Ménière's disease

Ménière's disease had been recognized prior to 1972, but it was still relatively vague and broad at the time. Committees at the Academy of Ophthalmology and Otolaryngology made set criteracriteria for diagnosing Ménière's, as well as defining two sub categories of Ménière's: cochlear (without vertigo) and vestibular (without deafness).

In 1972, the academy defined criteracriteria for diagnosing Ménière's disease as the following:

Fluctuating, progressive, sensorineural deafness. Episodic, characteristic definitive spells of vertigo lasting 20 minutes to 24 hours with no unconsciousness,without loss of consciousness and associated with the presence of vestibular nystagmus always presentnystagmus. Usually tinnitus. Attacks are characterized by periods of remission and exacerbation. In 1985, this list changed to alter wording, such as changing "deafness" changed to "hearing loss associated with tinnitus, characteristicallycharacteristic of low frequencies" and requiringrequired more than one attack of vertigo to diagnose. Finally in 1995, the list was again altered to allow for various degrees of the disease:.

Certain - Definite disease with histopathological confirmation Definite - Requires two or more definitive episodes of vertigo with hearing loss plus tinnitus and/or aural fullness Probable - Only one definitive episode of vertigo and the other symptoms and signssigns and symptoms Possible - Definitive vertigo with no associated hearing loss Cause The exact cause of Ménière's disease is not remains unknown, but it is believed to be related to endolymphatic hydrops or excess fluid in the inner ear. It is thought that the endolymphatic fluid burstsdeviates from its flow through the normal channels in the earchannel pathway and flows into other areas of the ear thereby causing damage. This may be related toattributes to the swelling of the endolymphatic sac or other tissues in the vestibular system of the inner ear, which is responsible for the body's sense of balance. The symptoms may occur in the presence of a middle ear infection, head trauma or an upper respiratory tract infection, or by using aspirin use, smoking cigarettes or drinking alcohol use. They may be further exacerbated by excessive consumption of caffeine and salt in some patients. Excessive levels of potassium in the body (usually caused by the consumption of potassium rich foods) may also exacerbate the symptoms.

It has also been proposed that Ménière's symptoms arecould be the result of damage caused by a the large family of DNA virus, herpes virusviridae. . Herpesviridae are presentis prevalent in a majoritydormant state in a majority of the population in a dormant state. It is suggested that the virus is reactivated when the immune system is depressed due to a stressor such as trauma, infection or surgery (under general anaesthesia). Symptoms then develop as the virus degrades the structure of the inner ear.

Symptoms The symptoms of Ménière's are variable; not all sufferers experience the same symptoms. However, the so-called "classic Ménière's" is considered to comprise of the following four symptoms:

Periodic episodes of rotary vertigo (the abnormal sensation of movement) or dizziness. Fluctuating, progressive, unilateral (in one ear) or bilateral (in both ears) hearing loss, oftensensorineural in origin often initially in the lowerlow frequency ranges. Unilateral or bilateral tinnitus (the perception of noises, often ringing, roaring, or whooshing), sometimes variable. A sensation of fullness or pressure in one or both ears., termed as aural fullness Ménière's often begins with one symptom, and gradually progresses. A diagnosis may be made in the absence of all four classic symptoms. However, having several symptoms at once is more conclusive than having each individual symptom had at a separate timestime.

Attacks of vertigo can be severe, incapacitating, and unpredictable. In some patients, attacks of vertigo can last for hours or days, and may be accompanied by an increase in the loudness of tinnitus and temporary, albeit significant, hearing loss in the affected ear(s). Hearing may improve after an attack, but often overtime becomes progressively worse. Vertigo attacks are sometimes accompanied by nausea, vomiting, and sweating.

Some sufferers experience what are informally known as "drop attacks" — a sudden, severe attackattacks of dizziness or vertigo that causes the sufferersufferers, if not seated, to fall. Patients may also experience the feeling of being pushed or pulled (Pulsion). Some patients may find it impossible to get up for some time, until the attack passes or medication takestakes its effect. There is also theassociated risk of injury from fallingwith falls.

In addition to hearing loss, sounds can seem tinny or distorted, and patients can experience unusual increased sensitivity to noises (hyperacusis). Some sufferers also experience nystagmus, or uncontrollable rhythmical and jerky eye movements, usually in the horizontal plane, reflecting the essential role of the balance system in coordinating eye movements.

