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FEATURE	DETAIL
Risk Factors	Recent or concurrent viral upper respiratory infection; herpes simplex virus type 1 (HSV-1) seropositivity; age 30 to 60 years; no strong sex predominance
Etiology	Inflammatory damage to the vestibular portion of cranial nerve VIII, most commonly the superior vestibular nerve; suspected viral neuritis or postviral immune-mediated injury
Patient Presentation	Acute onset of severe, persistent, continuous rotational vertigo lasting days, with nausea, vomiting, and postural instability; NO hearing loss and NO focal neurological deficits
Classic Physical Exam	Spontaneous unidirectional horizontal-torsional nystagmus beating AWAY from the affected ear; positive head impulse test (HIT) with corrective saccade toward the lesion side; gait deviation toward the affected side; no skew deviation
Key Diagnostic Results	Clinical diagnosis; caloric testing shows unilateral vestibular hypofunction (canal paresis on the affected side); MRI of the brain with diffusion-weighted imaging (DWI) is normal and used primarily to exclude posterior fossa stroke
Management	Short-term vestibular suppressants (dimenhydrinate, meclizine) for symptom control in the first 48 to 72 hours only; early vestibular rehabilitation exercises; a short course of corticosteroids (methylprednisolone taper) may be considered within 72 hours of onset
Keywords	"Acute continuous vertigo," "follows a viral illness," "no hearing loss," "positive head impulse test," "nystagmus suppressed by visual fixation," "horizontal-torsional nystagmus"

1. Pathophysiology

Vestibular neuritis results from inflammation of the vestibular nerve, predominantly involving the superior division of the vestibular nerve (which innervates the superior and lateral semicircular canals and the utricle). The most widely accepted theory attributes the inflammation to reactivation of herpes simplex virus type 1 (HSV-1) latent in the vestibular ganglion (Scarpa's ganglion), analogous to how HSV reactivates in the geniculate ganglion in Bell's palsy. Histopathologic studies of temporal bones from patients who had vestibular neuritis have demonstrated viral particles and demyelination confined to the vestibular nerve.

The inflammation causes a sudden unilateral loss of vestibular afferent input to the brainstem vestibular nuclei. Under normal conditions, both vestibular nuclei maintain a balanced tonic firing rate. When one side is acutely silenced, the intact contralateral side generates an unopposed tonic signal. The brainstem interprets this asymmetry as continuous head rotation toward the healthy side, which is why the patient perceives relentless rotational vertigo.

This vestibular tone imbalance also explains the nystagmus pattern. The slow phase drifts toward the lesion side (because vestibular output from that side is reduced), and the fast corrective phase (which defines the direction of nystagmus) beats away from the affected ear. Because the superior vestibular nerve also carries some otolithic and torsional canal information, the nystagmus has both a horizontal and a torsional component.

The head impulse test (HIT) is positive because the damaged vestibular nerve cannot generate the brisk vestibulo-ocular reflex (VOR) needed to stabilize gaze during rapid head turns toward the affected side. The eyes lag behind, producing a visible corrective catch-up saccade back to the target. This is a critical peripheral localizing sign.

Importantly, the cochlear nerve is not involved in vestibular neuritis. The cochlear nerve and the inferior vestibular nerve run through a separate bony channel (the foramen singulare), which provides some anatomic protection. This is why hearing is preserved. If hearing loss accompanies the vertigo, the diagnosis shifts to labyrinthitis, not vestibular neuritis.

Over days to weeks, the brainstem undergoes central vestibular compensation: the intact side recalibrates its tonic output, and cerebellar circuits rebalance the vestibular nuclei. This is why symptoms gradually improve, and it is also why early mobilization and vestibular rehabilitation are essential for recovery.

2. Classification and Clinical Manifestation

Vestibular neuritis is classified by which division of the vestibular nerve is affected, and this determines which semicircular canals and otolith organs show dysfunction on testing.

