Updated: Sep 02, 2020
Author: Mark E Boston, MD; Chief Editor: Robert A Egan, MD 



Labyrinthitis is an inflammatory disorder of the inner ear, or labyrinth. Clinically, this condition produces disturbances of balance and hearing to varying degrees and may affect one or both ears. Bacteria or viruses can cause acute inflammation of the labyrinth in conjunction with either local or systemic infections. Autoimmune processes may also cause labyrinthitis. Vascular ischemia may result in acute labyrinthine dysfunction that mimics labyrinthitis. (See Etiology and Presentation.)


The anatomic relationships of the labyrinth, middle ear, mastoid, and subarachnoid space are essential to understanding the pathophysiology of labyrinthitis. The labyrinth is composed of an outer osseous framework surrounding a delicate, membranous network that contains the peripheral sensory organs for balance and hearing. (See the image below.)

Anatomy of the labyrinth. Anatomy of the labyrinth.

These sensory organs include the utricle, saccule, semicircular canals, and cochlea. Symptoms of labyrinthitis occur when infectious microorganisms or inflammatory mediators invade the membranous labyrinth and damage the vestibular and auditory end organs.

The labyrinth lies within the petrous portion of the temporal bone adjacent to the mastoid cavity and connects with the middle ear at the oval and round windows. The labyrinth maintains connections with the central nervous system (CNS) and subarachnoid space by way of the internal auditory canal and cochlear aqueduct. Bacteria may gain access to the membranous labyrinth by these pathways or through congenital or acquired defects of the bony labyrinth. Viruses may spread to labyrinthine structures hematogenously or by way of the aforementioned preformed pathways.

Viral and bacterial labyrinthitis are sufficiently different to warrant discussing them as separate disease processes.

Viral labyrinthitis

Viral infections can cause congenital and acquired hearing loss. Rubella and cytomegalovirus are the best-recognized viral causes of prenatal hearing loss. Virally induced hearing loss in the postnatal period is usually due to mumps or measles. Viral infections are also implicated in idiopathic, sudden sensorineural hearing loss (SNHL). Experimental evidence suggests that inflammatory proteins play a critical role in the pathogenesis of cytomegalovirus-induced hearing loss.[1]

A unique form of viral labyrinthitis is herpes zoster oticus, or Ramsay-Hunt syndrome. The cause of this disorder is reactivation of a latent varicella-zoster virus infection occurring years after the primary infection. Evidence suggests that the virus may attack the spiral and vestibular ganglion in addition to the cochlear and vestibular nerves.[2] Auditory and vestibular symptoms develop in approximately 25% of patients with herpes oticus, in addition to the facial paralysis and vesicular rash that characterize the disease.[3]

Bacterial labyrinthitis

Bacterial labyrinthitis is a potential consequence of meningitis or otitis media and may occur by either direct bacterial invasion (suppurative labyrinthitis) or through the passage of bacterial toxins and other inflammatory mediators into the inner ear (serous labyrinthitis).  Labyrinthitis is the most common complication of otitis media, accounting for 32% of all intracranial and extracranial complications in one study.[4]

Although bacterial labyrinthitis is rare in the postantibiotic era, bacterial meningitis remains a significant cause of hearing loss.[5] Auditory symptoms, vestibular symptoms, or both may be present in as many as 20% of children with meningitis.[6] Meningitis typically affects both ears, whereas otogenic infections typically cause unilateral symptoms.

Suppurative labyrinthitis

In patients with meningitis, bacteria can spread from the cerebrospinal fluid to the membranous labyrinth by way of the internal auditory canal or cochlear aqueduct. Bacterial infections of the middle ear or mastoid most commonly spread to the labyrinth through a dehiscent horizontal semicircular canal.[7] Usually, the dehiscence is the result of erosion by a cholesteatoma. Suppurative labyrinthitis resulting from otitis media is uncommon in the postantibiotic era. When suppurative labyrinthitis occurs, it is almost always associated with cholesteatoma. Profound hearing loss, severe vertigo, ataxia, and nausea and vomiting are common symptoms of bacterial labyrinthitis.