Other symptoms include so-called "brain fog" (temporary loss of shortshort term memory loss, forgetfulness, and confusion), exhaustion and drowsiness, headaches, vision problems, and depression. Many of these latter symptoms are common to manyly associated with several chronic diseasesconditions.

Differential Diagnosis Diseases Clinical manifestations Para-clinical findings Gold standard Additional findings Symptoms Physical examination Lab Findings Imaging Acute onset Recurrency Nystagmus Hearing problems Peripheral BPPV + + +/− − + Dix-Hallpike maneuver − − Dix-Hallpike maneuver May be associated with nausea, vomiting, and gait instability Vestibular neuritis + +/− + /− (unilateral)

− + Head thrust test − − History/ Physical exam May be associated with nausea, vomiting, gait instability and previous upper respiratory infection HSV oticus + +/− − +/− Taste loss in the front two-thirds of the tongue Acute facial nerve paralysis Vesicles in the ear canal, the tongue, and/or hard palate + VZV antibody titres In MRI with gadolinium dye we may have enhancement of the facial nerve and cranial nerve VIII History/ Physical exam May be associated with otalgia, dry mouth, and dry eyes Meniere disease +/− + +/− + (Progressive) Sensorineural hearing loss − In CT scan we may see small or invisible vestibular aqueduct History/ Physical exam/ Rulling out other diagnoses May be associated with nausea, vomiting, and tinnitus Labyrinthine concussion + − − + high frequency hearing loss − We may see other evidences of head trauma or temporal bone fracture History/ Physical exam It happens following blunt head trauma May be associated with dizziness or tinnitus Perilymphatic fistula +/− + − + Tullio phenomenon − CT scan may show fluid around the round window recess History/ Physical exam/Imaging Can be a complication of a stapedectomy, head injury, or heavy lifting It may be provoked by sneezing, lifting, straining, coughing, and loud sounds Semicircular canal dehiscence syndrome

+/− + − + (air-bone gaps on audiometry)

Tullio phenomenon − CT scan may show defect in the arcuate eminence of the superior semicircular canal History/ Physical exam/Imaging It may be provoked by Valsalva maneuver, coughing, and sneezing Vestibular paroxysmia + + +/− (Induced by hyperventilation)

− Impaired caloric testing − We may see evidence of vestibulocochlear nerve compression on MRI History/ Physical exam/Imaging It may be provoked by head turn or other action They respond well to treatment with carbamazepine or oxcarbazepine Cogan syndrome − + +/− + Interstitial keratitis Oscillopsia Absent vestibular function on caloric test Systemic vasculitis (Aortitis) Increased ESR and cryoglobulins In CT scan we may see calcification or soft tissue attenuation obliterating the intralabyrinthine fluid spaces History/ Physical exam It may cause Ménière-like attacks Vestibular schwannoma − + +/− + Sensorineural hearing loss + Rinne test Lateralization of Weber test to the normal ear − In CT scan we may see erosion, and widening of the internal acoustic meatus Hypointense mass on T1-weighted MRI, and hyperintense mass on T2-weighted MRI Imaging Gadolinium-enhanced MRI scan is definitive diagnostic test of acoutic neuroma Otitis media + − − +/− Fever Presence of effusion in the middle ear Increased acute phase reactants Opacification of the middle ear History/ Physical exam Patient may show other signs and symptoms of upper respiratory infection such az cough, nasal discharge, and fever Aminoglycoside toxicity + − − + Oscillopsia − − History/ Physical exam May be associated with nausea, vomiting, and ataxia It may be irreversible Gentamicin is the most common one Recurrent vestibulopathy + − − − − − − History/ Physical exam The underlying pathophysiology is unknown It may happen infrequently, every one to two years It may be associated with nausea and vomiting It may overlap with vestibular migraine Central Vestibular migrain – + +/− +/− History of migraine headaches − They may have white-matter hyperintensities (WMHs) on MRI ICHD-3 criteria It may be associated with anxiety and depression Epileptic vertigo − + +/− − They may experience loss of consciousness and motor/sensory problems − − EEG They response well to anti-seizure drugs Multiple sclerosis − + +/− − Lhermitte's sign Spasticity Increased reflexes Internuclear ophthalmoplegia Optic neuritis Gait disturbance Elevated concentration of CSF oligoclonal bands Brain atrophy and some contrast enhancing plaques on CT scan Cerebral plaques disseminating in space and time on MRI History and physical examination Imaging CSF analysis MS is at least two times more common among women than men The onset of symptoms is mostly between the age of fifteen to forty years, rarely before age fifteen or after age sixty Brain tumors +/− + + + Papilledema Focal neurological deficits Cerebral spinal fluid (CSF) may show cancerous cells On CT scan most of the brain tumors appears as a hypodense mass lesions On MRI most of the brain tumors appears as a hypointense or isointense on T1-weighted scans, or hyperintense on T2-weighted MRI. Imaging Biopsy Patieny may experience headache, seizures, visual changes and changes in personality, mood and concentration Cerebellar infarction/hemorrhage + − ++/− − Limb ataxia Gait disturbance Dysarthria − Based on the time interval between stroke and imaging we may have different presentations Imaging Posterior inferior cerebellar artery is the most common artery that causes vertigo Brain stem ischemia + − +/− − Contralateral body weakness Visual field deficits Oculomotor abnormalities Bulbar findings − Based on the time interval between stroke and imaging we may have different presentations For more information click here Imaging It may be associated with subclavian steal syndrome Chiari malformation − + + − Tachycardia Pupillary dilatation Impaired gag reflex Impaired coordination − In CT scan we may see hydrocephalus, herniated cerebellar tonsils, and a flattened spinal cord In MRI we may see cerebellar tonsillar herniation, wedge shaped tonsils, syringohydromyelia, small posterior fossa, obstructive hydrocephalus, and brainstem anomalies Imaging Patient may experience ringing in the ears Parkinson − + − − Hypomimia Cogwheel rigidity Resting tremor Gait problems Bradykinesia − On brain CT scan, Parkinson disease is characterized by cortical and subcortical atrophy MRI findings in Parkinson disease are reduction in T2 relaxation time and reduced iron content in putamen and GPe History and physical examination Patients may present with slowness of movement (bradykinesia), shaking hands while they are at rest (resting tremor) and muscle stiffness (rigidity). Diseases Clinical manifestations Para-clinical findings Gold standard Additional findings Symptoms Physical examination Lab Findings Imaging Acute onset Recurrency Nystagmus Hearing problems Peripheral BPPV + + +/− − + Dix-Hallpike maneuver − − Dix-Hallpike maneuver May be associated with nausea, vomiting, and gait instability Vestibular neuritis + +/− + /− (unilateral)

