A unique association of bifacial weakness, paresthesia and vestibulocochlear neuritis as post-COVID-19 manifestation in pregnant women: a case report.

SARS-CoV-2 is an infection due to a novel virus belonging to the coronavirus family. Since December 2019, first human cases of COVID-19 have been identified in Wuhan (China) and rapidly has been progressed to a global pandemic declared by the world health organization (WHO) on March 11th 2020. The major complication of COVID-19, is pneumonia, but other presentations like cardiovascular and neurological complications have been reported. Herein, we report a first case of pregnant women presented with bifacial weakness and paraesthesia (BFP) associated to a vestibulocochlear neuritis as post-COVID-19 manifestation. This is a 36-year-old Moroccan female patient with a history of SARS-CoV-2 positive 6 weeks before admission. She presented to the emergency department with rapid bifacial paralysis, bilateral lower extremity paresthesia, vertigo, nausea, vomiting and right auricular pain. An acute stroke was ruled out after neurological examination and brain MRI. Clinical presentation, neurophysiological, audiometry and videonystagmography workup additionally to CSF findings were suggestive of a variant of Guillain Barré Syndrome (GBS), which is BFP associated to right vestibulocochlear neuritis. The patient was treated with Intravenous immunoglobulins (IVIG) therapy associated with intravenous steroids. The patient made a complete recovery of the right facial palsy and the sensorineural hearing loss but still have tingling in lower limbs and left facial palsy at 2 weeks´ follow-up. BFP can be induced by COVID-19 as a postinfectious immune-mediated complication. Regarding the pathophysiology of vestibular neuritis, is probably similar to other viral infection causing nerve damage. Clinicians should consider the association of vestibulocochlear neuritis and BFP as a post SARS-CoV-2 manifestation.

Vestibular and cochlear nerve enhancement on MRI and its correlation with vestibulocochlear functional deficits in patients with Ramsay Hunt syndrome.

OBJECTIVE: The correlation between enhancement of the vestibulocochlear nerves on gadolinium-enhanced magnetic resonance imaging (MRI) and vestibulocochlear functional deficits was examined in patients with Ramsay Hunt syndrome (RHS). METHODS: Nineteen patients with RHS who showed herpes zoster oticus, peripheral facial palsy, and vertigo were enrolled. Canal paresis (CP) in the caloric test, abnormal response to ocular and cervical vestibular myogenic potentials (oVEMP and cVEMP), and refractory sensorineural hearing loss were evaluated. MRI images perpendicular to the internal auditory canal were reconstructed to identify the superior (SVN) and inferior vestibular nerves (IVN) and the cochlear nerve (CV). The signal intensity increase (SIinc) of the four-nerve enhancement was calculated as an index. RESULTS: Among RHS patients, 79%, 53%, 17% and 26% showed CP in the caloric test, abnormal responses to oVEMP and cVEMP, and refractory sensorineural hearing loss, respectively. SIinc rates of the SVN were significantly increased in RHS patients with CP in the caloric test, and with abnormal responses to oVEMP and cVEMP. SIinc rates of the SVN tended to increase in RHS patients with refractory sensorineural hearing loss (p = 0.052). SIinc rates of the IVN were significantly increased in RHS patients with abnormal responses to oVEMP and cVEMP, and refractory sensorineural hearing loss, but not in those with CP in the caloric test. SIinc rates of the CN were significantly increased in RHS patients with CP in the caloric test, abnormal response to oVEMP and refractory sensorineural hearing loss, but not in those with abnormal response to cVEMP. CONCLUSION: In patients with RHS, the origin of vertigo may be superior vestibular neuritis, which is affected by reactive varicella-zoster virus from the geniculate ganglion of the facial nerve through the faciovestibular anastomosis. The results also suggested that in some RHS patients, inferior vestibular neuritis contributes to the development of vertigo and that the origin of refractory sensorineural hearing loss is cochlear neuritis.

