A typical attack of Meniere's disease is preceded by fullness in one ear. Hearing fluctuation or changes in tinnitus may also precede an attack. A Meniere's episode or "attack" generally involves severe vertigo spinning -- generally a horizontal merri-go-round type sensation , imbalance, nausea and vomiting as well as acute reduction of hearing. The average attack lasts two to four hours. Following a severe attack, most people find that they are exhausted and must sleep for several hours.
There is a large amount of variability in the duration of symptoms. Some people experience brief "shocks", and others have constant unsteadiness. An unusual variant is the "invisible hand", where individuals feel as if they are being pushed over.
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High sensitivity to visual stimuli visual dependence is common. Lacour, During the attack the eyes jump this is called "nystagmus". Supplemental material : Movie of nystagmus during a Meniere's disease attack. A particularly disabling symptom is a sudden fall. These typically occur without warning. These falls, a variant of " drop attacks ", are called "otolithic crisis of Tumarkin", from the original description of Tumarkin They are attributed to sudden mechanical deformation of the otolith organs utricle and saccule , causing a sudden activation of vestibular reflexes.
Patients suddenly feel that they are tilted or falling although they may be straight , and bring about much of the rapid repositioning themselves.
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This is a very disabling symptom as it occurs without warning and can result in severe injury. Often destructive treatment e. Other otologic conditions also occasionally are associated with Tumarkin type falls Black et al, ; Ishiyama et al, See here for more information about drop attacks. Meniere's episodes may occur in clusters; that is, several attacks may occur within a short period of time.
However, years may pass between episodes. Between the acute attacks, most people are free of symptoms or note mild imbalance and tinnitus. Meniere's affects roughly 0. In our clinical practice , where we care for large numbers of Meniere's patients, the most common age of presentation is in the 6th decade. This probably reflects the age distribution of Meniere's in Chicago Illinois, which of course is also a function of the age of the population in Chicago.
It is a little older than the typical age of presentation of vestibular migraine which is in the 5th decade, much older than the reported highest prevalence age for non-vestibular migraine about 35 , and is similar to the age of presentation of BPPV. The ratio of women to men in our Meniere's population is about Suh et al found the prevalence was only 5. We do generally agree that there is often minor symptoms on the other ear, and also that it is rare that both ears are severely impacted. We would say these statistics differ because they are comparing different things. Other possibilities, however, are selection bias and different patterns of the disease in different countries.
We would not agree with this in our own wide experience at Chicago Dizzienss and Hearing. Even if one does become bilateral, usually the second ear is affected only to a mild extent -- perhaps a little tinnitus or fullness.
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Suh et al, In most cases, a progressive hearing loss occurs in the affected ear s. A low-frequency sensorineural pattern is commonly found initially, but as time goes on, it usually changes into either a flat loss or a peaked pattern click here for more information about hearing testing.
Although an acute attack can be incapacitating, the Meniere's disease is not fatal. What causes Meniere's Disease? Click here for a more detailed discussion. The origin of Meniere's disease is presently controversial.
While in the past, it was felt that plumbing problems hydrops in the ear were responsible for the disease, the most current opinion is that hydrops is a marker for the Meniere's disease, rather than necessarily being responsible for the symptoms. Traditional thinking on the origin of Meniere's disease : The most prevalent opinion is that an acute attack of Meniere's disease results from fluctuating pressure of the fluid within the inner ear.
A system of membranes, called the membranous labyrinth, contains a fluid called endolymph. The membranes can become dilated like a balloon when pressure increases. This is called "hydrops".
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One way for this to happen is when the drainage system, called the endolymphatic duct or sac is blocked. In some cases, the endolymphatic duct may be obstructed by scar tissue, as might be true in some cases of the closely related condition of " delayed endolymphatic hydrops ", or may be narrow from birth. In some cases there may be too much fluid secreted by the stria vascularis. Besides a stoppage of drainage pathways, abnormally enlarged fluid pathways into the ear such as the vestibular aqueduct.
