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Labyrinthitis

Updated : August 17, 2023





Background

Inflammatory of the membranous labyrinth of the inner ear is known as labyrinthitis, and it frequently causes nausea, vertigo, tinnitus, vomiting, & hearing loss. Labyrinthitis has minimal epidemiological information, but the incidence seems to rise with age.

Before making a diagnosis of labyrinthitis, it is necessary to conduct a complete history, examination, and investigations because many other dangerous illnesses, such as CVA (cerebrovascular accident), can mirror the symptoms of labyrinthitis.

It is typically brought on by a viral or bacterial infection, but it can also be a symptom of an autoimmune disorder or HIV (human immunodeficiency virus). In addition to symptom management, treatment is targeted to the etiology. Whereas most cases will fully recover, some people may continue to have balance and hearing issues.

Anatomy

The membranous labyrinth and the bone labyrinth are the two components of the inner ear. The temporal bone of the skull contains a number of bony cavities that make up the bony labyrinth. The cochlea, vestibule, & 3 semicircular canals make up its three primary components. Perilymph is a material found in all 3 of these structures. The utricle, saccule, semicircular ducts, & cochlear ducts are the four parts of the membrane labyrinth, which is a part of the bone labyrinth.

They are all stuffed with something called endolymph. The inner ear has two connections to the middle ear & two connections to the nervous system. The middle ear is joined by the cochlear duct through a round window and the vestibule by an oval window. The cochlear aqueduct & internal auditory canal link the inner ear to the brain (CNS).

 

Epidemiology

Meanwhile, in South Korea, the frequency of vestibular dysfunction ranged from 3.1% – 35.4% and the prevalence increased with age. There is limited information on the frequency & severity of labyrinthitis. The most typical type of labyrinthitis is viral, and it typically develops as a result of an infection of the upper airways. Females are twice as likely as males to have it when they are adults between the ages of 30 and 60.

The most common complication of deafness in children under the age of two is suppurative bacteria labyrinthitis, which develops as a side effect of bacterial meningitis. Fortunately, in the post-antibiotic era, this is extremely uncommon. Otogenic suppurative labyrinthitis can strike at any age and is frequently associated with cholesteatoma or develops as a result of chronic otitis media that has gone untreated.

 

 

Anatomy

 

 

Pathophysiology

 

 

Etiology

An inflammatory of the membranous labyrinth is called labyrinthitis. Systemic illnesses, germs, or viruses may be the culprits. Labyrinthitis ossificans, when pathologic new bone growth takes place inside the membranous labyrinth, is a rare but possible outcome. Due to the similarities in the symptoms & clinical presentation of vestibular neuritis & labyrinthitis, the terms are frequently used interchangeably. True vestibular neuritis, on the other hand, does not involve inflammation of the membranous labyrinth and is restricted to the vestibular nerve itself.

Viral Labyrinthitis

Labyrinthitis typically develops as a result of an upper respiratory viral infection. One of the most typical causes of congenital deafness is labyrinthitis owing to maternal rubella and CMV (cytomegalovirus) infections. Mumps & measles are the most common viruses that cause hearing loss in the postnatal period. Herpes zoster oticus, also known as Ramsay-Hunt syndrome, is brought on by the latent varicella-zoster viral disease becoming triggered, frequently years after the initial viral illness.

Peripheral facial nerve dysfunction and a vesicular rash, typically on the ear or mouth mucosa, are the typical effects of this. In 25% of instances, the virus might also affect the vestibular & cochlear nerves. Last but not least, although the precise cause of abrupt SNHL (sensorineural hearing loss) is uncertain, recent evidence suggests that it may be brought on by a CMV inflammatory protein.

Bacterial Labyrinthitis

Bacterial meningitis (20 percent of adolescents with bacterial meningitis will suffer auditory and vestibular complaints) and otitis media are the two most common causes of bacterial labyrinthitis. Two separate methods can cause inflammation. In serous labyrinthitis, the round or oval window allows bacterial toxins, host cytokines, & proinflammatory cytokines to enter the membrane labyrinth & cause secondary inflammation.

An infection with germs can result in inflammation, known as suppurative labyrinthitis. This will have reached the inner ear via the auditory canal or cochlear aqueduct of the central nervous or by the aforementioned round or oval window connecting the inner ear to the middle ear. The most frequent entrance is through a circular window. In the bony labyrinth, they may also result from inherited & congenital abnormalities.

