COVID-19 has infected millions of people worldwide causing millions of deaths. COVID-19 has many serious effects on organs of the body especially the respiratory system causing pneumonia and acute respiratory distress syndrome (ARDS). The disease also has severe complications on other different organs; kidneys and liver which may end in multi-organ failure. Most common symptoms that have been detected in large section of patients were fever, cough and loss of taste or smell and less commonly sore throat, headache and muscle pain. The incidence of vertigo or dizziness is a rare symptom of COVID-19. In this case report, we introduce a 59-year-old male patient suffering from acute vertigo attack after COVID-19 infection. The patient had negative medical history of vertigo and any ear diseases. The patient received REGEN-COV (casirivimab and imdevimab) for COVID-19 and meclizine for vertigo. Vertigo attacks lasted for the two weeks follow up after disappearance of COVID-19 symptoms despite receiving vertigo medication. In conclusion, vertigo may be the sole neurological manifestation of COVID-19. More observational studies should address this symptom and researchers should also focus on identifying the origin of developing vertigo and the direct or indirect mechanisms that SARS-CoV-2 triggers to develop dizziness in general. This research should deliver a clear message, especially to ER physicians to consider proper referral of these patients without underestimating the risk of developing more serious COVID-19 symptoms as ARDS and multi-organ failure if no proper testing and follow-up are provided.

Extensive research has been conducted on the pathophysiological sequelae of the SARS-CoV-2 virus. Newer symptoms pertaining to cardiovascular, gastrointestinal, and neurological systems, apart from the recognized respiratory system, are constantly being reported. We report a case of a 22-year-old female with a seven-day history of COVID-19 who presented to the emergency department with an acute vertigo attack associated with nausea and vomiting for three hours. Physical examination and audiometry showed no neurological and auditory deficits; she was diagnosed with vestibular neuritis. The patient was managed with betahistine hydrochloride and an antihistamine. There was a complete resolution of symptoms after seven days. There have been reports of new-onset vertigo associated with SARS-CoV-2 infection, but more well-designed studies are needed to establish an association between COVID-19 and vertigo.

In addition to the known pathophysiological sequelae of the SARS-COV-2 virus and its related respiratory symptoms, several studies have recently reported cardiovascular, gastrointestinal, and neurological symptoms of new-onset after a history of infection. Vertigo is a symptom indicating dysfunction of the vestibular system and this report of a 60-year-old female patient points out the possible association between new-onset vertigo and SARS-COV-2 infection. A 60-year-old diabetic and hypertensive female patient with a 9-days history of COVID-19 symptoms presented to the emergency department with acute vertigo attack without nausea or vomiting. A full physical examination showed no other auditory or neurological symptoms and she never experienced vertigo before. Laboratory findings confirmed a current COVID-19 infection. The patient was managed with antihypertensive, anti-vertigo medications, and COVID-19 protocol for mild cases. After discharge, the patient was advised to continue the anti-vertigo drugs and COVID-19 medications. SARS-COV-2 may lead to vestibular neuritis causing vertigo and other related symptoms, but more well-designed observational studies with a large sample size are needed to establish a definite association between COVID-19 and vertigo.

Vestibular neuritis is a disorder selectively affecting the vestibular portion of the eighth cranial nerve generally considered to be inflammatory in nature. There have been no reports of severe acute respiratory syndrome coronavirus 2 causing vestibular neuritis. We present the case of a 42-year-old Caucasian male physician, providing care to COVID-19 patients, with no significant past medical history, who developed acute vestibular neuritis, 2 weeks following a mild respiratory illness, later diagnosed as COVID-19. Physicians should keep severe acute respiratory syndrome coronavirus 2 high on the list as a possible etiology when suspecting vestibular neuritis, given the extent and implications of the current pandemic and the high contagiousness potential.

The coronavirus disease 2019 (COVID-19) pandemic has created a global health crisis. Though respiratory symptoms have been the usual manifestations, the presentation in some cases may be atypical with various neurological and cutaneous manifestations. We present a case of a 63-year-old female diagnosed with COVID-19 and associated rare manifestations during her visit to Europe.

Differentiating central vestibulopathy from more common vestibular disorders is crucial because it often necessitates different treatment strategies, and early detection can help to minimize potential complications. Isolated nodular infarct is one of the central brain lesions that can mimic peripheral vertigo. We present a case of isolated nodular infarct that had been misdiagnosed as vestibular neuritis on the contralateral side at the initial evaluation. The patient was successfully treated with anticoagulants and antihyperlipidemic agents. Clinicians should keep in mind that some causes of central vertigo mimic peripheral vestibulopathy at the early stage.