Labyrinthitis ossificans, the deposition of bone in the fluid-filled spaces of the inner ear, often follows suppurative labyrinthitis; therefore, decisions regarding cochlear implantation must be made early. Meningitis may also result in progressive hearing loss secondary to necrosis and fibrosis of the membranous cochlea and labyrinth.[8]

Serous labyrinthitis

Serous labyrinthitis occurs when bacterial toxins and host inflammatory mediators, such as cytokines, enzymes, and complement, cross the round window membrane, causing inflammation of the labyrinth in the absence of direct bacterial contamination.[9] This condition is associated with acute or chronic middle ear disease and is believed to be one of the most common complications of otitis media.

Toxins, enzymes, and other inflammatory products infiltrate the scala tympani, forming a fine precipitate just medial to the round window membrane. Penetration of the inflammatory agents into the endolymph at the basilar turn of the cochlea results in a mild to moderate, high-frequency SNHL.

Audiometric testing reveals a mixed hearing loss when a middle ear effusion is present. Vestibular symptoms may occur but are less common. Treatment is aimed at eliminating the underlying infection and clearing the middle ear space of effusion. The hearing loss is usually transient but may persist if the otitis is left untreated.

Causative viruses and bacteria

Little direct evidence suggests a viral cause for labyrinthitis; however, a wealth of epidemiologic evidence implicates a number of viruses as potentially causing inflammation of the labyrinth. Viral labyrinthitis is often preceded by an upper respiratory tract infection and occurs in epidemics. The histologic finding of axonal degeneration in the vestibular nerve suggests a viral etiology for vestibular neuritis.[10]

The bacteria that cause labyrinthitis are the same bacteria responsible for meningitis and otitis. Gram-negative organisms are found more commonly when cholesteatoma is the inciting factor.

Potential viral causes of labyrinthitis include the following:

  • Cytomegalovirus

  • Mumps virus

  • Varicella-zoster virus

  • Rubeola virus

  • Influenza virus

  • Parainfluenza virus

  • Rubella virus

  • Herpes simplex virus 1

  • Adenovirus

  • Coxsackievirus

  • Respiratory syncytial virus

Potential bacterial causes of labyrinthitis include the following:

  • Streptococcus pneumoniae

  • Haemophilus influenzae

  • Moraxella catarrhalis

  • Neisseria meningitidis

  • Streptococcus species

  • Staphylococcus species

  • Proteus species

  • Bacteroides species

  • Escherichia coli

  • Mycobacterium tuberculosis

Autoimmune labyrinthitis

Autoimmune labyrinthitis is an uncommon cause of sensorineural hearing loss and may occur as a local, inner ear process or as part of a systemic autoimmune disease such as Wegener granulomatosis or polyarteritis nodosa.[11, 12]


Occurrence in the United States

Although definitive epidemiologic data are lacking, viral labyrinthitis is the most common form of labyrinthitis observed in clinical practice. The prevalence of sudden SNHL is estimated at 1 case in 10,000 persons, with up to 40% of these patients complaining of vertigo or dysequilibrium.[13] One study reported that 37 of 240 patients presenting with positional vertigo had viral labyrinthitis.[14]

Age-related demographics

Viral labyrinthitis is usually observed in adults aged 30-60 years and is rarely observed in children. Meningogenic suppurative labyrinthitis is usually observed in children younger than 2 years, which is the population most at risk for meningitis. Otogenic suppurative labyrinthitis can be observed in persons of any age in the presence of cholesteatoma or as a complication of untreated acute otitis media.[9] Serous labyrinthitis is more common in the pediatric age group, in which the vast majority of acute and chronic otitis media cases are observed.


The acute symptoms of vertigo and nausea and vomiting resolve after several days to weeks in all forms of labyrinthitis; however, hearing loss is more variable.

Suppurative labyrinthitis nearly always results in permanent and profound hearing loss, whereas patients with viral labyrinthitis may recover from hearing loss. Dysequilibrium and/or positional vertigo also may be present for weeks following resolution of the acute infection.

