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Summary Table

Category	Detail
Risk Factors	Recent or concurrent upper respiratory tract infection (viral), history of otitis media (bacterial), autoimmune disease, rarely post-meningitis
Etiology	Inflammation of the membranous labyrinth affecting both the vestibular and cochlear apparatus; most commonly viral (HSV, CMV, influenza, parainfluenza, adenovirus), less commonly bacterial extension from middle ear or meninges
Patient Presentation	Acute onset of continuous rotational vertigo lasting days, accompanied by unilateral hearing loss and tinnitus
Classic Physical Exam	Spontaneous unidirectional horizontal nystagmus beating away from the affected ear, positive head impulse test toward the affected side, sensorineural hearing loss on the affected side, unsteady gait deviating toward the lesion
Key Diagnostic Results	Clinical diagnosis; audiometry confirms unilateral sensorineural hearing loss; caloric testing shows reduced vestibular response on the affected side; MRI with gadolinium if atypical features or suspicion of central pathology
Management	Supportive care with short-term vestibular suppressants (diazepam, meclizine, promethazine) for acute phase; corticosteroids (oral prednisone) for hearing preservation; early vestibular rehabilitation; antibiotics only if bacterial etiology confirmed
Keywords	"Vertigo with hearing loss," "post-URI vertigo with tinnitus," "continuous vertigo for days," "sensorineural hearing loss with vestibular symptoms," "cochlear and vestibular involvement"

1. Pathophysiology

Labyrinthitis is an inflammatory process that involves the membranous labyrinth, the fluid-filled structure within the inner ear that houses both the vestibular organs (semicircular canals, utricle, saccule) and the cochlea. The critical distinction from vestibular neuritis is that labyrinthitis affects both the vestibular and cochlear compartments simultaneously, whereas vestibular neuritis is confined to the vestibular nerve and spares hearing.

In viral labyrinthitis, the most common form, a viral pathogen reaches the inner ear through hematogenous spread or by direct extension along neural pathways. The virus triggers an inflammatory cascade within the perilymphatic and endolymphatic spaces, causing edema, cellular infiltration, and potential damage to the hair cells of both the organ of Corti (cochlea) and the vestibular sensory epithelium. This dual involvement is why the patient simultaneously experiences vertigo and hearing loss.

The vestibular component produces a sudden asymmetry in tonic neural firing between the two vestibular nuclei. Under normal conditions, both vestibular apparatuses send balanced resting signals to the brainstem. When one side is acutely inflamed and hypofunction develops, the contralateral (healthy) side dominates. The brain interprets this imbalance as rotation, producing the sensation of vertigo. The nystagmus that results follows Alexander's law: the fast phase of nystagmus beats away from the lesioned side, and nystagmus intensity increases when the patient gazes in the direction of the fast phase.

The cochlear component leads to sensorineural hearing loss because the inflammatory process damages hair cells in the organ of Corti or disrupts the ionic environment of the endolymph (particularly the endocochlear potential maintained by the stria vascularis). Tinnitus results from aberrant spontaneous firing of damaged cochlear nerve fibers. Unlike the vestibular symptoms, which often recover substantially through central compensation, the hearing loss may be permanent depending on the degree of hair cell destruction.

Bacterial labyrinthitis follows a different route. It most often arises as a complication of otitis media (tympanogenic labyrinthitis), where bacteria or bacterial toxins penetrate through the round window membrane into the inner ear. It can also occur as a complication of bacterial meningitis (meningogenic labyrinthitis), where infection spreads from the subarachnoid space through the cochlear aqueduct. Bacterial labyrinthitis carries a far worse prognosis for hearing and can progress to labyrinthine ossification, particularly in post-meningitic cases, which is why urgent treatment and early cochlear implant evaluation matter in this subset.

The head impulse test is positive in labyrinthitis because the vestibulo-ocular reflex (VOR) on the affected side is impaired. When the examiner rapidly turns the patient's head toward the lesioned ear, the eyes cannot maintain fixation on the target, and a corrective catch-up saccade is observed. This finding localizes the lesion to the peripheral vestibular system and helps distinguish it from central causes where the VOR is typically preserved.

