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The diagnosis of "classic" Meniere's disease is easy to make. Unfortunately, Meniere's disease is a diagnosis of exclusion and many disease entities can mimic Meniere's disease. Thus, it is essential to eliminate other possible etiologic agents for complaints that could be related to Meniere's disease before making this diagnosis. This article evaluates the differential diagnosis in Meniere's disease.
Medical therapy of Meniere's disease is geared not only toward the differential diagnosis that has led to Meniere's disease and the supportive therapy for the physical manifestations of the disease but also for the psychologic sequelae of the disease such as mild-to-moderate situational depression and even chronic depression. Overall, with adequate medical therapy, allergy workup, and immunotherapy for patients with known diagnoses of allergies, the author's clinic has been able to help more than 85% of its patients who present with symptoms of Meniere's disease. For intractable cases where autoimmune phenomena can be suspected with a strong degree of suspicion, the author's clinic has also treated patients with immunosuppressive medications such as azathioprine and/or methotrexate in a low dose.
The etiologies of Meniere's disease and otosclerosis are largely unknown. An association between these two diseases has been proposed on both a clinical and histopathologic basis but the causal relationship is controversial. In this paper we report two families in which both otosclerosis and Meniere's disease are inherited as independent phenotypes suggesting that the two diseases represent different outcomes of the same mutation. Thus the Meniere's disease occasionally seen in otosclerotic patients might not be caused by otosclerosis, but rather by a molecular defect leading to endolymphatic hydrops and/or clinical otosclerosis.
Meniere's disease can compromise the quality of life of some patients in a manner so seriously that it can cause social segregation, even from family. Hearing loss, tinnitus, aural pressure, and disturbances in equilibrium added to an emotional instability frequently present in these patients may take them to a progressive state of solitude and depression, marking their lives by personal tragedy and making life a living hell. The clinical picture of Meniere's disease fluctuates, however. Individually, subsidiary examinations become impotent in diagnosing Meniere's disease. To be called Meniere's disease, the cause must be unknown; otherwise it would constitute Meniere's syndrome. Taking all of this into consideration, one would call this an unusual situation, or at least confusing. The lack of an etiologic diagnosis in medicine always creates anxiety for doctors and patients. What is considered to be either a routine or an extended test may change from service to service. The physician does not need to order all tests. What the physician needs is a protocol he or she trusts. Test results can vary, even depending on the moment when they are performed. More important than the number of tests ordered is the strategy by which the tests should be put together at that certain moment. The authors believe that one should have his or her own protocol for diagnosis, always beginning with a detailed history taking being guided by them most of the time. It is the authors' understanding that patients with Meniere's disease should be followed closely by their ear, nose, and throat doctor in episodes of vertigo or fluctuation of their hearing, tinnitus, or aural pressure. Should the patient be experiencing a stable period, a clinical visit along with an audiovestibular workup should be performed at least once a year. By monitoring the course of the disease, clinicians would be able to detect early changes in symptoms and/or test results, giving them the possibility to intervene clinically as early as possible in acute episodes of vestibulocochlear disorganization, protecting the inner ear, and minimizing sequelae from spells of hydrops. The authors believe that only the association of clinical sense and as many subsidiary tests as are useful will lead to a desirable level of certainty in the diagnosis of Meniere's disease, and will allow clinicians to presume bilateral involvement, monitor the development of the disease, intervene in its natural course, and idealize appropriate treatment.
Medical management of Meniere's disease is successful in approximately 70% of patients. Surgical intervention is the treatment option when medication fails. Middle ear installation of aminoglycosides provides significant control of vertigo. This article addresses the role of aminoglycoside ablation of vestibular function in Meniere's disease.
In Meniere's disease, spontaneous nystagmus beating toward the affected ear (ipsilateral nystagmus) is frequently observed especially during vertiginous periods. VOR against horizontal rotation was recorded in 19 patients with Meniere's disease exhibiting ispilateral beating nystagmus, and the dynamic aspect of vestibular function during vertiginous periods was examined by determining VOR gain and directional preponderance (DP). The patients sat on a rotation chair and were passively rotated at about 0.3-0.6 Hz. The maximal head velocity ranged from 80 to 120 deg/s and the duration of rotation from 20 to 30 s. In most patients exhibiting ipsilateral nystagmus, VOR gain toward the affected side was higher than that toward the intact side, indicating that the peripheral vestibular system on the affected side could still respond to head movements and that its dynamic function was increased. This asymmetry disappeared along with disappearance of ipsilateral nystagmus. During the period with contralateral nystagmus, VOR gain toward the affected side became lower than that toward the intact side. These findings indicate that alterations in the dynamic property of the peripheral vestibular system may correlate with the directional change of spontaneous nystagmus. However, the degree of VOR DP (VOR DP%) did not correlate with the slow phase velocity of spontaneous nystagmus, indicating that observation of spontaneous nystagmus alone cannot determine with precision the degree of imbalance in the dynamic aspect of vestibular function.
