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VESTIBULAR AND BALANCE DISORDERS

Vestibular Neuritis — Specialist Diagnosis and Rehabilitation in Hyderabad at KIMS

Vestibular neuritis is an acute, usually monophasic inflammatory disorder of the vestibular nerve that produces sudden, severe, continuous vertigo lasting hours to several days. It is the second most common cause of peripheral vestibular disorders after BPPV and the most common cause of acute severe vertigo requiring hospitalisation. The condition is caused by viral inflammation — usually from herpes simplex virus type 1 reactivation in the vestibular ganglion (Scarpa's ganglion), or occasionally from other viral infections — that selectively destroys or impairs the function of the vestibular nerve, usually the superior division (which supplies the anterior and horizontal semicircular canals and the utricle).

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Vestibular neuritis is an acute, usually monophasic inflammatory disorder of the vestibular nerve producing sudden, severe, continuous vertigo lasting hours to days. It is the second most common peripheral vestibular disorder after BPPV and the most common cause of acute severe vertigo requiring hospitalisation. Cause: viral inflammation — most commonly HSV-1 reactivation in Scarpa's ganglion (the vestibular ganglion), usually affecting the superior vestibular division (supplying the anterior and horizontal semicircular canals and the utricle). Hearing is preserved because the cochlea is supplied by the inferior vestibular nerve (usually spared). Clinical features: sudden severe continuous vertigo (not positional, unlike BPPV), intense nausea and vomiting, inability to walk, spontaneous horizontal nystagmus with fast phase away from the affected ear. NO hearing loss (distinguishes from labyrinthitis), no focal neurological deficit. The HINTS exam at KIMS distinguishes peripheral vestibular neuritis from a posterior-fossa stroke with sensitivity higher than early MRI. Treatment: vestibular suppressants (short-term, 48–72 hours), prednisolone (100 mg tapering over 3 weeks), and VRT — the cornerstone of long-term recovery.

HINTS exam — better than early MRI in first 24 hours: Head Impulse test: examiner rapidly rotates head 10–20°. PERIPHERAL (vestibular neuritis): the VOR fails on the affected side — eyes move with the head briefly, then make a catch-up saccade. CENTRAL (posterior fossa stroke): head impulse is NORMAL (no saccade needed) — paradoxically a NORMAL head impulse in acute severe vertigo is the danger sign. Nystagmus: unidirectional horizontal = peripheral; direction-changing or vertical = central. Test of Skew: cover-uncover, vertical refixation = skew deviation = central.
Video Head Impulse Test (vHIT) — quantifying the VOR deficit: vHIT uses a video-oculography goggle to quantify the VOR gain in each of the six semicircular canals. In superior division vestibular neuritis: VOR gain is reduced on the affected side for the anterior and horizontal canals. Covert saccades (during the head impulse, too fast for the naked eye) and overt saccades (visible catch-up after) confirm unilateral vestibular hypofunction. vHIT provides an objective measure that confirms the diagnosis and guides the prognosis for compensation.
Prednisolone 100 mg tapering — the evidence-based dose: The Strupp 2004 randomised trial showed methylprednisolone (equivalent to prednisolone 100 mg) significantly improved recovery of vestibular function on caloric testing at 12 months. KIMS protocol: prednisolone 100 mg daily for 3 days, then tapered over 3 weeks (80, 60, 40, 20, 10 mg). Side effects managed with PPI and glucose monitoring. Antiviral therapy (valaciclovir) is controversial — Strupp 2004 showed no additional benefit over prednisolone alone, and valaciclovir is not routinely recommended at KIMS.
VRT — the cornerstone of long-term recovery: Vestibular Rehabilitation Therapy is the most important long-term intervention. The brain compensates for unilateral vestibular hypofunction through central adaptation — rebalancing tonic firing rates between the two vestibular nuclei, recalibrating the VOR, and substituting visual and proprioceptive cues. VRT accelerates this by exposing the brain to movement challenges that drive adaptation. Components at KIMS: gaze stabilisation exercises; balance exercises (Romberg, tandem, standing on foam, walking with head turns); secondary BPPV management (BPPV develops in 5–10% of patients and must be treated with Epley).
30% incomplete compensation — who is at risk: Approximately 30% of vestibular neuritis patients develop chronic residual symptoms — persistent unsteadiness, movement-triggered dizziness, visual vertigo (dizziness in visually complex environments). Risk factors: older age (reduced neuroplasticity), delayed start of VRT, severe initial vestibular deficit, high anxiety (anxiety perpetuates avoidance and prevents adaptation), and pre-existing CNS changes. At KIMS, early initiation of VRT (within the first week) is prioritised. Patients with incomplete compensation receive intensive VRT and, in some cases, optokinetic therapy.
Labyrinthitis vs vestibular neuritis — the hearing distinction: Labyrinthitis (acute vestibulocochlear neuritis) produces the same acute severe vertigo as vestibular neuritis, but adds sensorineural hearing loss in the affected ear. This occurs because both the vestibular nerve and the cochlear nerve (or the labyrinth itself) are simultaneously inflamed. Hearing loss is typically moderate to severe and may be permanent. When acute vertigo is accompanied by simultaneous acute hearing loss in the same ear, labyrinthitis is more likely. At KIMS, urgent audiometry is performed in all patients with acute vertigo to identify co-existing hearing loss.
HSV-1 mechanism — the viral pathology: HSV-1 has a predilection for the vestibular ganglion (Scarpa's ganglion). In viral latency, HSV-1 resides in the ganglion cell bodies — the same cells that house the vestibular nerve cell bodies. Reactivation triggered by physiological stress, immune suppression, or other factors causes viral replication and inflammatory destruction of the ganglion and nerve fibres. Histopathological studies of temporal bones from patients who died after vestibular neuritis show HSV-1 antigens and inflammatory infiltrates in Scarpa's ganglion. The superior division (supplying the anterior and horizontal canals and the utricle) is preferentially affected because it runs through a narrower bony canal, making it more susceptible to inflammatory compression.