Elevation of cardiac troponin (cTn), a sensitive biomarker of myocardial injury, is frequently observed in severe acute neurological disorders. Case reports suggest that cardiac dysfunction may also occur in patients with transient global amnesia (TGA). Until now, no study has systematically assessed this phenomenon.
We performed a case-control study using data of consecutive patients presenting with TGA from 2010 to 2015. Multiple logistic regression analysis accounting for age, sex and cardiovascular risk factors was performed to compare the likelihood of myocardial injury [defined as elevation of cTn > 99th percentile (≥14 ng/L); highly sensitive cardiac troponin T assay] in TGA with three reference groups: migraine with aura, vestibular neuritis and transient ischaemic attack (TIA).
Cardiac troponin elevation occurred in 28 (25%) of 113 patients with TGA. Patients with TGA with cTn elevation were significantly older, more likely to be female and had higher blood pressure on admission compared with those without. The likelihood of myocardial injury following TGA was at least more than twofold higher compared with all three reference groups [adjusted odds ratio, 5.5; 95% confidence interval (CI), 1.2-26.4, compared with migraine with aura; adjusted odds ratio, 2.2; 95% CI, 1.2-4.4, compared with vestibular neuritis; adjusted odds ratio, 2.3; 95% CI, 1.3-4.2, compared with TIA].
One out of four patients with TGA had evidence of myocardial injury as assessed by highly sensitive cTn assays. The likelihood of myocardial injury associated with TGA was even higher than in TIA patients with a more pronounced cardiovascular risk profile. Our findings suggest the presence of a TGA-related disturbance of brain-heart interaction that deserves further investigation.

The term vestibular paroxysmia (VP) was introduced for the first time by Brandt and Dieterich in 1994. In 2016, the Barany Society formulated the International Classification of VP, focusing in particular on the number and duration of attacks, on the differential diagnosis and on the therapy. Ephaptic discharges in the proximal part of the eighth cranial nerve, which is covered by oligodendrocytes, are assumed to be the neural basis of VP. We report the first case in literature of an onset of symptoms and signs typical of VP in a young man following acute unilateral vestibular loss not combined with auditory symptoms. Indeed, the pathogenic mechanism affected only the vestibular nerve as confirmed by the presence of a stereotyped nystagmus pattern. The magnetic resonance imaging didn\'t reveal any specific cause therefore we suggest the possible role of a neuritis triggering an ephaptic discharge as the neural mechanism of VP.

This retrospective, observer blinded case-control study aims to compare the prevalence of neurovascular conflicts (NVCs) of the vestibulocochlear nerve and the anterior inferior cerebellar artery (AICA) in patients presenting with clinical signs of acute vestibular neuritis with and without subsequent objective vestibular function loss (VFL). 58 acute cases of clinically suspected acute vestibular neuritis were investigated with same day cranial MRI at a tertiary referral centre and compared to 61 asymptomatic controls. The prevalence of NVCs in cases with objective VFL were also compared to cases without VFL. Radiologists described the NVC as \"no contact\" (Grade 0), \"contact < 2 mm\" (Grade 1), \"contact > 2 mm\" (Grade 2) and \"vascular loop presence\" (Grade 3) without knowledge of neurotological data. Neurotological data was collected without knowledge of MRI findings. Vestibular function was tested by bithermic caloric irrigation. 26 cases (45%) showed caloric VFL (Group A), whereas 32 (55%) exhibited no VFL (Group B). Group A included 13 cases with NVCs (50%), Group B included 26 NVC cases (82%) (p = 0.012) and the control group included 16 individuals (26%) (p < 0.001 for comparison of all 3 groups). Group B had a significantly higher NVC-Grading than Group A (p = 0.009). There was no statistically significant association between NVCs and either SNHL or tinnitus (p > 0.05). Our results suggest that patients presenting with clinical signs of acute vestibular neuritis who show symmetrical caloric vestibular function test results have a significantly higher NVC prevalence in the cerebellopontine angle.
Il presente studio retrospettivo a singolo cieco si pone come obbiettivo quello di valutare in che percentuale di casi di pazienti che si presentano con sintomatologia compatibile con neurite vestibolare acuta, con e senza perdita oggettiva della funzione vestibulare (VFL), sia presente un conflitto neurovascolare fra il nervo vestibolococleare e la arteria cerebellare anteroinferiore (AICA). 58 pazienti con sintomatologia suggestiva per neurite vestibolare acuta, valutati con RMN presso un centro di terzo livello, sono stati confrontati con 61 pazienti asintomatici. I radiologi hanno dato valutato la presenza di conflitto neurovascolare, in assenza di dati clinici, conferendo ai rilievi oggettivi una valutazione in una scala da 0 a 3 a seconda che il contatto fosse: nesuno; inferiore a 2 mm; superiore ai 2 mm; presenza di vacular loop. I reperti neurootologici sono stati quindi raccolti all’oscuro del risultato dell’imaging. La funzione vestibolare è stata testata con prova calorica bitermica. Alla prova calorica 26 casi (45%) hanno mostrato segni oggettivi di deficit vestibolare (Gruppo A), 32 casi (55%) non hanno invece mostrato alcun deficit labirintico (Gruppo B). Il gruppo A ha incluso 13 casi (50%) con evidenza di conflitto neurovascolare (NVC), il gruppo B ha incluso 26 casi con NVC (82%) (p = 0.012) mentre i controlli hanno incluso 16 casi con NVC (26%). La differenza fra i tre gruppi ha mostrato significatività statistica (p<0.001). Il Gruppo B ha mostrati un associazione con un grading di conflitto piu elevato rispetto al Gruppo A (p = 0.009). La presenza di NVC non ha avuto un associazione statisticamente significativa ne con la presenza di SNHL ne con la presenza di acufene (p > 0.05). I nostri dati indicano che la presenza di conflitti neurovascolari a livello dell’angolo pontocerebellare è superiore in quei pazienti che in presenza di una sintomatologia compatibile con neurite vestibolare acuta abbiano una funzionalità simmetrica alla prova calorica.