Autoimmune Labyrinthitis

It has been established that labyrinthitis is an uncommon side effect of both polyarteritis nodosa & granulomatosis with polyangiitis.

Syphilis/ HIV

Labyrinthitis has been linked to both syphilis & HIV. Nevertheless, there is little information on whether the virus itself or opportunistic infections brought on by HIV-related immunodeficiency are to blame for the inflammation.

 

 

Genetics

 

 

Prognostic Factors

Labyrinthitis’s extreme vertigo should go away in a few days, but mild symptoms may last for some weeks. If the patient has no significant neurological aftereffects, the prognosis is typically favorable. However, the prognosis becomes more guarded since neurological problems may necessitate additional treatments.

For instance, patients with hydrocephalus brought on by bacterial meningitis may require ventriculoperitoneal shunts. Individuals who are prescribed antihistamines and benzodiazepines for a lengthy period of time to treat their vertigo seem to experience a prolonged vestibular recovery. Therefore, suppurative labyrinthitis seems to be more probable to result in long-term hearing loss.

 

 

Clinical History

Clinical History

The diagnosis of labyrinthitis as the cause of the patient’s vertigo and loss of hearing requires a detailed medical history that includes symptoms, past medical history, & medications. In the patient’s medical history, the following symptoms should be considered:

  • Visual changes
  • Symptoms of an upper respiratory infection that are present before or after
  • Stiffness/neck pain
  • Asymmetry or facial weakness
  • Fever
  • Vomiting or nausea
  • Otalgia
  • Otorrhea
  • Tinnitus
  • Aural fullness
  • Hearing loss
  • Vertigo

It is important to look into the patient’s past medical history for the following:

  • Family background of ear disease or hearing loss
  • Trauma (cervical spine or head)
  • Migraine
  • Stroke
  • Diabetes
  • Ear surgery
  • Sick contacts
  • Infections
  • Episodes of hearing loss or dizziness

The patient’s past medical history should also be considered. Look for the following drug usage:

  • Illicit drugs
  • Alcohol
  • Antiepileptics
  • Tranquilizers
  • Beta-blockers
  • Aminoglycosides & other ototoxic drugs
  • Viral labyrinthitis

One of the main symptoms of viral labyrinthitis is rapid, unilateral hearing loss & vestibular function. This illness is characterized by an abrupt onset of severe, frequently incapacitating vertigo that is frequently accompanied by vomiting and nausea. While the symptoms progressively go away, the patient is frequently bedridden. Vertigo usually goes away after a few days to a few weeks, but positional vertigo and unsteadiness might linger for several months.

Hearing loss is a frequent condition that many individuals may have as their main presenting symptom. Up to 50% of the time, cochleovestibular symptoms begin before an upper respiratory illness. Recurring attacks have been described; however, they are uncommon and could be mistaken for Ménière illness. Vertigo & disequilibrium frequently go away after a short while, and this is caused by a partial return of vestibular function and contemporaneous cerebral compensation for the remaining unilateral vestibular impairment.

Normal hearing recovery follows normal vestibular recovery. The previously stated herpes zoster oticus, as well as Ramsay-Hunt syndrome, is a distinct kind of viral labyrinthitis. Reactivation of a latent varicella-zoster virus infection that occurred years after the initial infection is the cause of this illness. Research suggests that in addition to the cochlear & vestibular nerves, the virus may also damage the spiral & vestibular ganglia.

Deep, throbbing auricular pain is one of the first signs of herpes zoster oticus. A few days later, a vesicular rash will appear in the external auditory canal and concha. Facial paralysis, hearing loss, & vertigo may appear separately or all at once. During a few weeks, symptoms usually get better, but patients frequently experience lifelong hearing loss or a persistent decline in caloric reactions.

Autoimmune labyrinthitis

A rare cause of sensorineural hearing loss, autoimmune labyrinthitis can develop in the inner ear or as part of a systemic autoimmune condition like Wegener granulomatosis and polyarteritis nodosa. With autoimmune inner ear disease, hearing loss is frequently bilateral and progresses over weeks to months. As many as 80 percent of patients with autoimmune inner ear infections may experience vestibular problems.

 

 

Physical Examination

Physical examinations

The physical exam comprises a thorough head and neck examination, with a focus on the cranial nerve, otologic, and eye parts of the examination. A quick neurologic evaluation is also required. If you are thinking about meningitis, look for meningeal signs.