Fact	Details
Definition	Acute inflammatory disorder of vestibular nerve · HSV-1 reactivation in Scarpa's ganglion · Superior division most affected · Hearing preserved (inferior division spared)
Clinical features	Sudden severe CONTINUOUS vertigo (not positional) · Intense nausea and vomiting · Unable to walk · Spontaneous horizontal nystagmus (fast phase away from affected ear) · NO hearing loss
HINTS exam	Head Impulse: corrective saccade = peripheral (safe) · Normal head impulse in severe vertigo = central = DANGER · Nystagmus: unidirectional horizontal = peripheral · Test of Skew: skew deviation = central
vHIT	Reduced VOR gain on affected side · Covert/overt corrective saccades · Quantifies unilateral vestibular hypofunction · Guides prognosis for compensation
Treatment	Vestibular suppressants (48–72h max) · Prednisolone 100 mg tapering over 3 weeks · VRT from week 1: gaze stabilisation + balance exercises + walking exercises
VRT at KIMS	Gaze stabilisation (head movement while fixating) · Balance exercises (Romberg, foam, tandem) · Dynamic walking · Secondary BPPV Epley if needed · 30% need intensive VRT for incomplete compensation
Contact	040-44885000 (outpatient) · 040-46324365 (emergency: acute severe vertigo with headache, focal signs, or inability to stand even with eyes open)

About This Condition

Vestibular Neuritis at a Glance

Epidemiology

Second most common peripheral vestibular disorder · Annual incidence 3.5–15 per 100,000 · Peak age 30–60 years · No sex predominance.

Cause

Viral inflammation of the vestibular nerve · HSV-1 reactivation in Scarpa's ganglion · Most commonly superior vestibular nerve (supplies HSCC, ASCC, utricle) · Rarely inferior branch (saccule, PSCC).

Clinical presentation

Sudden severe continuous vertigo (not positional) · Intense nausea and vomiting · Unable to walk · Falls toward affected side · Spontaneous horizontal nystagmus (fast phase away from affected ear) · NO hearing loss (distinguishes from labyrinthitis) · No focal neurological deficit.

Duration

Acute phase: 1–3 days (severe continuous vertigo) · Recovery phase: 1–3 weeks (unsteadiness, movement-triggered dizziness) · Chronic compensation: weeks to months (incomplete in 30%).

HINTS exam

Head Impulse (corrective saccade toward affected side = peripheral = safe) · Nystagmus direction (unidirectional horizontal = peripheral) · Test of Skew (no skew deviation = peripheral) · All three peripheral = vestibular neuritis · Any one central finding = STROKE until proven otherwise.

Video head impulse test (vHIT)

Quantitative assessment of vestibulo-ocular reflex (VOR) function · Reduced VOR gain on the affected side + covert/overt corrective saccades · Confirms unilateral vestibular hypofunction.

Treatment

Vestibular suppressants (short-term, 48–72 hours max): prochlorperazine, dimenhydrinate · Corticosteroids: prednisolone 100 mg tapering over 3 weeks · VRT: the most important long-term intervention · Antiviral: valaciclovir (controversial, not routinely recommended).

Incomplete compensation

30% of patients have chronic residual symptoms · Risk factors: older age, delayed VRT, severe initial deficit, pre-existing central pathway disease · Management: intensive VRT.