− + Head thrust test − − History/ Physical exam May be associated with nausea, vomiting, gait instability Triggered by viralupper respiratory tract infections

HSV oticus + +/− − +/− Taste loss in the front two-thirds of the tongue Acute facial nerve paralysis Vesicles in the ear canal, the tongue, and/or hard palate + VZV antibody titres Gadolinium-enhanced MRI scan shows enhancement of the facial nerve and vestibulocochlear nerve History/ Physical exam May be associated with otalgia, dry mouth and dry eyes Meniere disease +/− + +/− + (Progressive) Sensorineural hearing loss − CT scan can show small or invisible vestibular aqueduct History/ Physical exam Ruling out other causes

May be associated with nausea, vomiting, and tinnitus Labyrinthine concussion + − − + high frequency hearing loss − Evidence of head trauma or temporal bone fracture History/ Physical exam It may be seen following blunt head trauma May be associated with dizziness or tinnitus Perilymphatic fistula +/− + − + Tullio phenomenon − CT scan can show fluid around the round window recess History/ Physical exam/ Imaging Can be a complication of a stapedectomy, head injury, or heavy lifting It may be provoked by sneezing, lifting, straining, coughing, and loud sounds(Tullio phenomenon) Semicircular canal dehiscence syndrome

+/− + − + (air-bone gaps on audiometry)

Tullio phenomenon − CT scan can show defect in the arcuate eminence of the superior semicircular canal History/ Physical exam Imaging

It may be provoked by Valsalva maneuver, coughing, and sneezing Vestibular paroxysmia + + +/− (Induced by hyperventilation)

− Impaired caloric testing − MRI can show evidence of vestibulocochlear nerve compression History/ Physical exam Imaging