Vestibular Neuritis: Recent Advances in Etiology, Diagnostic Evaluation, and Treatment.

Purpose of Chapter: This chapter highlights the recent advances in etiology, diagnostic evaluation, and management of vestibular neuritis (VN). Recent Findings: The viral hypothesis has been strengthened with new evidence as the main etiology of VN. Recent evidence indicates that bedside oculomotor findings play a critical role in differentiating VN from stroke. The implementation of cervical and ocular vestibular evoked myogenic potential, and video head impulse test in vestibular function testing has made it possible to diagnose selective damage of the vestibular nerves. The management of the acute phase of VN is primarily medical, while long-term treatment is designed to improve vestibular compensation. Summary: VN is clearly defined as an important viral inner ear disorder.

[Vestibular function features and prognosis of vestibular neuritis in children].

Objective: To investigate the clinical characteristics, prognosis and affected branches of vestibular neuritis in children. Methods: Twenty-five patients with vestibular neuritis in ENT department, Beijing Children's Hospital, from October 2015 to October 2016, were collected. All patients were 4-14 (mean 9.8) years old including 17 boys and 8 girls. The clinical manifestations history, pure tone audiometry (PTA), vestibular function tests were done for each patient. We also took the blood samples for pathogenic virus in order to analyze the premorbid risk factors. Results: Rotational vertigo were complained by all presents. There were 17 cases (68%, 17/25) with nausea and vomiting and 19 cases (76%, 19/25) with balance dysfunction. There were 12 cases (60%, 12/20) with positive results in 20 blood samples for virology, among which 6 cases of influenza B virus and 4 cases of herpes simplex virus, 1 case of cytomegalovirus and 1 case of coxsackie were identified. The results of PTA were normal. Bithermal caloric test was abnormal in 22 cases (88%, 22/25). The ocular vestibular-evoked myogenic potential (oVEMP) in 12 cases (48%, 12/25) and cervical vestibular-evoked myogenic potential (cVEMP) in 5 cases (20%, 5/25) were abnormal. The bithermal caloric test along with oVEMP and cVEMP in 4 cases (16%, 4/25) were abnormal. The bithermal caloric test and oVEMP in 7 cases (28%, 7/25) were abnormal. The bithermal caloric test in 11 cases (44%, 11/25) were abnormal. The oVEMP in 1 cases (4%, 1/25) was abnormal. The cVEMP in 1 cases (4%, 1/25) was abnormal. All patients recovered well, but the time varied. The symptoms of 21 patients were complete recovery within 1 month. 3 patients were complete recovery within 2 months (aged 8 - 14 years old). One patient was complete recovery within 6 months (aged 13 years old). Conclusion: Rotary vertigo is most commonly in children with vestibular neuritis, accompany with imbalance and vomiting. The vestibular neuritis in children might be related with upper respiratory tract infection. Audiometry test is normal. Because of the bithermal caloric test and oVEMP are obvious abnormality, therefore it is speculated that the superior vestibular nerve may most commonly be affected. The younger patients with vestibular neuritis recovered more quickly than the older children.

Management of Recurrent Vestibular Neuritis in a Patient Treated for Rheumatoid Arthritis.