Morbidity and mortality

Deaths associated with labyrinthitis are not reported except in cases of meningitis or overwhelming sepsis. The morbidity of labyrinthitis, especially bacterial labyrinthitis, is significant.

Bacterial labyrinthitis, regardless of etiology, accounts for one third of all cases of acquired hearing loss.

In the pediatric population, the risk of hearing loss secondary to meningitis is estimated to be 10-20%.[6, 15] Permanent hearing loss occurs in 10-20% of children with meningitis.[6, 15] One study reported dizziness following pneumococcal meningitis in 23% of patients.[16]

Permanent SNHL occurs in approximately 6% of patients with herpes zoster oticus who present with hearing loss.[7] S pneumoniae appears to be the agent most likely associated with meningitis-associated hearing loss.[17]

Ménière disease may follow an episode of suppurative or serous labyrinthitis and is most likely due to fibrosis of the endolymphatic sac and altered Na+/K+ transport.

Patient Education

Counsel patients regarding the potential for injury to themselves or others if they operate heavy machinery or drive a vehicle while vertiginous or while taking certain medications to control symptoms. (See Treatment and Medication.)

For patient education information, see the Ear, Nose and Throat Center, as well as Labyrinthitis and Vertigo.




A thorough medical history, including symptoms, past medical history, and medications, is essential to diagnosing labyrinthitis as the cause of the patient's vertigo or hearing loss. Symptoms to consider in the patient’s medical history include the following:

  • Vertigo - Timing and duration, association with movement, head position, and other characteristics

  • Hearing loss - Unilateral or bilateral, mild or profound, duration, and other characteristics

  • Aural fullness

  • Tinnitus

  • Otorrhea

  • Otalgia

  • Nausea or vomiting

  • Fever

  • Facial weakness or asymmetry

  • Neck pain/stiffness

  • Upper respiratory tract infection symptoms - Preceding or concurrent

  • Visual changes

The patient’s past medical history should be examined for the following:

  • Episodes of dizziness or hearing loss

  • Infections

  • Sick contacts

  • Ear surgery

  • Hypertension/hypotension

  • Diabetes

  • Stroke

  • Migraine

  • Trauma (head or cervical spine)

  • Family history of hearing loss or ear disease

The patient’s medication history should also be taken into account. Check for use of the following drugs:

  • Aminoglycosides and other ototoxic medications

  • Beta-blockers and other antihypertensives

  • Tranquilizers, including benzodiazepines

  • Antiepileptics

  • Alcohol

  • Illicit drugs

Viral labyrinthitis

Viral labyrinthitis is characterized by a sudden, unilateral loss of vestibular function and hearing. The acute onset of severe, often incapacitating, vertigo, frequently associated with nausea and vomiting, is characteristic of this disorder. The patient is often bedridden while the symptoms gradually subside. Vertigo eventually resolves after several days to weeks; however, unsteadiness and positional vertigo may persist for several months. Hearing loss is common and may be the primary presenting symptom in many patients.

An upper respiratory tract infection precedes the onset of cochleovestibular symptoms in up to 50% of cases. Recurrent attacks are reported but are rare and may be confused with Ménière disease. Resolution of vertigo and dysequilibrium is common and is due to partial recovery of vestibular function, with concurrent central compensation of the remaining unilateral vestibular deficit. Return of hearing usually mirrors the return of vestibular function.

A unique form of viral labyrinthitis is the aforementioned herpes zoster oticus, or Ramsay-Hunt syndrome. The cause of this disorder is reactivation of a latent varicella-zoster virus infection occurring years after the primary infection. Evidence suggests that the virus may attack the spiral and vestibular ganglion in addition to the cochlear and vestibular nerves.[2]

The initial symptoms of herpes zoster oticus are deep, burning, auricular pain followed a few days later by the eruption of a vesicular rash in the external auditory canal and concha. Vertigo, hearing loss, and facial weakness may follow singly or collectively. Symptoms typically improve over a few weeks; however, patients often suffer permanent hearing loss and persistent reduction of caloric responses.[3]

Autoimmune labyrinthitis

Autoimmune labyrinthitis is an uncommon cause of sensorineural hearing loss and may occur as a local, inner ear process or as part of a systemic autoimmune disease such as Wegener granulomatosis or polyarteritis nodosa. Hearing loss in autoimmune inner ear disease is typically bilateral and progressive over weeks to months. Vestibular complaints may occur in up to 80% of patients with autoimmune inner ear disease.[11, 12]


The physical examination includes a complete head and neck examination, with emphasis on the otologic, ocular, and cranial nerve portions of the examination. A brief neurologic examination is also necessary. Seek the presence of meningeal signs if meningitis is a consideration.