It may be provoked by head turning Responds well to treatment with carbamazepine or oxcarbazepine Cogan syndrome − + +/− + Interstitial keratitis Oscillopsia Absent vestibular function on caloric test Systemic vasculitis (Aortitis) Increased ESR and cryoglobulins CT scan can show calcification or soft tissue attenuation obliterating the intralabyrinthine fluid spaces History/ Physical exam It may cause Ménière's disease like attacks Vestibular schwannoma − + +/− + Sensorineural hearing loss + Rinne test Lateralization of Weber test to the normal ear − CT scan can show erosion and widening of the internal acoustic meatus T1-weighted MRI may show a hypointense mass whereas a T2- weighted MRI may show a hyperintense mass Imaging Gadolinium-enhanced MRI scan is definitive diagnostic test of acoutic neuroma Otitis media + − − +/− Fever Presence of effusion in the middle ear Increased acute phase reactants Opacification of the middle ear History/ Physical exam Patient may present with other signs and symptoms of upper respiratory infection such as cough, nasal discharge, and fever Aminoglycoside toxicity + − − + Oscillopsia − − History/ Physical exam May be associated with nausea, vomiting, and ataxia It may be irreversible Gentamicin is the most common one Recurrent vestibulopathy + − − − − − − History/ Physical exam The underlying pathophysiology is unknown It may happen infrequently and varies every one to two years It may be associated with nausea and vomiting It may overlap with symptoms of vestibular migraine Central Vestibular migraine – + +/− +/− History of migraine headaches − MRI can demonstrate white-matter hyper-intensities (WMHs) ICHD-3 criteria It may be associated with anxiety and depression Epileptic vertigo − + +/− − They may experience loss of consciousness and motor/sensory problems − − EEG Respond well to anti-epileptic drugs. Multiple sclerosis − + +/− − Lhermitte's sign Spasticity Hyperreflexia Internuclear ophthalmoplegia Optic neuritis Gait disturbance Elevated concentration of CSF oligoclonal bands CT scan can show brain atrophy and some contrast enhanced demyelinating plaques MRI shows cerebral plaques disseminated in time and space History and physical examination Imaging CSF analysis MS is twice as common in women than in men The onset of symptoms is most prevalent between the age of fifteen to forty years and rarely before the age fifteen or after the age of sixty years. Brain tumors +/− + + + Papilledema Focal neurological deficits Cerebral spinal fluid (CSF) may show cancerous cells CT scan demonstrates most of the brain tumors as hypodense mass lesions T1- weighted MRI demonstrates most tumors as either a hypointense or isointense lesion and on the T2-weighted MRI as a hyperintense lesion Imaging Biopsy May experience headache, seizures, visual changes and changes in personality, mood and concentration Cerebellar infarction/hemorrhage + − +/− − Limb ataxia Gait disturbance Dysarthria − Based on the time interval between stroke and imaging we may have different presentations Imaging Posterior inferior cerebellar artery is the most common artery that causes vertigo Brain stem ischemia + − +/− − Contralateral body weakness Visual field deficits Oculomotor abnormalities Bulbar findings − Based on the time interval between the onset of stroke and the time of imaging we may have different presentations For more information click here Imaging It may be associated with subclavian steal syndrome Chiari malformation − + + − Tachycardia Pupillary dilatation Impaired gag reflex Impaired coordination − CT scan can show hydrocephalus, herniated cerebellar tonsils, and a flattened spinal cord MRI may show cerebellar tonsillar herniation, wedge shaped tonsils, syringohydromyelia, small posterior fossa, obstructive hydrocephalus, and brainstem anomalies Imaging May experience a sensation of ringing of ears (tinnitus) Parkinson − + − − Hypomimia Cogwheel rigidity Resting tremor Gait problems Bradykinesia Autonomic dysfunction( Dizziness, orthostatic hypotension)

− CT scan can demonstrate cortical and subcortical atrophy MRI can show reduction in T2 relaxation time and reduced iron content in putamen and GPe History and physical examination May present with slowing of movement (bradykinesia), resting tremorand muscle stiffness (rigidity). ABBREVIATIONS

⋮ Diagnosis Many disorders have symptoms similar to Ménière's. The diagnosis is usually established by clinical findings and medical history. However, a detailed oto-neurological examination, audiometry and head magnetic resonance imaging (MRI) scan should be performed to exclude a tumour of the cranial nerve VIII (vestibulocochlear nerve) or superior canal dehiscence which would cause similar symptoms. Because there is no definitive test for Ménière's, it is only diagnosed when all other causes have been ruled out.

Ménière’s disease typically starts between the ages of 20 and 50 years. Men and women are affected in equal numbers.- American Academy of Otolaryngology−Head and Neck Surgery

Ménière's typically begins between the ages of 30 and 60 and affects men slightly more than women.

Many CNS and Ear disorders have signs and symptoms similar to that seen in Ménière's Disease. The diagnosis is usually established by clinical findings and medical history. However, a detailed oto-neurological examination, audiometry and magnetic resonance imaging (MRI) scan should be performed to exclude a tumour of the vestibulocochlear nerve or superior canal dehiscence which would cause similar symptoms. Since there is no definitive test for Ménière's, it is only diagnosed when all other causes have been ruled out.