The following steps should be taken to do the otologic examination:

  • Check the outside of your body for indications of cellulitis, mastoiditis, or previous ear surgery.
  • Check for vesicles, otorrhea, and otitis externa in the ear canal.
  • Check the tympanic membrane and middle ear for signs of acute otitis media, cholesteatoma, perforation, or effusion.

The following should be done during the ocular investigation:

  • Check the pupillary response and ocular range of motion.
  • Conduct a funduscopy to check for papilledema.
  • Watch for nystagmus (spontaneous, gaze-evoked, & positional); if the patient is able, perform a Dix-Hallpike test.
  • See an ophthalmologist if suggestions for visual alterations are made.

The following should be done during the neurologic examination:

  • Do a thorough cranial nerve examination.
  • Tandem gait and the Romberg test are used to evaluate balance.
  • Testing the cerebellum with the finger-to-nose and heel-to-shin methods

Viral labyrinthitis

After a physical examination, it was discovered that the affected ear had decreased or no caloric responses and that there was spontaneous nystagmus it towards the unaffected side. Although any degree or kind of hearing loss may exist, it is often mild to moderate and is most noticeable in the higher frequencies (>2000 Hz).

 

 

Age group

Associated comorbidity

Associated activity

Acuity of presentation

Differential Diagnoses

Differential diagnosis

Multiple sclerosis

Temporal bone neoplasm

Inner ear hemorrhage

Temporal bone fracture

Inner ear malformations

Posterior fossa CVA

Acoustic neuroma

Benign positional vertigo

Meniere disease

Vestibular neuritis

 

 

Laboratory Studies

 

 

Imaging Studies

 

 

Procedures

 

 

Histologic Findings

 

 

Staging

 

 

Treatment Paradigm

The course of treatment must be determined by the cause & symptoms. Hydration & bed rest should be the mainstays of treatment for viral labyrinthitis in an outpatient environment. However, if a patient’s symptoms worsen or they exhibit any neurological symptoms (such as numbness/ weakness, slurred speech, diplopia, or gait disturbance), they should be advised to contact a doctor right once. There is currently little data supporting the usage of steroids and antiviral drugs.

Antibiotic type and administration method in bacterial labyrinthitis depend on the source. For acute media otitis with an intact tympanic membrane, oral antibiotics are the primary line of treatment, although intravenous antibiotics may be required if the disease does not improve. If bacterial meningitis is suspected, start intravenous antibiotic therapy right away and perform confirmatory radiography and CSF collection. Corticosteroids are the first line of treatment for autoimmune labyrinthitis. Other immunomodulators, such as etanercept, cyclophosphamide, or azathioprine, may be tried if individuals are resistant to corticosteroid treatment.

Because they have fewer negative effects than corticosteroids, these medications are frequently used to treat chronic diseases. Nonetheless, a specialist should be in charge of this treatment. If a patient’s syphilis and HIV serology are positive, the proper therapy should be initiated, and a specialist should be consulted. Those who initially experience vertigo will wish to lie still and close their eyes. It is imperative that they try to move around as soon as they can, even if doing so increases their vertigo, as this is thought to aid in vestibular compensation & prognosis.

The earliest symptoms of vertigo can be treated with benzodiazepines & antihistamines. Nonetheless, symptoms shouldn’t last more than 72 hours. Due to their potential to impair vestibular compensation, only brief courses of these drugs should be recommended. Prochlorperazine and other antiemetics should help manage vomiting and nausea. The term corticosteroids should be given to patients who experience sudden hearing loss, and they should be directed to a specialist.

A small percentage of people who suffer from sensorineural hearing impairment could still have tinnitus after treatment. It’s critical to understand the connection between this and responsive depression and to take early action with therapies like biofeedback, tinnitus, tinnitus re-training, maskers, & hearing aids. Just a small percentage of instances necessitate surgical intervention, such as mastoidectomy in people with cholesteatoma and serious mastoiditis.

Occasionally, patients with labyrinthitis brought on by otitis media may need effusion drainage or a myringotomy. Patients may experience lasting vestibular problems after the acute labyrinthitis has subsided, which can negatively affect their quality of life. Referrals for vestibular rehabilitation for these patients are necessary.