Enlarged vestibular aqueducts are one of the most commonly identified inner ear bony malformations in children with sensorineural hearing loss of unknown cause Oh et al, The vestibular aqueduct extends from the medial wall of the vestibule to the posterior surface of the petrous temporal bone. Most persons with enlarged vestibular aqueducts with ear disorders have hearing loss, but occasionally there is an association with vestibular problems Shessel and Nedzelski, There may be a genetic link between enlarged vestibular aqueduct and Pendred syndrome, which is a congenital thyroid disorder.
More recent thought on the origin of Meniere's disease. Because Meniere's disease occurs in roughly 0. Thus logically, there must be something more than simply hydrops involved in the origin of Meniere's disease see following paragraph about immunologic function as well as pages on autoimmune inner ear disease and allergy in Meniere's disease. Recently attention has also been focused on the immunologic function of the endolymphatic sac -- immune disease may contribute to a substantial percentage of Meniere's disease.
On the other hand, Ruckenstein and others recently obtained a large number of autoimmune blood tests in a group of 40 patients with unilateral Meniere's disease including CBC, ANA, Anti-Sjoegren, RF, Complement, antiphospholipid antibody, western blot for heat shock protein, MHA syphilis test , and Lyme. They concluded that it is unlikely that autoimmune etiologies play a significant role in their population of unilateral Meniere's Ruckenstein, Another interpretation of their data is that they may simply not have had an appropriate marker for autoimmune involvement, as well as unilateral Meniere's may have less autoimmune cause than bilateral.
One can also build a reasonable case for Migraine being the cause of some cases of Meniere's disease. Meniere's disease hearing loss does not follow the expected pattern for an inner ear disease i. Non-drug treatment of Meniere's i. Thus, the bottom line is that in most patients with Meniere's disease in , the underlying cause of Meniere's disease is unknown. It is most often attributed to viral infections of the inner ear, head injury, a hereditary predisposition, and allergy. Migraine may cause symptoms that overlap with Meniere's disease, or in some, may even be identical to Meniere's disease, at the level that we can resolve disorders in the clinic i.
What damage is done by Meniere's Disease? Hair cell death: Conventional thought is that repeated attacks of Meniere's kills hair cells in the inner ear. Cochlear hearing hair cells are the most sensitive. Vestibular hair cells seem more resilient but there is also a slow decline in the caloric response in the diseased ear over roughly 15 years Stahle et al, Mechanical changes to the ear.
Mechanical disruption of the inner ear is also likely with dilation of the utricle and saccule of the ear being a well known pathological finding. The saccule may dilate so that in later stages, it is adherent to the underside of the stapes footplate. This mechanical disruption and distortion of normal inner ear structures may result in the gradual onset of a chronic unsteadiness, even when patients are not having attacks. The periodic dilation and shrinkage of the utricle is also a reasonable explanation for periodic attacks of another inner ear disorder, BPPV.
Finally, it also seems likely that there may be rupture of the suspensory system for the membranous labyrinth, related to vestibular atelectasis.
This might create some mechanical instability of the utricle and saccule and consequently some chronic unsteadiness. Some investigators suggest that experimental Meniere's disease kills the cochleovestibular nerve through neurotoxicity in mice and guinea pigs Megarian et al, However, the evidence is against this being the main mechanism in human beings see Kitamura et al, ; Nadol et al, Rather, it seems that Meniere's disease damages both hair cells and nerve fibers in humans.
Studies of humans are handicapped by the possibility that Meniere's is the final common pathway of a variety of illnesses of the ear. This is roughly the same prevalence as multiple sclerosis MS. The majority of people with Meniere's disease are over 40 years of age, with equal distribution between males and females. At the present time there is no cure for Meniere's disease, but there are ways to manage the condition and help control symptoms.
Some recently refined treatments are rather close to a cure i. While some have suggested that Meniere's may "burn out", research studies suggest that this is not likely Havia and Kentala How does the doctor know I have Meniere's disease?
Diagnosis of Meniere's is based on a combination of the right set of symptoms usually episodic dizziness and hearing disturbance , hearing tests which document that hearing is reduced after an attack, and then gets better, and exclusion of alternative causes. Several committees have offered diagnostic criteria -- these are reviewed in the link. In spite of more recent additions, we continue to favor the AAO criteria for "definite" Meniere's disease.