The classical symptoms of VN comprise an abrupt, acute attack of severe, debilitating vertigo which worsens with head movement, persistent nausea and vomiting, sustained, horizontal, spontaneous nystagmus directed towards the unaffected ear, postural imbalance and complete absence of auditory and neurological symptoms. The symptoms typically last for 7 to 10 days. Within days to weeks, the episodes of VN slowly subside without treatment [10]. The entire period of illness typically lasts for 6 weeks but in some cases, may persist for more than 9 weeks [11] [12]. The hallmark of VN which distinguishes it from Meniere disease and Labyrinthitis is the complete absence of auditory symptoms (tinnitus and hearing loss) and other neurological symptoms (diplopia and dysarthria). Other symptoms of VN that might ensue due to underlying vestibular injury are presence of residual dysequilibrium and rapid head movements [10].

Patients with symptoms characteristic of VN are recommended a series of tests and assessments in order to establish a definite diagnosis of the disease. A complete history and thorough physical examination is performed which is followed by an audiologic assessment along with electronystagmography, caloric testing, imaging, laboratory studies and Hallpike maneuver.

MRI is performed to locate the vertigo and to rule out the presence of central vertigo. It is the preferred method of imaging compared to computed topography (CT) scan as the former method shows visible augmentation of the vestibular nerve and provides a vague image of internal auditory canals and. Imaging helps in ruling out other diagnoses and should therefore only be considered in patients suspected of suffering from other illnesses as well. 

Laboratory studies are usually indicated to exclude other diagnoses and to differentiate among types of vertigo which may be found in other disease conditions. For instance, presence of abnormal serum glucose levels and anemia along with dizziness can be suggestive of cardiac dysrhythmia. 

Another specific diagnostic test that helps in determining the cause of vertigo is Hallpike maneuver. The patient is instructed to turn the head in three different angles in a lied back supine position and is checked for the presence of nystagmus. 

As described earlier, determination of the type of vertigo and distinguishing the disorder from other forms with similar symptoms is of paramount importance in order to establish accurate diagnosis and initiate treatment. VN is a self-limiting condition and the symptoms often subside without treatment through physiological vestibular compensation. Management of VN is largely symptomatic with the use of anticholinergics, antiemetics, antihistamines, benzodiazepines and corticosteroids. Presence of dehydration due to severe vomiting must be corrected by starting an intravenous (IV) line. Physical therapy aimed at performing vestibular rehabilitation also helps in improving vestibular function.

In a study performed to determine possible treatment options that may help in protecting the vestibular apparatus and restoring vestibular function, it was found that administration of methylprednisolone in tapered doses can help in sustaining vestibular function. Furthermore, use of antiviral agent (valacyclovir) alone and in combination with methylprednisolone has also proved to be helpful [13].

The majority of patients suffering from VN typically recovers from episodes of severe vertigo and imbalance within a week without treatment. A small percentage of patients may experience recurrent, less severe attacks with prolonged symptoms [7]. The prognosis of VN is reported to be better in children than in adults [9]. In a clinical study conducted by Matsuo and Sekitani, it was reported that VN shows partial resolution in some cases with 15% of cases out of total 38 patients demonstrating recurrence of vestibular symptoms after 1 year [8]. 

As described earlier, the definite cause of VN is not discovered yet. According to most researchers, underlying viral infection might lead to the development of VN by some uncertain mechanism. Another suspected cause that may precipitate VN is localized ischemia of the vestibular apparatus.

Presumably, viral infection of the vestibular nerve, vestibular ganglion or vestibular labyrinth is thought to be one of the most common causes of VN [3]. It is believed that VN may occur in children with preceding viral infection of the inner ear, viral infection caused by herpes virus in different parts of the body (cold sores, shingles, chicken pox) or other viral infections such as measles, flu, mumps, hepatitis and polio.

The incidence rate of VN is reported to be approximately 3.5 cases among 100,000 people [5]. In the United States, about 5.6% cases of dizziness reported in emergency are due to VN [4]. The disease can occur in both males or females with no established gender predominance. Studies have shown that VN typically effects middle-aged individuals in between 30 and 60 years [5].

