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Emergency Medicine
Primary Care
Neurology

Labyrinthitis

High EvidenceUpdated: 2025-12-22

On This Page

Red Flags

  • Negative head impulse test (suggests central cause - STROKE)
  • Vertical nystagmus (central)
  • Direction-changing nystagmus (central)
  • Focal neurological deficits
  • Unable to walk independently
Overview

Labyrinthitis

1. Clinical Overview

Summary

Labyrinthitis is acute inflammation of the membranous labyrinth (inner ear), affecting both vestibular and cochlear function. It is typically viral (post-URI) and presents with sudden-onset sustained vertigo, nausea, vomiting, and unilateral hearing loss/tinnitus. The key differentiator from vestibular neuritis is the presence of hearing loss (labyrinthitis = vertigo + hearing loss). The main diagnostic challenge is distinguishing peripheral labyrinthitis from central causes (posterior circulation stroke). The HINTS examination is more sensitive than early MRI for detecting stroke. Management involves short-term vestibular suppressants (48-72 hours only) and early vestibular rehabilitation.

Key Facts

  • Definition: Inflammation of inner ear affecting vestibular AND cochlear portions
  • Difference from Vestibular Neuritis: Labyrinthitis = vertigo + HEARING LOSS
  • Cause: Usually viral (30% post-viral URI)
  • Duration: Acute phase 3-7 days; weeks to months for full compensation
  • Key Test: HINTS exam (distinguishes peripheral from central)
  • Management: Short-term suppressants + early mobilisation/vestibular rehab

Clinical Pearls

"Hearing Loss = Labyrinthitis": If there's vertigo WITH hearing loss → Labyrinthitis. If vertigo WITHOUT hearing loss → Vestibular neuritis. Both are treated similarly.

"HINTS Beats MRI Early": In acute vertigo, the HINTS exam is more sensitive than MRI in the first 48 hours for detecting posterior circulation stroke.

"Limit Suppressants to 72 Hours": Vestibular suppressants (prochlorperazine, cinnarizine) delay central compensation. Use only for severe symptoms in first 3 days.

"Positive Head Impulse = Peripheral = Safe": If the head impulse test is positive (corrective saccade), the lesion is peripheral. Negative HIT in acute vertigo = think STROKE.


2. Epidemiology

Incidence

  • 3.5 per 100,000 per year
  • Less common than vestibular neuritis
  • Peak age: 30-60 years

Demographics

  • M = F
  • All ages, but rare in children
  • Often follows upper respiratory tract infection

Aetiology

CauseFrequencyNotes
Viral70%HSV, VZV, CMV, Influenza, Adenovirus
BacterialRareComplication of otitis media, meningitis
Post-infectiousCommonFollows 1-3 weeks after URI
AutoimmuneRareAssociated with autoimmune inner ear disease

3. Pathophysiology

Anatomy

  • Labyrinth = bony and membranous structures containing:
    • Vestibular portion: Semicircular canals (angular motion), Otolith organs (linear motion)
    • Cochlear portion: Organ of Corti (hearing)

Mechanism

  1. Viral infection (usually HSV reactivation) affects inner ear
  2. Inflammation damages both vestibular AND cochlear hair cells
  3. Unilateral vestibular hypofunction → Vestibular asymmetry → Vertigo
  4. Cochlear damage → Sensorineural hearing loss, tinnitus

Why Vertigo Occurs

  • Normal bilateral vestibular input = balanced = no vertigo
  • Sudden unilateral loss = perceived rotation toward intact side
  • Brain interprets asymmetry as movement

Vestibular Compensation

  • Brain adapts to unilateral loss over weeks
  • Central recalibration using visual and proprioceptive inputs
  • EARLY MOBILISATION promotes faster compensation

4. Clinical Presentation

Symptoms

FeatureDescription
VertigoSevere, rotational, sustained (not positional)
DurationDays (not seconds like BPPV)
Nausea/VomitingVery common, can be severe
Hearing lossUnilateral, sensorineural (KEY differentiator)
TinnitusOften present
Aural fullnessMay occur

Time Course

Distinguishing Labyrinthitis vs Vestibular Neuritis

FeatureLabyrinthitisVestibular Neuritis
VertigoYesYes
Hearing lossYESNo
TinnitusOftenNo
TreatmentSameSame