2. Classification and Clinical Manifestation

By Etiology

Type	Cause	Route	Hearing Prognosis	Association
Viral labyrinthitis	HSV, CMV, influenza, adenovirus, mumps, rubella, EBV	Hematogenous spread or neural route	Partial to full recovery possible; some permanent loss in ~30-50%	Preceding or concurrent upper respiratory infection
Bacterial (tympanogenic)	Extension from acute or chronic otitis media	Bacterial toxins or direct invasion through the round window membrane	Poor; often permanent severe to profound loss	Concurrent middle ear infection; may see otorrhea, otalgia, fever
Bacterial (meningogenic)	Complication of bacterial meningitis (especially S. pneumoniae, N. meningitidis, H. influenzae)	Through the cochlear aqueduct or internal auditory canal	Very poor; frequently bilateral and profound	Can lead to labyrinthine ossification; cochlear implantation must be considered early
Autoimmune labyrinthitis	Autoimmune inner ear disease, systemic autoimmune conditions (Cogan syndrome, granulomatosis with polyangiitis, SLE)	Immune-mediated inflammation	Variable; may be steroid-responsive	Bilateral fluctuating hearing loss; may present with interstitial keratitis in Cogan syndrome

By Clinical Phase

Phase	Duration	Vestibular Symptoms	Cochlear Symptoms	Nystagmus
Acute phase	First 1-3 days	Severe continuous vertigo, nausea, vomiting, inability to stand or walk	Hearing loss (often sudden), tinnitus, aural fullness	Spontaneous horizontal or horizontal-torsional, fast phase beating away from the affected ear
Subacute phase	Days 3-14	Gradually improving vertigo, persistent imbalance especially with head movement	Hearing may stabilize or partially recover	Nystagmus intensity decreasing; may only be visible with Frenzel goggles
Chronic/compensatory phase	Weeks to months	Residual imbalance and motion sensitivity; true vertigo resolves	Hearing loss may be permanent; tinnitus may persist	Nystagmus resolved at rest; may be provoked by head-shaking

Distinguishing Feature from Vestibular Neuritis

Feature	Labyrinthitis	Vestibular Neuritis
Vertigo	Present	Present
Hearing loss	Yes (sensorineural)	No
Tinnitus	Often present	Absent
Nystagmus pattern	Same peripheral pattern	Same peripheral pattern
Head impulse test	Positive toward affected side	Positive toward affected side
Core distinction	Cochlear + vestibular involvement	Vestibular involvement only

3. Diagnostic Workup

Test	Role	Expected Finding
Clinical examination (head impulse test, nystagmus assessment, Rinne/Weber)	Best initial evaluation	Positive head impulse test toward the affected ear; spontaneous nystagmus with fast phase away from lesion; Weber lateralizes to the unaffected ear; Rinne positive bilaterally (air > bone)
Audiometry	Best initial test for documenting cochlear involvement	Unilateral sensorineural hearing loss on the affected side; this is what separates labyrinthitis from vestibular neuritis
Caloric testing (electronystagmography/videonystagmography)	Confirms vestibular hypofunction	Reduced or absent caloric response (canal paresis) on the affected side
MRI with gadolinium	Most accurate test to exclude central pathology	Enhancement of the labyrinth or vestibulocochlear nerve may be seen in inflammation; primarily ordered to rule out cerebellopontine angle tumors (vestibular schwannoma), stroke, or demyelinating disease
Tympanometry and otoscopic exam	Rule out middle ear pathology	Normal in viral labyrinthitis; abnormal (effusion, perforation, cholesteatoma) in tympanogenic bacterial labyrinthitis
CBC, CRP, ESR	Supportive if bacterial or autoimmune etiology suspected	Elevated inflammatory markers suggest bacterial infection or autoimmune process
Blood cultures, lumbar puncture	If meningogenic labyrinthitis suspected	Positive cultures, elevated CSF WBC, low glucose, elevated protein in bacterial meningitis