The otologic examination should be carried out as follows:

  • Perform an external inspection for signs of mastoiditis, cellulitis, or prior ear surgery

  • Inspect the ear canal for otitis externa, otorrhea, or vesicles

  • Inspect the tympanic membrane and middle ear for the presence of perforation, cholesteatoma, middle ear effusion, or acute otitis media

The ocular examination should be performed as follows:

  • Inspect the ocular range of motion and pupillary response

  • Perform a funduscopic examination to assess for papilledema

  • Observe for nystagmus (spontaneous, gaze-evoked, and positional); perform a Dix-Hallpike test if the patient can tolerate it

  • If visual changes are suggested, consult an ophthalmologist

The neurologic examination should be performed as follows:

  • Perform a complete cranial nerve examination

  • Assess for balance using the Romberg test and tandem gait

  • Assess cerebellar function by performing finger-to-nose and heel-to-shin tests

Viral labyrinthitis

Physical examination findings include spontaneous nystagmus towards the unaffected side, with diminished or absent caloric responses in the affected ear. The hearing loss is usually mild to moderate and is typically evident in the higher frequencies (>2000 Hz), although any degree or type of hearing loss may be present.



Diagnostic Considerations

Vestibular neuritis

Viral labyrinthitis is often confused with vestibular neuritis, and the terms are occasionally used interchangeably in the literature. However, most authors agree that vestibular neuritis is a disorder of the vestibular nerve and is not associated with hearing loss.[10] Because the cochlea is affected in pan-labyrinthine inflammation, hearing loss is always present in persons with viral labyrinthitis.

Vestibular neuritis typically manifests as sudden, acute vertigo without hearing loss in an otherwise healthy patient. The condition is more common in the fourth and fifth decades of life and affects men and women equally. An upper respiratory tract infection often precedes the condition, and the disorder is more common in the spring and early summer.

Histopathologic nerve studies of patients with vestibular neuritis demonstrate axonal loss, endoneurial fibrosis, and atrophy.[10] These findings are consistent with a viral inflammatory etiology. The treatment of vestibular neuritis and viral labyrinthitis is similar.

Other conditions

A 2009 case report suggests that an early anterior inferior cerebellar artery infarction should be considered in patients presenting with acute hearing loss and vertigo.[18]

Noninfectious labyrinthitis is very rare in children; therefore, seek an alternative diagnosis in patients this age. Labyrinthitis resulting from otitis media or meningitis is not uncommon in children.

Conditions to consider in the differential diagnosis of labyrinthitis also include the following:

  • Vertebrobasilar insufficiency

  • Presyncopal dizziness

  • Cerebellar infarct

  • Dysequilibrium of aging

  • Drug-induced vertigo and/or hearing loss

Differential Diagnoses



Approach Considerations

No specific laboratory studies are available for labyrinthitis. Routine serology testing often fails to reveal an infectious organism, and when results are positive, methods to determine if the same organism caused the damage to the membranous labyrinth are not available. Obtain appropriate tests to help exclude other possible etiologies in the differential diagnosis.

Examine cerebrospinal fluid if meningitis is suggested. If a systemic infection is considered, a complete blood count (CBC) and blood cultures are indicated. Perform culture and sensitivity testing of middle ear effusions, if present, and select appropriate antibiotic therapy accordingly.

Currently, no accurate or reliable autoimmune test is commercially available for autoimmune labyrinthitis. The diagnosis of the condition rests on a positive clinical response to steroid therapy.[19]

Imaging Studies

CT scanning

Consider a computed tomography (CT) scan prior to lumbar puncture in cases of possible meningitis. A CT scan is also useful to help rule out mastoiditis as a potential cause. A temporal bone CT scan may aid in the management of patients with cholesteatoma and labyrinthitis.