Acute phase
3-7 days of severe symptoms
Recovery
Gradual over weeks to months
Residual
Some patients have persistent imbalance
5. Clinical Examination

Vestibular Examination

Head Impulse Test (HIT)

  • Rapidly rotate head and observe for corrective saccade
  • POSITIVE (corrective saccade) = Peripheral lesion (reassuring)
  • NEGATIVE = Central lesion or normal (if negative in acute vertigo = WORRY)

Nystagmus Assessment

  • Peripheral: Unidirectional, horizontal-torsional, suppressed by fixation
  • Central: Any direction, vertical, direction-changing, not suppressed

Test of Skew

  • Cover-uncover test looking for vertical correction
  • Positive = Central lesion

HINTS Examination (Head Impulse, Nystagmus, Test of Skew)

┌──────────────────────────────────────────────────────────┐
│   HINTS: INFARCT = CENTRAL (DANGEROUS)                   │
├──────────────────────────────────────────────────────────┤
│                                                          │
│  Impulse Negative (no corrective saccade)              │
│  +                                                      │
│  Fast phase Alternating (direction-changing nystagmus)  │
│  +                                                      │
│  Refixation on Cover Test (skew deviation)             │
│                                                          │
│  ANY of these = Central cause until proven otherwise     │
│  → Urgent neurology/stroke team                         │
│                                                          │
└──────────────────────────────────────────────────────────┘

Hearing Assessment

  • Weber test: Lateralises to UNAFFECTED ear (sensorineural loss)
  • Rinne test: Air > Bone (but reduced on affected side)
  • Audiometry: Documents hearing loss

6. Investigations

Clinical Diagnosis

  • Usually clinical in typical presentation
  • HINTS exam is key to distinguish central

Audiometry

  • Confirms sensorineural hearing loss
  • Documents severity
  • Useful for monitoring recovery

Imaging

ModalityIndication
MRI brainIf central cause suspected (abnormal HINTS), atypical features
CT headAcute setting if MRI unavailable

Important Note on Early MRI

  • MRI may be FALSE NEGATIVE in first 24-48 hours for posterior fossa stroke
  • HINTS examination is MORE SENSITIVE than early MRI

Other Tests

  • Caloric testing: Confirms unilateral vestibular hypofunction
  • VNG: Objective vestibular assessment
  • Bloods: Inflammatory markers if infection suspected

7. Management

Acute Phase (First 72 Hours)

Vestibular Suppressants (SHORT-TERM ONLY)

MedicationDoseNotes
Prochlorperazine5mg TDS or 25mg PRAntiemetic + vestibular suppressant
Cinnarizine15-30mg TDSLess sedating
Promethazine25mg TDSAlternative
Diazepam2mg TDSReserve for severe symptoms

Important: LIMIT to 48-72 hours maximum. Longer use delays vestibular compensation.

Supportive Care

  • IV fluids if unable to tolerate oral (vomiting)
  • Bed rest only in acute phase
  • Safety precautions (falls risk)

Corticosteroids (Controversial)

  • Some evidence for vestibular neuritis (not conclusive)
  • May be considered: Prednisone 40-60mg daily tapering over 10 days
  • No strong evidence for labyrinthitis specifically

Recovery Phase

Vestibular Rehabilitation (CRITICAL)

  • EARLY mobilisation promotes faster compensation
  • Gaze stabilisation exercises
  • Balance retraining
  • Habituation exercises (controlled symptom provocation)
  • Referral to vestibular physiotherapy

Hearing Loss Management

  • Often some recovery occurs
  • Audiological monitoring
  • Hearing aids if persistent significant loss
  • Rarely cochlear implant (severe bilateral cases)

8. Complications

Acute

  • Severe dehydration (vomiting)
  • Falls and injury
  • Aspiration (severe nausea)

Long-Term

  • Persistent vestibular hypofunction (40%)
  • Chronic dizziness/imbalance
  • Permanent hearing loss (variable)
  • BPPV (can develop after labyrinthitis)
  • Anxiety/depression related to chronic imbalance

9. Prognosis & Outcomes

Vestibular Recovery

  • 50-60% recover fully
  • 40% have some residual imbalance
  • Most improve significantly with vestibular rehabilitation