Labyrinthitis is fundamentally a clinical diagnosis supported by audiometry. The bedside evaluation is where the diagnosis begins. The examiner should first assess for spontaneous nystagmus. In labyrinthitis, the nystagmus is unidirectional, horizontal or horizontal-torsional, with the fast phase beating toward the healthy ear. It obeys Alexander's law and suppresses with visual fixation. These features are what classify it as a peripheral pattern and distinguish it from central causes.

The head impulse test (HIT) is performed next. The examiner asks the patient to fixate on the examiner's nose while the head is rapidly turned to each side. A corrective saccade when turning toward the affected ear confirms a peripheral vestibular deficit. A negative head impulse test in a patient with acute vertigo should raise concern for a central lesion, particularly posterior circulation stroke, and should prompt urgent imaging.

Audiometry is the single most important ancillary test. It is the study that distinguishes labyrinthitis from vestibular neuritis. The audiogram will show a unilateral sensorineural hearing loss on the affected side. The pattern may be low-frequency predominant, high-frequency predominant, or flat, depending on which portion of the cochlea is most affected. If the audiogram is completely normal, the diagnosis is vestibular neuritis, not labyrinthitis.

Tuning fork tests at the bedside serve as a rapid screen. The Weber test will lateralize to the unaffected ear (because the affected ear has sensorineural loss). The Rinne test will be positive bilaterally (air conduction greater than bone conduction on both sides), which confirms the loss is sensorineural rather than conductive.

MRI with gadolinium is not needed in every case but becomes the most accurate test when there is diagnostic uncertainty. It is ordered when the presentation is atypical: vertigo lasting beyond the expected timeframe, progressive hearing loss, neurologic signs, or failure to improve. MRI can show labyrinthine enhancement on post-contrast T1-weighted images in active inflammation and can exclude a vestibular schwannoma (which would present more insidiously with gradual unilateral hearing loss and may show a cerebellopontine angle mass). In post-meningitic labyrinthitis, MRI and CT temporal bone can detect early labyrinthine fibrosis or ossification, which is critical for timing of cochlear implantation.

Caloric testing via videonystagmography (VNG) provides objective documentation of vestibular hypofunction. Warm and cold water or air are irrigated into the ear canal, and the induced nystagmus is measured. A canal paresis greater than 20-25% on the affected side confirms unilateral vestibular loss. This test is useful for medicolegal documentation and for monitoring recovery but is not required for the initial clinical diagnosis.

4. Management and Treatment

Clinical Scenario	Treatment	Dose/Details
Acute symptom control (first 48-72 hours)	Vestibular suppressants	Diazepam 2-5 mg IV/PO every 8 hours, OR meclizine 25 mg PO every 8 hours, OR promethazine 25 mg PO/IM/IV every 6-8 hours
Anti-emetic support	Ondansetron	4-8 mg IV/PO every 8 hours as needed
Hearing preservation	Oral corticosteroids	Prednisone 1 mg/kg/day (max 60 mg) for 7-14 days with taper; begin as early as possible
Vestibular rehabilitation	Physical therapy	Begin once acute symptoms stabilize (usually after day 3-5); continue for weeks to months
Bacterial labyrinthitis (tympanogenic)	IV antibiotics + possible surgical drainage	Ceftriaxone 2 g IV daily or culture-directed therapy; myringotomy if middle ear source; mastoidectomy if cholesteatoma
Bacterial labyrinthitis (meningogenic)	Treat the meningitis + dexamethasone	Meningitis-directed antibiotics; dexamethasone 0.15 mg/kg IV every 6 hours for 4 days (started before or with first antibiotic dose)
Post-meningitic hearing loss	Early cochlear implant evaluation	MRI/CT temporal bone to assess for labyrinthine ossification; implantation before ossification obliterates the cochlea

Acute Stabilization

The immediate priority in the acute phase is symptom relief. Patients with labyrinthitis are often incapacitated by vertigo, nausea, and vomiting. Vestibular suppressants work by dampening the asymmetric vestibular input reaching the brainstem. Diazepam is often preferred in the emergency setting because it acts on GABA receptors in the vestibular nuclei, providing both anxiolytic and direct vestibular suppression. Meclizine, an antihistamine with anticholinergic properties, is a reasonable alternative for outpatient management.