PURPOSE: This clinical report is presented to describe how results of vestibular function testing were considered along with other medical history to develop a management plan that was ultimately successful. METHOD: The patient underwent audio-vestibular assessment including comprehensive audiogram, videonystagmography, cervical vestibular evoked myogenic potential, and postural stability testing. RESULTS: Results from initial testing were most consistent with uncompensated peripheral vestibular dysfunction affecting the right superior vestibular nerve. These results, considered along with history and symptoms, supported vestibular neuritis. After a second vertigo event, we became concerned about the potential temporal association between the patient's rheumatoid arthritis treatment and symptom onset. It is established that treatment for rheumatoid arthritis can exacerbate latent viral issues, but this has not specifically been reported for vestibular neuritis. There are reports in the literature in which patients successfully used viral suppressant medication to decrease viral activity while they were able to continue benefiting from immunosuppressive therapy. We hypothesized that, if the current patient's vestibular neuritis events were related to her treatment for rheumatoid arthritis, she may also benefit from use of viral suppressant medication while continuing her otherwise successful immunosuppressive intervention. CONCLUSIONS: Patients treated with biologic disease-modifying antirheumatic drugs are more susceptible to viral issues, and this may include vestibular neuritis. For the current case, identifying this possibility and recommending viral suppressant medication allowed her to continue with successful treatment of rheumatoid arthritis while avoiding additional vertigo events.

Differential Involvement during Latent Herpes Simplex Virus 1 Infection of the Superior and Inferior Divisions of the Vestibular Ganglia: Implications for Vestibular Neuritis.

Controversy still surrounds both the etiology and pathophysiology of vestibular neuritis (VN). Especially uncertain is why the superior vestibular nerve (SVN) is more frequently affected than the inferior vestibular nerve (IVN), which is partially or totally spared. To address this question, we developed an improved method for preparing human vestibular ganglia (VG) and nerve. Subsequently, macro- and microanatomical as well as PCR studies were performed on 38 human ganglia from 38 individuals. The SVN was 2.4 mm longer than the IVN, and in 65% of the cases, the IVN ran in two separate bony canals, which was not the case for the SVN. Anastomoses between the facial and cochlear nerves were more common for the SVN (14/38 and 9/38, respectively) than for the IVN (7/38 and 2/38, respectively). Using reverse transcription-quantitative PCR (RT-qPCR), we found only a few latently herpes simplex virus 1 (HSV-1)-infected VG (18.4%). In cases of two separate neuronal fields, infected neurons were located in the superior part only. In summary, these PCR and micro- and macroanatomical studies provide possible explanations for the high frequency of SVN infection in vestibular neuritis.IMPORTANCE Vestibular neuritis is known to affect the superior part of the vestibular nerve more frequently than the inferior part. The reason for this clinical phenomenon remains unclear. Anatomical differences may play a role, or if latent HSV-1 infection is assumed, the etiology may be due to the different distribution of the infection. To shed further light on this subject, we conducted different macro- and microanatomical studies. We also assessed the presence of HSV-1 in VG and in different sections of the VG. Our findings add new information on the macro- and microanatomy of the VG as well as the pathophysiology of vestibular neuritis. We also show that latent HSV-1 infection of VG neurons is less frequent than previously reported.

Superior Versus Inferior Vestibular Neuritis: Are There Intrinsic Differences in Infection, Reactivation, or Production of Infectious Particles Between the Vestibular Ganglia?

HYPOTHESIS: Intrinsic differences in neurons of the vestibular ganglia result in the increased likelihood of superior vestibular ganglion involvement in vestibular neuritis. BACKGROUND: Vestibular neuritis is hypothesized to result from herpes simplex type I (HSV1) infection or reactivation in vestibular ganglia. Involvement of the inferior vestibular ganglion is extremely rare in patients with vestibular neuritis. METHODS: Primary cultures of rat superior and inferior vestibular ganglion neurons (VGNs) were cultivated separately. Neurons were lytically and latently infected with HSV1 with a US11-green fluorescent protein (GFP) chimera. Percentage lytic infection and baseline reactivation was assessed by microscopy for GFP fluorescence. Trichostatin-A (TSA) was used to stimulate HSV1 reactivation. Virion production was assessed by viral titers. Relative numbers of latency-associated (LAT) transcripts were determined by real-time reverse-transcription polymerase chain reaction (real-time RT-PCR). RESULTS: Lytic infection rates were equivalent between the two ganglia (p > 0.05). Lytic infections yielded similar amounts of plaque-forming units (p > 0.05). Relative amounts of LAT transcripts did not differ between latently infected superior and inferior VGNs. Latently infected cultures showed no differences in rates of baseline and TSA-induced HSV1 reactivation (p > 0.05). Production of virions was not significantly different between reactivated, latently infected superior versus inferior VGNs (p = 0.45). CONCLUSION: Differences in prevalence of superior and inferior vestibular neuritis do not result from intrinsic differences in HSV1 infection or virion production of these neurons. Other factors, such as the length and width of the bony canal containing the ganglia and nerves, account for the greater involvement of the superior vestibular ganglion in vestibular neuritis.