Hearing Recovery

  • Variable
  • Some recovery common if viral
  • Complete recovery less common than vestibular improvement
  • Bacterial labyrinthitis: Often permanent hearing loss

Factors Affecting Prognosis

Better PrognosisPoorer Prognosis
Young ageElderly
Early vestibular rehabProlonged suppressant use
Viral aetiologyBacterial aetiology
No comorbiditiesVascular risk factors

10. Evidence & Guidelines

Key Guidelines

  1. NICE CKS: Vestibular Neuronitis/Labyrinthitis
  2. AAO-HNS Guidelines
  3. Bárány Society Diagnostic Criteria

Key Evidence

HINTS Exam

  • Kattah et al (2009): HINTS more sensitive than MRI in first 48h for stroke
  • Sensitivity 100%, Specificity 96% for central cause

Corticosteroids

  • Cochrane Review: Moderate evidence steroids improve vestibular recovery
  • NNT ~4 for significant improvement with steroids

Vestibular Rehabilitation

  • Cochrane Review: Strong evidence for benefit
  • Improves symptoms and function more than no treatment

11. Patient/Layperson Explanation

What is Labyrinthitis?

Labyrinthitis is an inflammation of the inner ear, usually caused by a viral infection. The inner ear contains the balance organs and the hearing part, so labyrinthitis causes both dizziness and hearing problems.

What Are the Symptoms?

  • Severe spinning sensation (vertigo) that lasts days, not seconds
  • Feeling sick and vomiting
  • Hearing loss in one ear
  • Ringing in the ear (tinnitus)
  • Difficulty balancing

How is it Different from Other Ear Problems?

Unlike a middle ear infection (which causes ear pain and fever), labyrinthitis affects the inner ear and causes balance problems. If you have vertigo WITHOUT hearing loss, it's likely "vestibular neuritis" - a similar condition treated the same way.

How is it Treated?

  • Anti-sickness tablets for the first few days
  • Rest during the acute phase
  • EARLY movement is important - staying in bed too long actually slows recovery
  • Balance exercises (vestibular rehabilitation) help your brain adapt

When to Seek Urgent Help

Go to A&E if you have:

  • New sudden hearing loss
  • Difficulty walking or standing
  • Weakness, numbness, or speech problems (could suggest stroke)
  • Symptoms getting worse after a few days

Recovery

Most people feel much better within 1-2 weeks, though full recovery can take several weeks to months. Some hearing loss may be permanent, but often some recovery occurs.


12. References

Primary Guidelines

  1. NICE Clinical Knowledge Summaries. Vestibular Neuronitis. cks.nice.org.uk
  2. Bárány Society. Diagnostic Criteria for Vestibular Disorders.

Key Studies

  1. Kattah JC, et al. HINTS to diagnose stroke in the acute vestibular syndrome. Stroke. 2009;40(11):3504-10. PMID: 19762709
  2. Hillier SL, McDonnell M. Vestibular rehabilitation for unilateral peripheral vestibular dysfunction. Cochrane Database Syst Rev. 2011. PMID: 21328277

Last updated: 2025-12-22

At a Glance

EvidenceHigh
Last Updated2025-12-22

Red Flags

  • Negative head impulse test (suggests central cause - STROKE)
  • Vertical nystagmus (central)
  • Direction-changing nystagmus (central)
  • Focal neurological deficits
  • Unable to walk independently

Clinical Pearls

  • **"Hearing Loss = Labyrinthitis"**: If there's vertigo WITH hearing loss → Labyrinthitis. If vertigo WITHOUT hearing loss → Vestibular neuritis. Both are treated similarly.
  • **"HINTS Beats MRI Early"**: In acute vertigo, the HINTS exam is more sensitive than MRI in the first 48 hours for detecting posterior circulation stroke.
  • **"Limit Suppressants to 72 Hours"**: Vestibular suppressants (prochlorperazine, cinnarizine) delay central compensation. Use only for severe symptoms in first 3 days.
  • **"Positive Head Impulse = Peripheral = Safe"**: If the head impulse test is positive (corrective saccade), the lesion is peripheral. Negative HIT in acute vertigo = think STROKE.
  • Bone (but reduced on affected side)

Guidelines

  • NICE Guidelines
  • BTS Guidelines
  • RCUK Guidelines