A noncontrast CT scan is best for visualizing fibrosis and calcification of the membranous labyrinth in persons with chronic labyrinthitis or labyrinthitis ossificans.


Magnetic resonance imaging (MRI) can be used to help rule out acoustic neuroma, stroke, brain abscess, or epidural hematoma as potential causes of vertigo and hearing loss.

The cochlea, vestibule, and semicircular canals enhance on T1-weighted, postcontrast images in persons with acute and subacute labyrinthitis.[20] This finding is highly specific and correlates with objective and subjective patient assessment. Improvements that have been made in MRI techniques may make this the study of choice for suspected labyrinthitis.[21]  The intensity of gadolinium enhancement on MRI can be useful in distinguishing intracochlear tumors from other inner ear pathology, including labyrinthitis.[22]


Obtain an audiogram in all patients who may have labyrinthitis. Evaluate critically ill and severely vertiginous patients when they are stable and able to tolerate the test. The audiogram may show different findings in relation to the etiology of the labyrinthine inflammation. For example, a patient with otitis media-induced labyrinthitis would most likely have a mixed hearing loss, whereas viral labyrinthitis would present with a sensorineural hearing loss. Otoacoustic emission (OAE) testing or auditory brainstem response (ABR) testing may be helpful in patients who are unable to cooperate for standard audiometry.

Persons with viral labyrinthitis have mild to moderate, high-frequency SNHL in the affected ear, although any frequency spectrum may be affected.

Suppurative (bacterial) labyrinthitis typically results in severe to profound, unilateral hearing loss. In cases of meningitis, the loss is often bilateral. Persons with serous (bacterial) labyrinthitis have unilateral, high-frequency hearing loss in the affected ear. A conductive loss in the same ear may occur secondary to effusion.

Vestibular Testing

Caloric testing and an electronystagmogram may help in diagnosing difficult cases and establishing a prognosis for recovery. Evidence suggests that careful evaluation of the vestibulo-ocular reflex may help to establish the etiology of the labyrinthitis.[23]

Persons with viral labyrinthitis have nystagmus with unilateral caloric vestibular paresis/hypofunction.

Persons with suppurative (bacterial) labyrinthitis have nystagmus and an absent caloric response on the affected side.

Persons with serous (bacterial) labyrinthitis usually have normal electronystagmogram results, but they may have a decreased caloric response in the affected ear. However, the presence of a middle ear effusion can attenuate the caloric response and cause a false-positive finding.



Approach Considerations

Viral labyrinthitis

The initial treatment for viral labyrinthitis consists of bed rest and hydration. Most patients can be treated on an outpatient basis. However, they should be cautioned to seek further medical care for worsening symptoms, especially neurologic symptoms (eg, diplopia, slurred speech, gait disturbances, localized weakness or numbness). Patients with severe nausea and vomiting may benefit from intravenous (IV) fluid and antiemetic medications.

Bacterial labyrinthitis

For bacterial labyrinthitis, antibiotic treatment is selected based on culture and sensitivity results. Treatment of suppurative labyrinthitis is aimed at eradicating the underlying infection, providing supportive care to the patient, draining middle ear effusions or mastoid infections, and preventing the spread of infection.

Surgical Care

In cases of labyrinthitis resulting from otitis media, perform a myringotomy and evacuate the effusion. A ventilation tube also may be indicated. Middle ear effusion should be sent for microscopic evaluation, as well as culture and sensitivity.

Mastoiditis and cholesteatoma are handled best with surgical drainage and debridement by way of a mastoidectomy.


Consult a neurosurgeon in the event of suppurative intracranial complications. Consultation with an infectious disease specialist may be warranted in the presence of systemic infection or unusual or atypical infections.

Inpatient care

Most patients with labyrinthitis can be evaluated and treated in the emergency department and then discharged. Some patients with intractable vertigo and vomiting may require admission.