To date, the etiology and definite pathophysiology of VN largely remain unknown. However, certain theories claim that the reactivation of a previously latent neurotropic virus (for instance, herpes simplex virus) in the vestibular ganglia accounts for the onset of an inflammatory reaction, leading to sudden dysfunction of afferent neuronal input of the vestibular apparatus. The disruption leads to self-limited episodes of vertigo. The evidence of suspected herpetic viral infection in pathophysiology of VN is suggested by histologic evaluation of the temporal bone that shows visible changes. The lesions occurring in VN are limited to vestibular neurons only with no involvement of cochlear and vestibular elements of inner ear. Therefore, the vertigo occurs solely in the absence of hearing loss and central involvement, a distinctive feature of VN [6].

Prevention of VN requires staying away from a possible viral infection as the disease is thought to occur due to such. Getting complete vaccination shots and following treatment regimen in patients who are already on antimicrobial therapy are also helpful measures in preventing VN. 

Vestibular neuronitis (VN), also referred to as vestibular neuropathy or acute peripheral vestibulopathy is described as acute, persistent dysfunction of the peripheral vestibular system that occurs as a result of inflammation of the vestibular division of the 8th cranial nerve. VN is characterized by prolonged episodes of nausea, vomiting and vertigo and is the second most common cause of peripheral vestibular vertigo [1] [2]. The etiology of VN is not completely known but it is thought to emerge from inflammatory reaction provoked by the herpes simplex virus where that effects the vestibular ganglion and vestibular nerve [3]. Diagnosis of VN requires meticulous assessment to rule out other similar diagnoses. VN, primarily exhibiting a peripheral cause, must be differentiated from other conditions possessing central cause. Such can be cerebral stroke and hemorrhage, the latter possibly fatal. In cases when central signs are suspected or vertigo is undifferentiated from others forms of dizziness, magnetic resonance imaging (MRI) is suggested to establish a definite diagnosis. Other diagnostic tests of VN comprise audiologic assessment, caloric testing, electronystagmography and Hallpike maneuver. Recovery following an episode of VN often occurs without definite treatment although symptomatic management helps in alleviating symptoms and improving the overall condition. Prolonged use of vestibular suppressants in order to reduce episodes of VN should be avoided as the physiologic compensation might be disrupted. Commonly used drugs to reduce symptoms of VN are anticholinergics, antiemetics, antihistamines, benzodiazepines and corticosteroids. Because the definite cause of VN is unknown, no specific preventive measures of the disease are established. Avoiding viral infection, getting appropriate vaccination and following complete course of antimicrobial drugs can be helpful in preventing VN. 

Vestibular neuronitis (VN) is a disorder of a part of the brain (called vestibular system) which results in a sudden, intensive episode of vertigo, (a type of dizziness in which the patient experiences false feeling of head spinning) followed by severe nausea and vomiting. 

The definite cause of VN is not known but it is thought to occur from a viral infection. Herpes simplex virus, a type of virus belonging to the neurotropic group of viruses, is suspected to be involved in the disease. It is believed that after entering the body, the virus resides in the brain in an inactive state and becomes reactivated later to cause infection which then results in VN. Other viral infections that may precipitate VN include measles, flu, mumps, hepatitis and polio. An ischemic attack in the vestibular apparatus may also cause VN.

The characteristic signs and symptoms of VN is a single, severe attack of vertigo that may last several days and may be followed by additional milder vertigo attacks later for several weeks. Other symptoms are nausea and vomiting which last for 7 to 10 days. Usually the initial episode of vertigo is the most severe one. It has been estimated that in the US, about 3.5% cases of dizziness reported in the ER are found to occur from VN. The disease equally affects males and females with no gender predominance. 

A series of hearing tests (audiologic assessment), tests for nystagmus (electronystagmography) and Hallpike maneuver are used to establish diagnosis. Laboratory studies and imaging (MRI scan) are performed to assure that the symptoms are characteristic of VN only and not caused by any other disease. Hallpike maneuver is a specific test used to identify the type of vertigo. In this test, the patient is instructed to lie down facing upwards three times with both eyes kept open. Throughout the assessment, the patient is checked for the appearance of nystagmus and symptoms of vertigo (appearance or worsening of symptoms). 

VN often subsides itself without medicinal intervention. However, the severe and recurring symptoms can be managed by symptomatic treatment. When diagnosed correctly and treated appropriately, the outcome is usually positive. Commonly prescribed medicines used to control symptoms of VN are anticholinergics, antiemetics, antihistamines, benzodiazepines and corticosteroids. Physical therapy is also applied to improve brain function in VN. It is recommended to stay away from all forms of viral infections and follow complete course of antimicrobial therapy during infection in order to prevent VN. 

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