies have examined the effect of photobiomodulation on balance dysfunction. We used a rat model to mimic human vestibulopathy resulting from gentamicin treatment and evaluated the effect of photobiomodulation on vestibular toxicity. Slow harmonic acceleration (SHA) rotating platform testing was used for functional evaluation and both qualitative and quantitative epifluorescence analyses of cupula histopathology were performed. Animals were divided into gentamicin only and gentamicin plus laser treatment groups. Laser treatment was applied to one ear, and function and histopathology were evaluated in both ears. Decreased function was observed in both ears after gentamicin treatment, demonstrated by low gain and no SHA asymmetry. Laser treatment minimized the damage resulting from gentamicin treatment as shown by SHA asymmetry and recovered gain in the treated ear. Histology results reflected the functional results, showing increased hair cell density and epifluorescence intensity in laser-treated cupulae.

Drug-induced aseptic meningitis, sensorineural hearing loss and vestibulopaty.

We report clinically rare and serious adverse reactions that occurred after the co-administration of ranitidine, ibuprofen and ciprofloxacin: completely reversible aseptic meningitis and irreversible bilateral sensorineural hearing loss, tinnitus, and vestibulopathy. Recurrent urinary inflammations treated with antibacterials, classic familial migraine, and allergy to trimethoprim-sulfamethoxazole and chromium were favourable predisposing factors for the adverse event in this patient. A close chronological relation between administration of drugs (especially ibuprofen) and adverse reactions was noted. No evidence of infection and/or autoimmune disease was found. The mechanism of these serious events may be explained as a hypersensitive reaction affecting the meninges and, partially, cochlea.

Mitochondrial 12S rRNA susceptibility mutations in aminoglycoside-associated and idiopathic bilateral vestibulopathy.

The mitochondrial 12S rRNA is considered a hotspot for mutations associated with nonsyndromic (NSHL) and aminoglycoside-induced hearing loss (AIHL). Although aminoglycoside ototoxicity is the most common cause of bilateral vestibular dysfunction, the conceivable role of 12S rRNA mutations has never been systematically investigated. We sequenced the 12S rRNA of 66 patients with bilateral vestibulopathy (BV) with (n=15) or without (n=51) prior exposure to aminoglycosides, as well as 155 healthy controls with intact vestibular function (sport pilots), and compared these to 2704 published sequences (Human Mitochondrial Genome Database). No mutations with a confirmed pathogenicity were found (A1555G, C1494T), but four mutations with a hitherto tentative status were detected (T669C, C960del, C960ins, T961G). Due to their predominant occurrence in patients without aminoglycoside exposure, their detection in controls and a weak evolutionary conservation, their pathogenic role in vestibulocochlear dysfunction remains provisional.

Follow-up of vestibular function in bilateral vestibulopathy.

OBJECTIVE: Bilateral vestibulopathy (BV) leads to a bilateral deficit of the vestibulo-ocular reflex and has various aetiologies. The main goal of this study was to determine the frequency and degree of recovery or worsening of vestibular function over time. METHODS: 82 patients (59 males, 23 females; mean age at the time of diagnosis 56.3 (SD 17.6) years) were re-examined 51 (36) months after the first examination. All patients underwent a standardised neuro-ophthalmological and neuro-otological examination. Electronystagmography with bithermal caloric irrigation was analysed by measurement of the mean peak slow phase velocity (SPV) of the induced nystagmus. Patients evaluated the course of their disease in terms of balance, gait unsteadiness and health related quality of life. RESULTS: Statistical analysis of the mean peak SPV of caloric induced nystagmus revealed a non-significant worsening over time (initial mean peak SPV 3.0 (3.5) degrees/s vs 2.1 (2.8) degrees/s). With respect to subgroups of aetiology, only patients with BV due to meningitis exhibited an increasing, but non-significant SPV (1.0 (1.4) degrees/s vs 1.9 (1.6) degrees/s). Vestibular outcome was independent of age, gender, time course of manifestation and severity of BV. Single analysis of all patients showed that a substantial improvement > or = 5 degrees/s occurred in two patients on both sides (idiopathic n = 1, Sjögren's syndrome n = 1) and in eight patients on one side (idiopathic n = 6, meningitis n = 1, Menière's disease n = 1). In 84% of patients there was impairment of their health related quality of life (42% slight, 24% moderate, 18% severe). Forty-three per cent of patients rated the course of their disease as stable, 28% as worsened and 29% as improved. CONCLUSIONS: Our data support the view that more than 80% of patients with BV do not improve. Thus the prognosis of BV is less favourable than assumed.