For patients with a possible severe, underlying condition (eg, vertebrobasilar ischemia or brainstem tumor), admission to the hospital may be appropriate under the direction of a neurologist, a neurosurgeon, or both.

Pharmacologic Therapy

Viral labyrinthitis

Diazepam or other benzodiazepines are occasionally helpful as a vestibular suppressant. A short course of oral corticosteroids may be helpful. Currently, the role of antiviral therapy is not established.

In a randomized, controlled trial by Strupp et al, steroids (methylprednisolone) were found to be more effective than antiviral agents (valacyclovir) for recovery of peripheral vestibular function in patients with vestibular neuritis.[24] This may also apply to the treatment of viral labyrinthitis.

The antiviral drugs acyclovir, famciclovir, and valacyclovir shorten the duration of viral shedding in persons with herpes zoster oticus and may prevent some auditory and vestibular damage if started early in the clinical course. Administer corticosteroids to reduce inflammation and edema in the facial canal and labyrinth.

Bacterial labyrinthitis

For bacterial labyrinthitis, antibiotic treatment is selected based on culture and sensitivity results. Antibiotic treatment should consist of broad-spectrum antibiotic or combination therapy with CNS penetration until culture results are available. Treat the vertigo symptomatically as indicated. The use of steroids in meningogenic hearing loss is controversial.

Studies have shown that antioxidant therapy and cochlear microperfusion may be useful adjuvant treatments.[25, 26]

Outpatient Care

Patients with persistent vestibular symptoms may be candidates for vestibular rehabilitation. For many patients with chronic vertigo due to a peripheral vestibular etiology, a simple home program of vestibular habituation head movement exercises reduces symptoms of imbalance during stance and gait.[27]

A follow-up audiogram should be performed in all patients with hearing loss and in patients who were not tested at presentation. An auditory brainstem response test is indicated for younger children.



Medication Summary

Medications may be indicated in persons with viral labyrinthitis to treat the symptoms of vertigo and nausea/vomiting. These medications include benzodiazepines and antiemetics and are typically used for a few days, until symptoms are relieved. (Avoid scopolamine, or use with extreme caution, in elderly patients.)

Corticosteroids should, in theory, reduce labyrinthine inflammation and prevent the sequelae of labyrinthitis due to infectious or inflammatory causes. Definitive evidence is lacking, however, for the efficacy of corticosteroids in the treatment of labyrinthitis and sudden SNHL.[28] Intratympanic steroids, either alone or in combination with systemic steroids, may be more effective than systemic steroids in the treatment of sudden hearing loss.[29, 30]

Antiviral agents may play a role in the treatment of labyrinthitis due to presumed viral infections. However, studies have not shown improvement in treatment outcomes when antivirals are combined with systemic steroids in the treatment of labyrinthitis.[31]

Antibiotic therapy for bacterial causes of labyrinthitis must be directed at the most likely causative organisms. A complete discussion of all the antibiotics available for the treatment of suppurative or toxic bacterial labyrinthitis is beyond the scope of this article.


Class Summary

These agents are used for the symptomatic treatment of vertigo.

Diazepam (Valium, Diastat)

Diazepam depresses all levels of the CNS (eg, limbic and reticular formation), possibly by increasing the activity of gamma-aminobutyric acid (GABA). Individualize the dosage and increase it cautiously to avoid adverse effects.

Lorazepam (Ativan)

By increasing the action of GABA, which is a major inhibitory neurotransmitter in the brain, lorazepam may depress all levels of the CNS, including the limbic and reticular formation.


Class Summary

These agents are used for the relief of nausea and vomiting.

Prochlorperazine (Compro)

Prochlorperazine may relieve nausea and vomiting by blocking postsynaptic mesolimbic dopamine receptors through anticholinergic effects and depressing the reticular activating system. In addition to having antiemetic effects, prochlorperazine has the advantage of augmenting the hypoxic ventilatory response, acting as a respiratory stimulant at high altitudes.

Antivirals, Other

Class Summary

Nucleoside analogs are initially phosphorylated by viral thymidine kinase to eventually form a nucleoside triphosphate. These molecules inhibit herpes simplex virus polymerase with 30-50 times the potency of human alpha–deoxyribonucleic acid (DNA) polymerase.