Herpes simplex virus type 1 in saliva of patients with vestibular neuronitis: a preliminary study.

OBJECTIVES: Vestibular neuronitis (VN) is an inflammatory disease of the vestibular nerve, presumably caused by reactivation of the herpes simplex virus type l (HSV-1). We hypothesized that HSV-1 might be detected in saliva of patients with VN due to migration of the reactivated virus from the vestibular ganglia to the parotid gland. METHODS: Twenty-one patients with VN and 15 healthy controls participated. HSV-1 DNA detection was performed using the real-time polymerase chain reaction method. Sera were collected and stored to be later analyzed for immunoglobulin (Ig) G and IgM antibody titers against HSV-1 by immunofluorescence and enzyme linked immunosorbent assay methods, respectively. RESULTS: HSV-1 was detected in saliva of 14% of VN patients and in 6% of controls (P>0.05). Serological testing revealed borderline IgM (optical density±10% average of 2 cut off serums) antibodies to HSV-1 in 75% of patients versus 13% of controls (P=0.01). The IgG antibody test was positive in 17 of 20 patients and borderline (IgG ≤1:16) in 2 of 20 patients tested whereas 13 of 15 controls had positive IgG test results (P>0.05). CONCLUSIONS: In this preliminary study we found serological evidence of higher exposure of patients with VN to HSV-1 in the past. We were not able to demonstrate that the virus can be detected in saliva of VN patients as evidence for herpetic infection or reactivation.

Ménière's disease is a viral neuropathy.

Morphological and clinical evidence supports a viral neuropathy in Ménière's disease (MD). Quantitative examination of 11 sectioned temporal bones (TBs) from 8 patients with a history of MD revealed a significant loss of vestibular ganglion cells in both the endolymph hydropic (EH) and non-EH ears. Transmission electron microscopy of vestibular ganglion cells excised from a patient with MD revealed viral particles enclosed in transport vesicles. Antiviral treatment controlled vertigo in 73 of 86 patients with vestibular neuronitis (85%) and 32 of 35 patients with MD (91%).

Evidence for a viral neuropathy in recurrent vertigo.

The concept that reactivation of latent neurotropic viruses (i.e. Herpesviridae group) in the vestibular ganglion is responsible for recurrent vestibulopathies is presented. A similar histopathologic degeneration of vestibular ganglion cells in vestibular neuronitis (VN), Ménière's disease and benign paroxysmal positional vertigo is presented to support this concept. The clinical response (relief of vertigo) to the administration of antiviral medication in these syndromes provides practical evidence of a viral neuropathy in patients with recurrent vertigo. Relief of vertigo after this treatment was 90% in VN, Ménière's disease and VN. The relief of positional vertigo (benign paroxysmal positional vertigo) was 66%.

A child with vestibular neuritis. is adenovirus implicated?