About This Condition

Vestibular Neuritis — Acute Viral Vestibular Nerve Inflammation That Mimics a Stroke

The most critical clinical challenge in vestibular neuritis is distinguishing it from an acute posterior fossa stroke — specifically, a cerebellar or brainstem infarction — which can present identically at first glance. Both cause sudden severe vertigo, nausea, vomiting, and inability to walk. The distinction determines whether the patient goes home with reassurance and prednisolone or goes straight to the stroke unit. The HINTS exam — three bedside eye movement tests — makes this distinction with high accuracy.

Acute Vertigo Assessment

Speak directly with the KIMS neurology and vestibular rehabilitation teams — for HINTS exam and video head impulse test, early prednisolone, structured VRT, and stroke exclusion in any patient with acute severe vertigo.

040-44885000Stroke / posterior fossa emergency: 040-46324365

Head Impulse · Nystagmus · Test of Skew · HINTS Accuracy

The HINTS Exam — The Most Important Bedside Test in Acute Vertigo

H — Head Impulse Test — the single most important test

The head impulse test (HIT) assesses the vestibulo-ocular reflex (VOR) — the reflex that keeps the eyes stable on a target when the head moves. The examiner asks the patient to fix their gaze on a target (the examiner's nose) and then applies a brief, rapid, small-amplitude (10–20°) head rotation to one side. Normal VOR: the eyes remain perfectly fixed on the target despite the head movement. Abnormal VOR (positive HIT): after the head impulse toward the affected side, the eyes are dragged off target by the head movement, then make a rapid corrective saccade back to the target — this corrective saccade is the positive finding. Peripheral interpretation: a positive HIT (corrective saccade visible after head impulse toward one side) indicates a peripheral unilateral vestibular lesion (vestibular neuritis) on that side. The VOR is impaired because the vestibular nerve is damaged. Central interpretation: a NORMAL HIT (no corrective saccade) in a patient with acute severe vertigo is alarming — it means the VOR is intact, which rules out peripheral vestibular neuritis and strongly suggests a central cause (brainstem or cerebellar stroke). In central vertigo, the brainstem still receives vestibular input but processes it incorrectly.

N — Nystagmus direction — unidirectional vs direction-changing

In peripheral vestibular neuritis, the spontaneous nystagmus is: unidirectional (beats consistently in one direction throughout all gaze positions) · Horizontal with a torsional component · Fast phase directed away from the damaged (hypoactive) ear · Suppressed by fixation (covering one eye with a Frenzel lens increases nystagmus intensity) · Increases with gaze in the direction of the fast phase (Alexander's law). Central nystagmus is: direction-changing (changes direction depending on gaze direction) · OR purely vertical (upbeat or downbeat) · OR not suppressed by fixation. Any direction-changing or vertical nystagmus in a patient with acute vertigo = central pathology = urgent MRI.

T — Test of Skew — the ocular misalignment sign

Skew deviation is a vertical misalignment of the eyes from an imbalance in otolithic input to the ocular motor nuclei. It is detected by the alternating cover test: cover one eye, then rapidly uncover it and watch for a vertical refixation movement. If the uncovered eye makes a vertical saccade to refixate (it was deviated up or down while covered), skew deviation is present. Skew deviation indicates a brainstem lesion affecting the otolith-ocular pathways (the utriculo-trochlear and utriculo-oculomotor pathways that cross in the MLF). Skew deviation is rare in peripheral vestibular neuritis. Its presence in acute vertigo = central pathology = stroke until proven otherwise.

HINTS accuracy — superior to early MRI

The HINTS exam (when performed by an experienced clinician) has a sensitivity of 100% and specificity of approximately 96% for distinguishing posterior fossa stroke from peripheral vestibular neuritis in acute vertigo. In the AVERT study, early MRI DWI in the first 48 hours had a sensitivity of only approximately 80% for posterior fossa ischaemia — meaning 1 in 5 strokes can be missed on early MRI. A HINTS exam suggesting peripheral vestibular disease, performed by an experienced clinician, is therefore more reliable than a normal early MRI for excluding posterior fossa stroke. At KIMS, all patients with acute vertigo undergo a formal HINTS examination before MRI decisions are made.

Treatment

Management at KIMS

Vestibular Rehabilitation Therapy (VRT) Is the Single Most Important Long-Term Treatment

Long-term Compensation and Recovery Pathway

Acute Phase — Vestibular suppressants (short-term only): Prochlorperazine 12.5 mg IM or 5 mg oral TDS · Or dimenhydrinate 50 mg every 6 hours · CRITICAL: use for maximum 48–72 hours only — prolonged use prevents central compensation and prolongs disability.

Corticosteroids: Prednisolone 100 mg/day tapering to zero over 3 weeks · Accelerates recovery of vestibular function on video-HIT and caloric testing · Start within first 3 days for maximum benefit.

IV fluids and antiemetics: For severe vomiting and dehydration · Ondansetron IV for nausea.

Early mobilisation: As soon as tolerable (24–48 hours) · Immobility delays central compensation · Gradual return to walking with support.