The key principle is that vestibular suppressants must be limited to the first 48-72 hours. Prolonged use impairs the brain's ability to undergo central compensation, the neuroplastic process by which the brainstem recalibrates to function with asymmetric vestibular input. Continuing these medications beyond the acute phase delays recovery and prolongs symptoms.

Corticosteroids for Hearing Preservation

Oral prednisone is started as early as possible, ideally within the first 72 hours of symptom onset, to reduce inflammation and improve the chance of hearing recovery. The mechanism parallels that used in sudden sensorineural hearing loss (SSNHL), as the cochlear component of labyrinthitis is essentially an inflammatory cause of sudden hearing loss. The typical regimen is prednisone 1 mg/kg/day (maximum 60 mg/day) for 7-14 days followed by a taper over 5-7 days.

If oral steroids fail to produce hearing recovery, intratympanic dexamethasone injection may be considered as salvage therapy. This delivers a high concentration of steroid directly to the round window membrane and into the inner ear. This is more commonly studied in isolated SSNHL, but the principle extends to the cochlear injury in labyrinthitis.

Vestibular Rehabilitation

Once acute nausea and vertigo begin to subside (typically after day 3-5), the patient should be started on a structured vestibular rehabilitation program. This is the cornerstone of long-term recovery. Exercises include gaze stabilization (head movement while maintaining visual fixation on a target), habituation exercises (repeated exposure to provocative movements), and balance retraining. Central compensation is an active process that requires vestibular challenge, which is why stopping suppressant medications and starting rehabilitation early is essential.

Bacterial Labyrinthitis

When bacterial extension from the middle ear is suspected (concurrent otitis media, otorrhea, fever), intravenous antibiotics must be started urgently. Ceftriaxone or a combination covering typical middle ear pathogens (S. pneumoniae, H. influenzae, Moraxella) is appropriate. Surgical intervention such as myringotomy with tube placement or mastoidectomy may be necessary to drain the source of infection and prevent further intracranial complications (meningitis, brain abscess, lateral sinus thrombosis).

In meningogenic labyrinthitis, treatment of the underlying meningitis takes priority. Dexamethasone administered before or concurrently with the first dose of antibiotics has been shown to reduce the incidence of hearing loss in pneumococcal meningitis. Serial audiometry should be performed, and if profound bilateral hearing loss develops, early cochlear implant evaluation is critical because labyrinthine ossification can begin within weeks, making future implantation technically difficult or impossible.

Contraindications and Cautions

Corticosteroids should be used cautiously in patients with uncontrolled diabetes, active peptic ulcer disease, or immunocompromised states. In diabetic patients, close glucose monitoring during the steroid course is necessary, and the potential benefit of hearing preservation must be weighed against the metabolic risks.

Benzodiazepines carry risks of sedation, respiratory depression, and dependence. In elderly patients, meclizine is generally preferred over diazepam due to the lower risk of falls and oversedation.