TYPE	NERVE DIVISION	STRUCTURES AFFECTED	CLINICAL FEATURES
Superior vestibular neuritis (most common, ~65 to 70% of cases)	Superior vestibular nerve	Superior semicircular canal, lateral semicircular canal, utricle	Horizontal-torsional nystagmus; positive HIT for lateral canal; abnormal caloric test; cervical VEMP may be abnormal (utricular involvement)
Inferior vestibular neuritis (less common)	Inferior vestibular nerve	Posterior semicircular canal, saccule	May present with less pronounced horizontal nystagmus; positive HIT for posterior canal; caloric testing may be normal; abnormal ocular VEMP (saccular involvement)
Total vestibular neuritis (both divisions)	Both superior and inferior	All three canals, utricle, saccule	Most severe presentation; all caloric and VEMP tests abnormal on the affected side

The natural course of vestibular neuritis follows a recognizable timeline:

PHASE	TIMEFRAME	CLINICAL FEATURES
Acute phase	Day 0 to 3	Severe continuous vertigo, nausea, vomiting, spontaneous nystagmus, inability to walk unassisted
Subacute phase	Day 3 to 14	Gradual reduction of vertigo at rest; persistent imbalance during movement; nystagmus may only be visible with Frenzel goggles or during head-shaking
Chronic compensatory phase	Weeks 2 to 12	Vertigo largely resolved at rest; residual unsteadiness with rapid head movements; caloric paresis may persist on testing even after clinical recovery

3. Diagnostic Workup

TEST	ROLE	EXPECTED FINDING
Bedside head impulse test (HIT)	Best initial test (peripheral localizer)	Positive: corrective saccade when head is thrust toward the affected ear
Nystagmus assessment (with/without Frenzel goggles)	Best initial test (direction of lesion)	Unidirectional horizontal-torsional nystagmus beating away from the lesion; suppressed by visual fixation
HINTS exam (HIT, Nystagmus, Test of Skew)	Best bedside battery to differentiate peripheral from central cause	Peripheral pattern: positive HIT + unidirectional nystagmus + no skew deviation
Caloric testing (videonystagmography/electronystagmography)	Most accurate test for confirming unilateral vestibular hypofunction	Unilateral canal paresis (reduced or absent caloric response on the affected side); >20 to 25% asymmetry is considered significant
Audiometry	Rule out labyrinthitis or other inner ear pathology	Normal hearing bilaterally
MRI brain with DWI	Rule out posterior fossa stroke (cerebellar or brainstem infarct)	Normal; no restricted diffusion in the cerebellum or brainstem

Walkthrough of the workup:

The diagnosis of vestibular neuritis is fundamentally clinical. In the exam setting, you are expected to recognize the pattern at the bedside, not by ordering advanced imaging.

The HINTS exam is the single most important bedside tool for a patient presenting with acute continuous vertigo. It stands for Head Impulse, Nystagmus, and Test of Skew. A "peripheral" or "benign" HINTS pattern consists of: (1) a positive head impulse test (corrective saccade present, indicating a peripheral VOR deficit), (2) unidirectional nystagmus that obeys Alexander's law (increases when gazing in the direction of the fast phase), and (3) no skew deviation on alternating cover test. If all three features point to a peripheral lesion, the sensitivity for identifying a peripheral cause exceeds 95%, and this pattern has been shown to outperform early MRI in detecting posterior fossa stroke.

A dangerous or "central" HINTS pattern would include any one of: a negative (normal) head impulse test in a patient with acute vertigo (meaning the VOR is intact despite the patient's severe symptoms, suggesting a central lesion bypassing the vestibular nerve), direction-changing nystagmus, or the presence of skew deviation. Any one of these central signs warrants urgent MRI with DWI sequences to rule out cerebellar or brainstem stroke, particularly posterior inferior cerebellar artery (PICA) territory infarction.

Caloric testing via videonystagmography (VNG) is the confirmatory test for documenting unilateral vestibular hypofunction. Warm and cool water (or air) are irrigated into each ear canal sequentially, and the resulting nystagmus is measured. A canal paresis greater than 20 to 25% on the affected side confirms the diagnosis. This test is typically ordered in the outpatient setting once the acute phase has passed, not in the emergency department.