Famciclovir (Famvir)

Famciclovir is a prodrug that, when biotransformed into an active metabolite (penciclovir), may inhibit viral DNA synthesis/replication.

Valacyclovir (Valtrex)

Valacyclovir is a prodrug that is rapidly converted to the active drug acyclovir. It is more expensive than acyclovir, but its dosing regimen is more convenient.

Acyclovir (Zovirax)

Acyclovir has an affinity for viral thymidine kinase and, once phosphorylated, causes DNA chain termination when acted upon by DNA polymerase. The drug, which requires 5 daily doses, can be associated with compliance problems.


Class Summary

Corticosteroids have anti-inflammatory properties and cause profound and varied metabolic effects. These drugs modify the body's immune response to diverse stimuli. These are standard agents administered in cases of sudden hearing loss; they may play a role in the treatment of viral labyrinthitis. Their role in the treatment of bacterial labyrinthitis and meningogenic hearing loss is controversial.


Prednisone is an immunosuppressant used in the treatment of autoimmune disorders. It may decrease inflammation by reversing increased capillary permeability and suppressing polymorphonuclear cell activity. Prednisone stabilizes lysosomal membranes and suppresses lymphocytes and antibody production and activity.

Methylprednisolone (A-Methapred, Solu-Medrol, Depo-Medrol)

Methylprednisolone is available in intravenous (IV)/intramuscular (IM) or oral (PO) form. Methylprednisolone may decrease inflammation by reversing increased capillary permeability and suppressing polymorphonuclear leukocyte activity.

Prednisolone (Pediapred, Prelone, Orapred)

Prednisolone may decrease inflammation by reversing increased capillary permeability and suppressing polymorphonuclear leukocyte activity. It is a commonly used oral agent.


Questions & Answers


What is labyrinthitis?

What causes labyrinthitis?

What is viral labyrinthitis?

What is bacterial labyrinthitis?

What is suppurative labyrinthitis?

What is serous labyrinthitis?

Which viruses cause labyrinthitis?

Which bacteria cause labyrinthitis?

What is autoimmune labyrinthitis?

What is the prevalence of labyrinthitis?

Which patient groups have the highest prevalence of labyrinthitis?

What is the prognosis of labyrinthitis?

What is the mortality and morbidity associated with labyrinthitis?

What is included in patient education about labyrinthitis?


Which clinical history findings are characteristic of labyrinthitis?

Which clinical history findings are characteristic of viral labyrinthitis?

Which clinical history findings are characteristic of autoimmune labyrinthitis?

Which physical findings are characteristic of labyrinthitis?

Which physical findings are characteristic of viral labyrinthitis?


How is labyrinthitis differentiated from vestibular neuritis?

Which conditions are included in the differential diagnoses of labyrinthitis?

What are the differential diagnoses for Labyrinthitis?


How is labyrinthitis diagnosed?

What is the role of CT scanning in the workup of labyrinthitis?

What is the role of MRI in the workup of labyrinthitis?

What is the role of audiography in the workup of labyrinthitis?

What is the role of vestibular testing in the workup of labyrinthitis?


How is viral labyrinthitis treated?

How is bacterial labyrinthitis treated?

What is the role of surgery in the treatment of labyrinthitis?

Which specialist consultations are beneficial to patients with labyrinthitis?

When is inpatient care indicated in the treatment of labyrinthitis?

What is the role of medications in the treatment of viral labyrinthitis?

What is the role of medications in the treatment of bacterial labyrinthitis?

What is the role of vestibular rehabilitation in the treatment of labyrinthitis?

When is a follow-up audiogram indicated in the treatment of labyrinthitis?


Which medications are used in the treatment of labyrinthitis?

Which medications in the drug class Corticosteroids are used in the treatment of Labyrinthitis?

Which medications in the drug class Antivirals, Other are used in the treatment of Labyrinthitis?

Which medications in the drug class Antiemetics are used in the treatment of Labyrinthitis?

Which medications in the drug class Benzodiazepines are used in the treatment of Labyrinthitis?