5. Differential Diagnosis and Distractors

Differential Diagnosis	Why It Looks Similar	Key Discriminator
Vestibular neuritis	Acute continuous vertigo, positive head impulse test, same peripheral nystagmus pattern	No hearing loss and no tinnitus in vestibular neuritis; audiometry is normal. If the vignette includes hearing loss, it is labyrinthitis
Meniere disease	Vertigo with hearing loss and tinnitus	Meniere presents with recurrent episodic attacks (20 minutes to several hours) with symptom-free intervals; labyrinthitis is a single prolonged continuous episode. Meniere also classically shows fluctuating low-frequency sensorineural hearing loss
Sudden sensorineural hearing loss (SSNHL)	Acute onset unilateral hearing loss	SSNHL presents with hearing loss as the dominant symptom, sometimes with mild imbalance but typically without sustained rotational vertigo. If vertigo is prominent and prolonged, labyrinthitis is favored
Posterior circulation stroke (AICA territory)	Acute vertigo with hearing loss	AICA stroke can mimic labyrinthitis closely because the anterior inferior cerebellar artery supplies both the labyrinth (via the labyrinthine artery) and the lateral pons/cerebellum. Key discriminators: negative head impulse test (VOR preserved centrally), direction-changing nystagmus, additional neurologic findings (facial weakness, Horner syndrome, limb ataxia, crossed sensory deficits). This is the most dangerous mimic
BPPV	Vertigo triggered by position changes	Episodes are seconds long, purely positional, with no hearing loss; positive Dix-Hallpike with characteristic latency and fatigability
Vestibular schwannoma (acoustic neuroma)	Unilateral hearing loss with vestibular symptoms	Onset is gradual over months to years, not acute; hearing loss is progressive and often high-frequency predominant; vertigo is typically mild or absent because the slow growth allows central compensation; MRI reveals a cerebellopontine angle mass
Otitis media with serous labyrinthitis	Ear infection with vertigo	Middle ear findings (bulging tympanic membrane, effusion, conductive hearing loss) dominate; if a conductive pattern is present on tuning fork tests with only mild imbalance, this is serous labyrinthitis from middle ear inflammation, not true suppurative labyrinthitis
Vestibular migraine	Episodic vertigo, sometimes with auditory symptoms	Episodes are recurrent, lasting minutes to 72 hours, with migrainous features (headache, photophobia, phonophobia, visual aura); hearing loss, if present, is mild and fluctuating rather than the sudden onset seen in labyrinthitis

6. Traps and High-Yield Pearls

The most common trap on this topic is the failure to distinguish labyrinthitis from vestibular neuritis. Both present with acute continuous vertigo, unidirectional nystagmus, and a positive head impulse test. The single discriminating feature is hearing loss. If the vignette mentions any degree of sensorineural hearing loss or tinnitus alongside acute vertigo, the answer is labyrinthitis. If hearing is explicitly normal, the answer is vestibular neuritis. Students who do not actively look for this detail in the stem will conflate the two diagnoses.

A second high-yield trap involves the AICA stroke mimic. The anterior inferior cerebellar artery gives off the labyrinthine artery, which supplies the inner ear. An AICA territory infarct can produce acute vertigo with ipsilateral hearing loss, looking identical to labyrinthitis on the surface. The exam tests whether you can apply the HINTS examination (Head Impulse, Nystagmus, Test of Skew) to differentiate peripheral from central causes. A negative head impulse test (no corrective saccade) in a patient with acute vertigo is a red flag for stroke, not a reassuring finding. This is counterintuitive and is a favorite test question.

A third pitfall is over-treating with vestibular suppressants. The vignette may describe a patient one week into labyrinthitis who is still taking meclizine three times daily and has not improved. The correct next step is to discontinue the suppressant and initiate vestibular rehabilitation, not to increase the medication dose or switch to a different suppressant.

Finally, in the setting of bacterial meningitis complicated by hearing loss, students must recognize the urgency of cochlear implant evaluation. Labyrinthine ossification can begin within weeks of meningitis, and a delay in imaging and referral may render the patient ineligible for implantation. When the vignette describes a post-meningitic child with bilateral profound hearing loss, the next step is temporal bone imaging and otologic referral, not a "wait and observe" approach.

The core competency being tested across labyrinthitis questions is the ability to localize an acute vestibular syndrome to the peripheral system using bedside examination, to identify cochlear involvement as the distinguishing feature from vestibular neuritis, and to recognize the one dangerous central mimic that can present with both vertigo and hearing loss.

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