Vestibular hair cell regeneration and restoration of balance function induced by math1 gene transfer.

HYPOTHESIS: Delivery of math1 using an adenovector (Admath1.11D) results in vestibular hair cell regeneration and recovery of balance function in ototoxin-treated adult mice. BACKGROUND: Loss of peripheral vestibular function is associated with disease processes such as vestibular neuronitis, aminoglycoside ototoxicity, and aging. Loss of vestibular hair cells is one of the mechanisms underlying balance dysfunction in all of these disorders. Currently, recovery from these diseases relies on central vestibular compensation rather than on local tissue recovery. Overexpression of the mammalian atonal homologue math1 has been demonstrated to induce generation of hair cells in neonatal organ of Corti cultures and in the guinea pig cochlea in vivo and could thus provide an approach to local tissue recovery. METHODS: Admath1.11D was applied to cultures of aminoglycoside-treated macular organs or in vivo in a mouse aminoglycoside ototoxicity model. Outcome measures included histologic examination, immunohistochemistry, swim testing, and evaluation of the horizontal vestibulo-ocular reflex. RESULTS: Delivery of math1 resulted in the generation of vestibular hair cells in vitro after aminoglycoside-mediated loss of hair cells. Math1-treated mice showed recovery of the vestibular neuroepithelium within 8 weeks after Admath1.11D treatment. Assessment of animals after vector infusion demonstrated a recovery of vestibular function compared with aminoglycoside-only-treated mice. CONCLUSION: Molecular replacement of math1 may provide a therapeutic means of restoring vestibular function related to vestibular hair cell loss.

Distal effects in a model of proximal axonopathy: 3,3'-iminodipropionitrile causes specific loss of neurofilaments in rat vestibular afferent endings.

3,3'-Iminodipropionitrile (IDPN) is a neurotoxic compound that causes both a proximal neurofilamentous axonopathy and loss of the vestibular sensory hair cells. We used immunocytochemistry to examine changes in the expression of heavy, medium and light neurofilament (NF-H, NF-M, NF-L) proteins in the afferent terminals of vestibular sensory epithelia after IDPN exposure in rats. Acute, repeated and subchronic IDPN exposure induced a marked loss of NFs in the nerve terminals. The effect of subchronic IDPN was specific, as demonstrated by comparison with the synaptic membrane protein SNAP-25. In addition, Western blot analysis indicated specific loss of NFs in the vestibular receptors. Ultrastructural analysis revealed that afferent endings in the vestibular receptors were significantly preserved in animals exposed to subchronic IDPN, but that these endings showed NF segregation from microtubules followed by NF loss. These effects were closely paralleled by ultrastructural changes in the nerve terminals, particularly in the afferent contacts with the hair cells, and preceded hair cell loss. Thus, distal NF loss and nerve terminal pathology occur in the IDPN model of proximal neurofilamentous axonopathy. Similar distal pathology could also occur in human diseases characterized by proximal axonal swellings, particularly in amyotrophic lateral sclerosis.

Vestibular symptoms as a complication of sildenafil: a case report.

Potential vasodilator side effects of sildenafil such as headache, flushing, dyspepsia, heartburn, nasal congestion, dizziness and visual changes have been frequently observed. We report a 79-year-old man who developed severe vestibular neuritis-like symptoms (horizontal nystagmus with rotatory components and vomiting) two hours after taking 50 mg sildenafil. Additionally, the patient complained of tinnitus in both ears. Internal and neurological examination revealed no pathological findings and the patient had no history of cardiovascular disease. The symptoms lasted for 24 hours and then resolved completely. All of the patient's complaints indicated a drug-related phenomenon. This drug related adverse reaction should be included in the long list of potential side effects of sildenafil.