 

 

by Stage

 

 

by Modality

 

 

Chemotherapy

 

 

Radiation Therapy

 

 

Surgical Interventions

 

 

Hormone Therapy

 

 

Immunotherapy

 

 

Hyperthermia

 

 

Photodynamic Therapy

 

 

Stem Cell Transplant

 

 

Targeted Therapy

 

 

Palliative Care

 

 

Medication

 

 

Media Gallary

References

https://www.ncbi.nlm.nih.gov/books/NBK560506/

https://emedicine.medscape.com/article/856215-clinical

 

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Labyrinthitis

Updated : August 17, 2023




Inflammatory of the membranous labyrinth of the inner ear is known as labyrinthitis, and it frequently causes nausea, vertigo, tinnitus, vomiting, & hearing loss. Labyrinthitis has minimal epidemiological information, but the incidence seems to rise with age.

Before making a diagnosis of labyrinthitis, it is necessary to conduct a complete history, examination, and investigations because many other dangerous illnesses, such as CVA (cerebrovascular accident), can mirror the symptoms of labyrinthitis.

It is typically brought on by a viral or bacterial infection, but it can also be a symptom of an autoimmune disorder or HIV (human immunodeficiency virus). In addition to symptom management, treatment is targeted to the etiology. Whereas most cases will fully recover, some people may continue to have balance and hearing issues.

Anatomy

The membranous labyrinth and the bone labyrinth are the two components of the inner ear. The temporal bone of the skull contains a number of bony cavities that make up the bony labyrinth. The cochlea, vestibule, & 3 semicircular canals make up its three primary components. Perilymph is a material found in all 3 of these structures. The utricle, saccule, semicircular ducts, & cochlear ducts are the four parts of the membrane labyrinth, which is a part of the bone labyrinth.

They are all stuffed with something called endolymph. The inner ear has two connections to the middle ear & two connections to the nervous system. The middle ear is joined by the cochlear duct through a round window and the vestibule by an oval window. The cochlear aqueduct & internal auditory canal link the inner ear to the brain (CNS).

 

Meanwhile, in South Korea, the frequency of vestibular dysfunction ranged from 3.1% – 35.4% and the prevalence increased with age. There is limited information on the frequency & severity of labyrinthitis. The most typical type of labyrinthitis is viral, and it typically develops as a result of an infection of the upper airways. Females are twice as likely as males to have it when they are adults between the ages of 30 and 60.

The most common complication of deafness in children under the age of two is suppurative bacteria labyrinthitis, which develops as a side effect of bacterial meningitis. Fortunately, in the post-antibiotic era, this is extremely uncommon. Otogenic suppurative labyrinthitis can strike at any age and is frequently associated with cholesteatoma or develops as a result of chronic otitis media that has gone untreated.

 

 

 

 

 

 

An inflammatory of the membranous labyrinth is called labyrinthitis. Systemic illnesses, germs, or viruses may be the culprits. Labyrinthitis ossificans, when pathologic new bone growth takes place inside the membranous labyrinth, is a rare but possible outcome. Due to the similarities in the symptoms & clinical presentation of vestibular neuritis & labyrinthitis, the terms are frequently used interchangeably. True vestibular neuritis, on the other hand, does not involve inflammation of the membranous labyrinth and is restricted to the vestibular nerve itself.

Viral Labyrinthitis

Labyrinthitis typically develops as a result of an upper respiratory viral infection. One of the most typical causes of congenital deafness is labyrinthitis owing to maternal rubella and CMV (cytomegalovirus) infections. Mumps & measles are the most common viruses that cause hearing loss in the postnatal period. Herpes zoster oticus, also known as Ramsay-Hunt syndrome, is brought on by the latent varicella-zoster viral disease becoming triggered, frequently years after the initial viral illness.

Peripheral facial nerve dysfunction and a vesicular rash, typically on the ear or mouth mucosa, are the typical effects of this. In 25% of instances, the virus might also affect the vestibular & cochlear nerves. Last but not least, although the precise cause of abrupt SNHL (sensorineural hearing loss) is uncertain, recent evidence suggests that it may be brought on by a CMV inflammatory protein.

Bacterial Labyrinthitis

Bacterial meningitis (20 percent of adolescents with bacterial meningitis will suffer auditory and vestibular complaints) and otitis media are the two most common causes of bacterial labyrinthitis. Two separate methods can cause inflammation. In serous labyrinthitis, the round or oval window allows bacterial toxins, host cytokines, & proinflammatory cytokines to enter the membrane labyrinth & cause secondary inflammation.