Ménière’s disease typically presents between the ages of 20 and 50 years. Men and women are affected in equal numbers.- American Academy of Otolaryngology−Head and Neck Surgery

Ménière's typically begins between the ages of 30 and 60 years and affects men slightly more than women.

Treatment Initial treatment is aimed at both dealing with immediate symptoms and preventing recurrence of symptoms, and so will vary from patient to patient. Doctors may recommend vestibular training, methods for dealing with tinnitus, stress reduction, hearing aids to deal with hearing loss, and medication to alleviate nausea and symptoms of vertigo.

Several environmental and dietary changes are thought to reduce the frequency or severity of symptom outbreaks. Most patients are advised to adopt a low-sodium diet, typically one to two grams (1000-2000mg) at first, but diets as low as 400mg are not uncommon. Patients are advised to avoid caffeine, alcohol and tobacco, all of which can aggravate symptoms of Ménière's. Some recommend avoiding Aspartame. Patients are often prescribed a mild diuretic (sometimes vitamin B6). Many patients will have allergy testing done to see if they are candidate for allergy desensitization as allergies have been shown to aggravate Ménière's symptoms.

Initial treatment is targeted at relieving immediate symptoms and preventing recurrence of symptoms in the future and thus varies from patient to patient. Doctors may recommend vestibular training, methods for dealing with tinnitus, stress reduction, hearing aids to deal with hearing loss, and medication to alleviate nausea and symptoms of vertigo.

Several environmental and dietary changes are thought to reduce the frequency or severity of symptom outbreaks. Most patients are advised to adopt a low-sodium diet, typically one to two grams (1000-2000mg) at first, but diets as low as 400mg are not uncommon. Patients are advised to avoid caffeine, alcohol and tobacco, all of which can aggravate symptoms of Ménière's. Some clinicians recommend avoiding Aspartame. Patients are often prescribed a mild diuretic to decrease the inner ear fluid build up. Many patients undergo allergen testing during initial evaluation as allergies have been shown to aggravate Ménière's symptoms.

Women may experience increased symptoms during pregnancy or shortly before menstruation, probably due to increased fluid retention.

Lipoflavonoid is also recommended for treatment by some doctors.

Many patients consider fluorescent lighting to be a trigger for symptoms. The plausibility of this can be explained by how important a part vision plays in the overall mechanism of human balance.

Lipoflavonoid, a natural bioflavanoid that contains some of the B vitamins namely B3, B6 and B12 of the B vitamin complex is recommended for treatment of the tinnitus component of the disease by some doctors.

Many patients consider fluorescent light as a trigger for their symptoms. The plausibility of this can be explained by the vital role that vision plays in the overall mechanism of human balance.

The endolymphatic shunt operation consists of opening the mastoid bone and identifying the endolymphatic sac which is located in the posterior fossa dura. To find the sac, the sigmoid sinus is denuded of its bony cover except for a small rectangle of thin bone named Bill's Island, after Dr. William House. The sigmoid sinus is then collapsed with gentle pressure and the sac exposed behind the posterior semicircular canal. The sac is then incised and a shunt tube is inserted. The picture on the right shows a Huang-Gibson tube with a one-way valve that allows fluid to seep out but not back into the sac. This procedure decreases the endolymphatic fluid pressure. Treatments aimed at lowering the pressure within the inner ear include antihistamines, anticholinergics, steroids, and diuretics. A medical device that provides transtympanic micropressure pulses is now showing some promise and is becoming more widely used as a treatment for Ménière's.

Surgery may be recommended if medical management does not control vertigo. Injection of steroid medication behind the eardrum, or surgery to decompress the endolymphatic sac may be used for symptom relief. Permanent surgical destruction of the balance part of the affected ear can be performed for severe cases if only one ear is affected. This can be achieved through chemical labyrinthectomy, in which a drug (such as gentamicin) that "kills" the vestibular apparatus is injected into the middle ear. The nerve to the balance portion of the inner ear can be cut (vestibular neurectomy), or the inner ear itself can be surgically removed (labyrinthectomy). These treatments eliminate vertigo, but because they are destructive, they are used only as a last resort. Typically balance returns to normal after these procedures, but hearing loss may continue to progress.