Audiometry is ordered not to confirm vestibular neuritis, but to exclude labyrinthitis. If the audiogram shows sensorineural hearing loss on the affected side, the diagnosis becomes labyrinthitis. Normal hearing is a defining feature of vestibular neuritis.

MRI of the brain is not required to diagnose vestibular neuritis, but it is the study you order when you are worried about a central cause. Its primary role is to exclude stroke. Note that early DWI can miss small cerebellar infarcts in the first 24 to 48 hours (up to 20% false-negative rate), which is why the HINTS exam is considered superior to MRI in the hyperacute period for distinguishing peripheral from central vertigo.

4. Management and Treatment

INTERVENTION	INDICATION	DETAILS
Vestibular suppressants	Acute symptom relief (first 48 to 72 hours only)	Meclizine 25 mg PO every 8 hours; OR dimenhydrinate 50 mg PO/IV every 6 hours; OR diazepam 2 to 5 mg PO every 8 hours
Antiemetics	Nausea and vomiting in the acute phase	Ondansetron 4 mg IV/PO every 8 hours; or promethazine 25 mg PO/IM/IV every 6 hours
Corticosteroids	Within 72 hours of symptom onset; may improve long-term vestibular recovery	Methylprednisolone starting at 100 mg/day PO, tapered over 3 weeks (e.g., decrease by 20 mg every 3 days); OR prednisone 1 mg/kg/day for 5 days then taper
Vestibular rehabilitation therapy (VRT)	Begin as early as possible once acute nausea/vomiting subsides	Supervised gaze stabilization exercises, balance retraining, habituation exercises; continue for 4 to 12 weeks
Discontinuation of suppressants	After 48 to 72 hours	Prolonged use delays central compensation and worsens long-term recovery

Acute stabilization (first 72 hours):

In the acute phase, the patient is often incapacitated with vertigo and vomiting. The immediate priority is symptomatic relief. Vestibular suppressants such as meclizine (an antihistamine), dimenhydrinate, or low-dose benzodiazepines (diazepam) reduce the tonic firing asymmetry perceived by the brainstem. Antiemetics are given concurrently.

If the patient presents within 72 hours of onset, a short course of corticosteroids should be considered. The most cited regimen is methylprednisolone 100 mg/day, tapered by 20 mg every 3 days over approximately 3 weeks. The rationale is to reduce inflammation and edema of the vestibular nerve within the bony canal, potentially preserving vestibular function. Evidence from the Strupp et al. (2004) trial showed improved caloric recovery at 12 months in steroid-treated patients. Antivirals (such as valacyclovir) have not been shown to add benefit beyond steroids alone and are not recommended.

The single most critical management point tested on exams: vestibular suppressants must be stopped after 48 to 72 hours. Continuing them beyond this window impairs the brainstem's ability to undergo central vestibular compensation, because the drugs dampen the very neural signals that drive the recalibration process. This is a commonly tested concept.

Long-term management:

The cornerstone of long-term recovery is vestibular rehabilitation therapy (VRT). This consists of graded exercises designed to promote central compensation:

Gaze stabilization exercises: the patient fixates on a stationary target while moving the head back and forth, retraining the VOR.
Habituation exercises: repeated exposure to movements that provoke dizziness, gradually desensitizing the vestibular system.
Balance and postural training: progressive exercises on unstable surfaces to retrain proprioceptive and visual-vestibular integration.

VRT should begin as soon as the patient can tolerate head movement (typically within 2 to 5 days of onset). Multiple randomized trials have demonstrated that early VRT significantly accelerates recovery and reduces the risk of chronic dizziness.

Contraindications and considerations:

Corticosteroids should be used cautiously in patients with uncontrolled diabetes, active peptic ulcer disease, or immunosuppression. In these populations, the risk-benefit ratio must be weighed individually. Benzodiazepines should be avoided in the elderly or in patients at risk for falls, as sedation compounds the existing postural instability.