An infection with germs can result in inflammation, known as suppurative labyrinthitis. This will have reached the inner ear via the auditory canal or cochlear aqueduct of the central nervous or by the aforementioned round or oval window connecting the inner ear to the middle ear. The most frequent entrance is through a circular window. In the bony labyrinth, they may also result from inherited & congenital abnormalities.

Autoimmune Labyrinthitis

It has been established that labyrinthitis is an uncommon side effect of both polyarteritis nodosa & granulomatosis with polyangiitis.

Syphilis/ HIV

Labyrinthitis has been linked to both syphilis & HIV. Nevertheless, there is little information on whether the virus itself or opportunistic infections brought on by HIV-related immunodeficiency are to blame for the inflammation.

 

 

 

 

Labyrinthitis’s extreme vertigo should go away in a few days, but mild symptoms may last for some weeks. If the patient has no significant neurological aftereffects, the prognosis is typically favorable. However, the prognosis becomes more guarded since neurological problems may necessitate additional treatments.

For instance, patients with hydrocephalus brought on by bacterial meningitis may require ventriculoperitoneal shunts. Individuals who are prescribed antihistamines and benzodiazepines for a lengthy period of time to treat their vertigo seem to experience a prolonged vestibular recovery. Therefore, suppurative labyrinthitis seems to be more probable to result in long-term hearing loss.

 

 

Clinical History

The diagnosis of labyrinthitis as the cause of the patient’s vertigo and loss of hearing requires a detailed medical history that includes symptoms, past medical history, & medications. In the patient’s medical history, the following symptoms should be considered:

  • Visual changes
  • Symptoms of an upper respiratory infection that are present before or after
  • Stiffness/neck pain
  • Asymmetry or facial weakness
  • Fever
  • Vomiting or nausea
  • Otalgia
  • Otorrhea
  • Tinnitus
  • Aural fullness
  • Hearing loss
  • Vertigo

It is important to look into the patient’s past medical history for the following:

  • Family background of ear disease or hearing loss
  • Trauma (cervical spine or head)
  • Migraine
  • Stroke
  • Diabetes
  • Ear surgery
  • Sick contacts
  • Infections
  • Episodes of hearing loss or dizziness

The patient’s past medical history should also be considered. Look for the following drug usage:

  • Illicit drugs
  • Alcohol
  • Antiepileptics
  • Tranquilizers
  • Beta-blockers
  • Aminoglycosides & other ototoxic drugs
  • Viral labyrinthitis

One of the main symptoms of viral labyrinthitis is rapid, unilateral hearing loss & vestibular function. This illness is characterized by an abrupt onset of severe, frequently incapacitating vertigo that is frequently accompanied by vomiting and nausea. While the symptoms progressively go away, the patient is frequently bedridden. Vertigo usually goes away after a few days to a few weeks, but positional vertigo and unsteadiness might linger for several months.

Hearing loss is a frequent condition that many individuals may have as their main presenting symptom. Up to 50% of the time, cochleovestibular symptoms begin before an upper respiratory illness. Recurring attacks have been described; however, they are uncommon and could be mistaken for Ménière illness. Vertigo & disequilibrium frequently go away after a short while, and this is caused by a partial return of vestibular function and contemporaneous cerebral compensation for the remaining unilateral vestibular impairment.

Normal hearing recovery follows normal vestibular recovery. The previously stated herpes zoster oticus, as well as Ramsay-Hunt syndrome, is a distinct kind of viral labyrinthitis. Reactivation of a latent varicella-zoster virus infection that occurred years after the initial infection is the cause of this illness. Research suggests that in addition to the cochlear & vestibular nerves, the virus may also damage the spiral & vestibular ganglia.

Deep, throbbing auricular pain is one of the first signs of herpes zoster oticus. A few days later, a vesicular rash will appear in the external auditory canal and concha. Facial paralysis, hearing loss, & vertigo may appear separately or all at once. During a few weeks, symptoms usually get better, but patients frequently experience lifelong hearing loss or a persistent decline in caloric reactions.

Autoimmune labyrinthitis

A rare cause of sensorineural hearing loss, autoimmune labyrinthitis can develop in the inner ear or as part of a systemic autoimmune condition like Wegener granulomatosis and polyarteritis nodosa. With autoimmune inner ear disease, hearing loss is frequently bilateral and progresses over weeks to months. As many as 80 percent of patients with autoimmune inner ear infections may experience vestibular problems.