Vestibular Rehabilitation Therapy (VRT) — Recovery Phase: VRT is the most important long-term treatment for vestibular neuritis and should be started as soon as the acute vertigo phase subsides (typically within 1–2 weeks of onset). VRT works by driving central compensation — the brain’s process of learning to use the remaining vestibular input (from the intact contralateral side), vision, and proprioception to replace the lost vestibular input from the affected side. Core VRT exercises: (1) Gaze stabilisation exercises: target fixation during head movements in the horizontal and vertical planes · (2) Balance retraining: progressively challenging balance tasks with reduced visual input (eyes closed) and unstable surfaces · (3) Habituation exercises: repeated exposure to motion stimuli that provoke residual symptoms, promoting adaptation. VRT at KIMS is provided by trained vestibular physiotherapists in individual and group sessions.

Related Conditions

Vestibular neuritis belongs to the family of vestibular and balance disorders evaluated and managed at KIMS Neuroscience. Explore related conditions

BPPV Menière's Disease Central Vertigo

FAQs

Frequently Asked Questions

Yes — what you are experiencing is the recovery phase of vestibular neuritis, which is entirely expected and normal. During the acute phase, one vestibular nerve was functioning and one was not, creating a profound imbalance in the signals reaching your brain. Your brain then began a process of central compensation: gradually learning to interpret the asymmetric vestibular input and use visual and proprioceptive information to compensate for the missing signal. This compensation takes weeks to months to complete. The residual movement-triggered dizziness (called oscillopsia or motion intolerance) will improve progressively. The most important thing you can do is vestibular rehabilitation therapy (VRT) — a structured exercise programme that actively drives the compensation process. At KIMS, VRT sessions begin within 1–2 weeks of the acute event and most patients achieve full compensation within 4–12 weeks. Do not take vestibular suppressant medications (cinnarizine, prochlorperazine) for the residual symptoms — they slow down the compensation process. Call 040-44885000.

Prolonged use of prochlorperazine (or any vestibular suppressant) beyond 48–72 hours in vestibular neuritis is a common and important error. These medications suppress the vestibular signal and make the patient feel temporarily better, but they actively prevent central compensation — the brain's natural recovery process. A patient taking prochlorperazine for 6 weeks has had her central vestibular compensation significantly impaired. The correct action: (1) Stop prochlorperazine now · (2) Referral to vestibular rehabilitation therapy (VRT) at KIMS immediately · (3) Reassessment with video-HIT to determine whether there is ongoing vestibular hypofunction that can be compensated. Even at 6 weeks, central compensation can still occur with intensive VRT — it is not too late. The principle: vestibular suppressants are crisis medications for the first 2–3 days, not long-term treatment. Call 040-44885000.

Yes — post-vestibular neuritis BPPV is a well-recognised complication, occurring in approximately 10–15% of vestibular neuritis patients. The mechanism: the viral inflammation that damages the vestibular nerve also disrupts the utricle and its otoconia, causing them to dislodge and migrate into the posterior semicircular canal. The resulting BPPV produces the classic brief positional vertigo (triggered by lying down or rolling over) that is distinct from the residual movement intolerance of the post-neuritis recovery phase. The distinction matters because BPPV is treated by the Epley manoeuvre, not by VRT alone. At KIMS, all patients with post-vestibular neuritis positional symptoms undergo the Dix-Hallpike test to check for BPPV. If BPPV is confirmed, the Epley manoeuvre is performed in the same visit. Call 040-44885000.

A normal CT scan does not mean the brain is free of a stroke in the posterior fossa. CT is very poor at visualising the cerebellum and brainstem — small strokes in these regions are regularly missed on CT. The correct test is MRI with DWI, which is far more sensitive. However, even early MRI DWI misses approximately 20% of posterior fossa strokes in the first 24–48 hours. The most reliable bedside test to distinguish inner ear vertigo from brain stroke is the HINTS exam — three simple eye movement assessments performed by an experienced clinician. The key warning signs that suggest brain rather than inner ear: direction-changing nystagmus (nystagmus that beats in different directions depending on where you look) · Vertical nystagmus (beating up or down) · A new severe headache with the vertigo · Skew deviation (one eye higher than the other) · Any weakness, numbness, double vision, or slurred speech · A normal head impulse test (corrective saccade is absent). At KIMS, any patient with acute vertigo is assessed with the HINTS exam by a neurologist. If any central feature is present, MRI is performed urgently. Call 040-44885000.

The worst vertigo you have ever had. Vomiting for hours. Unable to walk. Vestibular neuritis resolves with the right treatment — and vestibular rehabilitation therapy returns most patients to full function within weeks.

At KIMS Hyderabad, the HINTS exam safely distinguishes inner ear disease from stroke, and the vestibular rehabilitation team restores balance. Call 040-44885000.

040-44885000

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