The anti herpesvirus drug Aciclovir has also been used with some success to treat Ménière's Disease. The likelihood of the effectiveness of the treatment was found to decrease with increasing duration of the disease possibly because the accumulation of viral damage to the inner ear over time meant that suppression of the virus made no significant difference to the symptoms. Morphological changes to the inner ear of Ménière's sufferers have also been found which it was considered likely to have resulted from attack by a herpes simplex virus. It was considered possible that long term treatment with an acyclovir (greater than six months) would be required to produce an appreciable effect on symptoms. Herpes viruses have the ability to remain dormant in nerve cells by a process known as HHV Latency Associated Transcript. Continued administration of the drug should prevent reactivation of the virus and allow for the possibility of an improvement in symptoms. Another consideration is that different strains of a herpes virus can have different characteristics which may result in differences in the precise effects of the virus. Further confirmation that Aciclovir can have a positive effect on Ménière's symptoms has been reported.

Treatments aimed at lowering the pressure within the inner ear include antihistamines, anticholinergics, steroids, and diuretics. A medical device that provides transtympanic micropressure pulses is now showing some promising results and is becoming more widely used as a treatment for Ménière's.

Surgery may be recommended if medical management does not control vertigo. Injection of steroid medication behind the eardrum, or surgery to decompress the endolymphatic sac may be used for symptom relief. Permanent surgical destruction of the balance component of the affected inner ear can be performed for severe and refractory cases of the disease if only one ear is affected. This can be achieved through chemical labyrinthectomy, in which a drug (such as gentamicin) that "kills" the vestibular apparatus is injected into the middle ear. The nerve to the balance portion of the inner ear can be cut (vestibular neurectomy), or the inner ear itself can be surgically removed (labyrinthectomy). These treatment options eliminate vertigo, but since they are typically destructive they are implemented only as a last resort. Usually balance returns to normal after these procedures, but hearing loss may continue to progress.

The anti herpesvirus drug Acyclovir has also been used with some success to treat Ménière's Disease. The likelihood of the effectiveness of the treatment was found to decrease with increasing duration of the disease possibly because of the overtime accumulation of viral damage to the inner ear and thus demonstrated that suppression of the virus made no significant difference to the symptoms if the exposure was present for prolonged periods. Morphological changes to the inner ear of Ménière's sufferers has also been found and is likely considered to have resulted from attack by the herpes simplex virus. It was considered possible that long term treatment with an acyclovir (greater than six months) would be required to produce a remarkable reduction in symptomatology. Herpes viruses have the ability to remain dormant in nerve cells by a process known as HHV Latency Associated Transcript. Continued administration of the drug should prevent reactivation of the virus and allow for the possibility of an improvement in symptoms. Another consideration is that different strains of herpes virus can have different characteristics which may result in differences in the pathophysiological effects of the virus. Further confirmation that Acyclovir can have a positive effect on Ménière's symptoms has been reported.

Progression Progression of Ménière's is unpredictable: symptoms may worsen, disappear altogether, or remain the same.

Sufferers whose Ménière's began with one or two of the classic symptoms may develop others with time. Attacks of vertigo can become worse and more frequent over time, resulting in loss of employment, loss of the ability to drive, and inability to travel. Some patients become largely housebound. Hearing loss can become more profound and may become permanent. Some patients become deaf in the affected ear. Tinnitus can also worsen over time. Some patients with unilateral symptoms, as many as fifty percent by some estimates, will develop symptoms in both ears. Some of these will become totally deaf.

Yet the disease may end spontaneously and never repeat again. Some sufferers find that after eight to ten years their vertigo attacks gradually become less frequent and less severe; in some patients they disappear completely. In some patients, symptoms of tinnitus will also disappear, and hearing will stabilize (though usually with some permanent loss).

Progression of Ménière's is unpredictable: symptoms may worsen, undergo complete resolution or remain the same.

Sufferers whose Ménière's began with one or two of the classical symptoms may develop other symptoms over time. Attacks of vertigo can progressively worsen and increase in frequency over time, resulting in unemployment and the inability to drive and travel. Some patients become largely housebound. Hearing loss can become profound and more permanent. Some patients may also develop deafness in the affected ear. It is estimated that in fifty percent of the cases patients with unilateral symptoms will develop symptoms bilaterally. Tinnitus is also known to worsen over time.

Some sufferers reported that after eight to ten years the vertigo attacks gradually became less frequent and lesser in severity; some patients reported that the symptoms disappeared completely.  In some patients, symptoms of tinnitus disappear overtime and the hearing partially stabilises although usually with some permanent hearing loss.