 

 

Physical examinations

The physical exam comprises a thorough head and neck examination, with a focus on the cranial nerve, otologic, and eye parts of the examination. A quick neurologic evaluation is also required. If you are thinking about meningitis, look for meningeal signs.

The following steps should be taken to do the otologic examination:

  • Check the outside of your body for indications of cellulitis, mastoiditis, or previous ear surgery.
  • Check for vesicles, otorrhea, and otitis externa in the ear canal.
  • Check the tympanic membrane and middle ear for signs of acute otitis media, cholesteatoma, perforation, or effusion.

The following should be done during the ocular investigation:

  • Check the pupillary response and ocular range of motion.
  • Conduct a funduscopy to check for papilledema.
  • Watch for nystagmus (spontaneous, gaze-evoked, & positional); if the patient is able, perform a Dix-Hallpike test.
  • See an ophthalmologist if suggestions for visual alterations are made.

The following should be done during the neurologic examination:

  • Do a thorough cranial nerve examination.
  • Tandem gait and the Romberg test are used to evaluate balance.
  • Testing the cerebellum with the finger-to-nose and heel-to-shin methods

Viral labyrinthitis

After a physical examination, it was discovered that the affected ear had decreased or no caloric responses and that there was spontaneous nystagmus it towards the unaffected side. Although any degree or kind of hearing loss may exist, it is often mild to moderate and is most noticeable in the higher frequencies (>2000 Hz).

 

 

Differential diagnosis

Multiple sclerosis

Temporal bone neoplasm

Inner ear hemorrhage

Temporal bone fracture

Inner ear malformations

Posterior fossa CVA

Acoustic neuroma

Benign positional vertigo

Meniere disease

Vestibular neuritis

 

 

 

 

 

 

 

 

 

 

 

 

The course of treatment must be determined by the cause & symptoms. Hydration & bed rest should be the mainstays of treatment for viral labyrinthitis in an outpatient environment. However, if a patient’s symptoms worsen or they exhibit any neurological symptoms (such as numbness/ weakness, slurred speech, diplopia, or gait disturbance), they should be advised to contact a doctor right once. There is currently little data supporting the usage of steroids and antiviral drugs.

Antibiotic type and administration method in bacterial labyrinthitis depend on the source. For acute media otitis with an intact tympanic membrane, oral antibiotics are the primary line of treatment, although intravenous antibiotics may be required if the disease does not improve. If bacterial meningitis is suspected, start intravenous antibiotic therapy right away and perform confirmatory radiography and CSF collection. Corticosteroids are the first line of treatment for autoimmune labyrinthitis. Other immunomodulators, such as etanercept, cyclophosphamide, or azathioprine, may be tried if individuals are resistant to corticosteroid treatment.

Because they have fewer negative effects than corticosteroids, these medications are frequently used to treat chronic diseases. Nonetheless, a specialist should be in charge of this treatment. If a patient’s syphilis and HIV serology are positive, the proper therapy should be initiated, and a specialist should be consulted. Those who initially experience vertigo will wish to lie still and close their eyes. It is imperative that they try to move around as soon as they can, even if doing so increases their vertigo, as this is thought to aid in vestibular compensation & prognosis.

The earliest symptoms of vertigo can be treated with benzodiazepines & antihistamines. Nonetheless, symptoms shouldn’t last more than 72 hours. Due to their potential to impair vestibular compensation, only brief courses of these drugs should be recommended. Prochlorperazine and other antiemetics should help manage vomiting and nausea. The term corticosteroids should be given to patients who experience sudden hearing loss, and they should be directed to a specialist.

A small percentage of people who suffer from sensorineural hearing impairment could still have tinnitus after treatment. It’s critical to understand the connection between this and responsive depression and to take early action with therapies like biofeedback, tinnitus, tinnitus re-training, maskers, & hearing aids. Just a small percentage of instances necessitate surgical intervention, such as mastoidectomy in people with cholesteatoma and serious mastoiditis.

Occasionally, patients with labyrinthitis brought on by otitis media may need effusion drainage or a myringotomy. Patients may experience lasting vestibular problems after the acute labyrinthitis has subsided, which can negatively affect their quality of life. Referrals for vestibular rehabilitation for these patients are necessary.

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

https://www.ncbi.nlm.nih.gov/books/NBK560506/

https://emedicine.medscape.com/article/856215-clinical

 

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