Vertigo in children is relatively under examined in the literature. Among its causes, vestibular neuritis (VN) represents only 2% of cases, with its etiology remaining unknown. We report for the first time a 4-year-old boy with vestibular neuritis and serological results compatible with adenoviral infection. Serological diagnosis was performed on the basis of a rise and consequent normalization of complement fixation (CF) titers of the plasma antibodies. Although we were not able to detect exactly when the infection started, we were able to detect an increased level of adenovirus antibodies by CF titers, followed by a decrease (i.e. 1/16, then 1/8, then <1/4) during the recovery. This is typical of a resolving infection. Furthermore, that this increase in antibodies was specific to an adenovirus infection was suggested by the observation that we did not detect increases in antibodies to other common viruses (i.e. herpes simplex and zoster viruses, Epstein-Barr virus, cytomegalovirus, influenza and parainfluenza viruses). This allows us to exclude the chance of nonspecific antibody activation. We concluded that, although our data do not formally demonstrate an involvement of adenovirus in VN, they suggest such an involvement. This may be of interest, given that a viral etiology for VN has been proposed but not definitively proven.

Vestibular neuritis caused by enteroviral infection.

Vestibular neuritis is characterized by the sudden onset of nausea, vomiting, and spontaneous horizontal or horizonto-rotatory nystagmus. The etiology of the disease is multifactorial. Mumps, rubella, herpes simplex virus type 1, cytomegalovirus, and Epstein-Barr virus may have a role in the disease. Enteroviruses are among the other rare causes. This report presents a 7-year-old male admitted with nausea, vomiting, rotatory vertigo, horizonto-rotatory nystagmus with positive Romberg's sign and positive head-thrust test. Cranial magnetic resonance imaging and audiometry of the patient were normal. He was diagnosed with vestibular neuritis, and steroid therapy was initiated. At the second month of follow-up, all symptoms had regressed. To the best of our knowledge, this case report describes the first pediatric patient in whom enteroviral ribonucleic acid is documented both in cerebrospinal fluid and in nasopharyngeal material in active disease. This finding supports the possible role of enteroviruses in the etiology of vestibular neuritis.

Herpes encephalitis preceded by ipsilateral vestibular neuronitis.

A 74-year-old woman developed vertigo and jerk nystagmus to the left with normal cerebral imaging. Three days later she developed fever, altered mental state and left medial temporal lobe hypodensity, confirmed on lumbar puncture to be due to herpes simplex type 1 encephalitis. We propose that the patient had vestibular neuronitis caused by HSV-1 that progressed to ipsilateral temporal lobe encephalitis.

Vestibular neuritis: etiopathogenesis.

Vestibular neuritis presents as sudden unilateral vertigo in the absence of hearing loss or neurologic involvement and is thought to be due to neurotropic viruses. Its morbidity is unknown and it affects both sexes equally, with the highest incidence at 40-50 years of age. The etiology of this condition has been ascribed to viral, bacterial and protozoan infections, as well as allergic and auto-immune causes. Inflammation of the vestibular nerve is followed by demyelination and loss of function, which is not always reversible. Higher plasma fibrinogen and CRP levels in the acute phase, longer BERA latency and I-III interval and increased gadolinium uptake in the vestibular nerve and Scarpa's ganglion on enhanced MRI confirm the inflammatory nature of the process. An animal model of vestibular neuritis using retroauricular inoculation of herpes simplex virus in mice, histologic findings in the temporal bone of individuals who had vestibular neuritis, and influenza A virus infection in cultured Schwann's cells suggest viral infection as the main aetiologic cause.

The three faces of vestibular ganglionitis.

We present temporal bone and clinical evidence that common syndromes of recurrent vertigo are caused by a viral infection of the vestibular ganglion. In the present series, histopathologic and radiologic changes in the vestibular ganglion and meatal ganglion were consistent with a viral inflammation of ganglion cells in cases of Meniere's disease, benign paroxysmal positional vertigo, and vestibular neuronitis. Clinical observations of multiple neuropathies involving cranial nerves V, VII, and VIII on the same side in patients with recurrent vertigo are best explained by a cranial polyganglionitis caused by a neurotrophic virus, which is reactivated by a stressful event later in life. The reactivation of the latent virus may manifest as one of the above vertigo syndromes, depending on the part of the vestibular ganglion that is inflamed, the type and strain of the virus, and host resistance.