A subset of patients (approximately 10 to 15%) develop benign paroxysmal positional vertigo (BPPV) as a secondary complication weeks after the initial neuritis, likely due to otoconia displacement from the damaged utricle. If the patient returns with brief positional vertigo triggered by rolling over in bed, the Dix-Hallpike test should be performed, and treatment is the Epley maneuver, not a repeat course of steroids.

5. Differential Diagnosis and Distractors

DIFFERENTIAL	WHY IT IS SIMILAR	KEY DISCRIMINATOR
Labyrinthitis	Also causes acute continuous vertigo with the same nystagmus pattern	Labyrinthitis includes unilateral sensorineural hearing loss and/or tinnitus; vestibular neuritis has normal hearing
Posterior fossa stroke (PICA or AICA territory)	Acute vertigo, nausea, imbalance; may mimic peripheral vertigo closely	Central HINTS pattern: negative (normal) head impulse test, direction-changing nystagmus, or skew deviation; may have cerebellar signs (dysmetria, truncal ataxia); stroke risk factors present
Benign paroxysmal positional vertigo (BPPV)	Causes vertigo and nystagmus	BPPV episodes are brief (seconds), triggered by positional changes, with symptom-free intervals; nystagmus is positional and fatigable on Dix-Hallpike; vestibular neuritis causes continuous vertigo lasting days
Meniere disease	Episodic vertigo involving the inner ear	Meniere episodes last 20 minutes to several hours, are recurrent, and include fluctuating sensorineural hearing loss, tinnitus, and aural fullness; vestibular neuritis is a single prolonged episode without hearing symptoms
Vestibular migraine	Acute vertigo that can last hours to days	Associated with headache (though not always present during the episode), photophobia, phonophobia, or visual aura; history of migraine; no canal paresis on caloric testing
Acoustic neuroma (vestibular schwannoma)	Involves the vestibular nerve	Presents with gradual progressive unilateral hearing loss and tinnitus over months to years, not acute vertigo; MRI shows enhancing mass at the cerebellopontine angle
Multiple sclerosis (brainstem plaque)	Can cause acute vertigo in young adults	Look for other neurological deficits separated in time and space; internuclear ophthalmoplegia; MRI shows periventricular white matter lesions

6. Traps and High-Yield Pearls

The most common way students lose points on vestibular neuritis questions is by confusing a peripheral pattern with a central pattern on the HINTS exam. The critical trap is this: a normal (negative) head impulse test in a patient with acute vertigo is not reassuring. It is actually an alarming sign. In vestibular neuritis, the VOR is broken on the affected side, so the HIT should be abnormal (positive). If the HIT is normal, the vestibular nerve and peripheral apparatus are functioning, which means the vertigo is originating centrally, and you must suspect stroke. Exam writers exploit this by presenting a patient with acute vertigo, nausea, and a "normal" HIT, hoping students will incorrectly choose vestibular neuritis because the symptoms sound peripheral.

The second common trap involves prolonged use of vestibular suppressants. When a vignette describes a patient with vestibular neuritis who is "not improving after two weeks," the answer is almost never to add stronger medication. Instead, the correct next step is to discontinue suppressants and initiate vestibular rehabilitation. The suppressants themselves are the obstacle to recovery.

Third, students often confuse vestibular neuritis with labyrinthitis. The distinguishing feature is straightforward but easily overlooked: hearing loss means labyrinthitis, no hearing loss means vestibular neuritis. If the stem includes any mention of reduced hearing, tinnitus, or abnormal audiometry on the affected side, do not select vestibular neuritis.

Finally, remember that MRI can be falsely negative in the first 24 to 48 hours after a posterior fossa stroke. A normal MRI in the hyperacute setting does not exclude stroke. The HINTS exam, when performed by a trained examiner, has been shown to be more sensitive than early DWI-MRI for detecting posterior circulation infarcts. If the HINTS pattern is central, pursue stroke workup regardless of initial MRI results.

The core competency being tested is the ability to differentiate peripheral from central vertigo at the bedside using the HINTS exam, to recognize the natural history of vestibular neuritis, and to understand why early vestibular rehabilitation and timely discontinuation of suppressants are the most important management decisions.

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