OBJECTIVE: The diagnosis of Meniere's disease has always been a source of confusion. There is no single test that is definitive for the diagnosis. Recent advances have enabled clinicians to noninvasively test the function of the inner ear and its associated neural pathways. The electrocochleogram (ECOG) has been advocated as a reliable test that is diagnostic for Meniere's disease. This study was undertaken to assess the value of ECOG in establishing the diagnosis of Meniere's disease. STUDY DESIGN: Patients who were suspected of having Meniere's disease were prospectively entered into a study of the diagnostic value of ECOG. Each patient had a complete evaluation including a detailed history, physical examination, laboratory studies, and audiometric tests. SETTING: University otolaryngology clinic. PATIENTS: A group of 199 patients who presented to a neurotology clinic and were suspected to have symptoms consistent with Meniere's disease. INTERVENTION: ECOG testing. MAIN OUTCOME MEASURES: Audiometric thresholds, action potential magnitude (AP), summating potential amplitude (SP), AP latency, and clinical evaluations were assessed. RESULTS: The ECOG was found to correlate with historical and audiometric criteria that are used to diagnose the disease. The percentage of abnormal ECOG did not correlate with stage of disease or duration of time that symptoms were present. CONCLUSIONS: The ECOG has limited value in the diagnosis of Meniere's disease. It appears to correlate with the length of time patients experience symptoms and their audiometric findings. It was not correlated with the number of symptoms that the patient experienced at the time that the study was conducted.
Meniere's disease is a disease of the inner ear characterized by a triad of symptoms: vestibular symptoms, auditory symptoms, and pressure. The pathologic correlate of Meniere's disease is endolymphatic hydrops and the etiopathogenesis involves a deficiency in the absorption of endolymph. The pathophysiology of the symptoms is still disputed: membranous ruptures, pressure and mechanical displacement of the end organs, or obstruction followed by an abrupt clearance of the endolymphatic duct. The course of the disease may be progressive or nonprogressive and, in addition to the typical presentation of Meniere's disease, two variations of the disorder have been identified: cochlear Meniere's disease, and vestibular Meniere's disease. It can be further broken into two subsets: Meniere's syndrome, with a known and well-established cause, and Meniere's disease, in which the cause seems to be idiopathic. It is likely that there are racial (genetic) as well as environmental factors that influence differences in incidence among countries and among various sections of countries. The disease is much more common in adults, with an average age of onset in the fourth decade, the symptoms beginning usually between ages 20 and 60 years. Meniere's disease is (grossly) equally common in each sex, and right and left ears are affected with fairly equal frequency. The diagnosis of Meniere's disease is by exclusion, and a careful history is the most important guide to a correct diagnosis. Its medical treatment is largely empiric. Surgery can be considered when, even after medical therapy, the disease progresses and the symptoms become intractable. Surgery may be either conservative or destructive. Bilaterality must be considered when deciding the best surgical option for a patient with Meniere's disease. It is the authors' opinion that endolymphatic sac surgery is an extension of conservative treatment.
Meniere's disease is a clinical syndrome of uncertain aetiology but it is a widespread belief that it is related to endolymphatic hydrops. Clinically, it is a paroxysmal disorder with vertigo and subsequent deafness. It is responsive to acetazolamide and sensitive to the sodium content in the diet, many of the features of the channelopathies. The present paper explores the possibility that it may be related to a channelopathy.
The ablation treatment of Meniere's disease by intratympanic streptomycin applications was first reported by Schuknecht in 1957. Streptomycin and gentamycin are the most frequent aminoglycosides used for the Meniere's disease treatment. Gentamycin is responsible for the damage of vestibular dark cells causing the impairment of endolymph production. This method gives the possibility for the control of the vertigo with a potential hearing preservation. Fifteen patients with unilateral Meniere's disease who had not responded to conventional therapy, were treated by intratympanic gentamycin injections. The hearing status and the caloric test were staged before and after treatment according to the AAO-HNS guidelines. Overall results after minimum 1 year follow-up in this group were as shown below: complete vertigo control--5 patients, substantial vertigo control--8 patients, complete relief of tinnitus--10, relief of aural fullness--12 patients, hearing loss--none. According to presented results, intratympanic injections of gentamycin is the useful alternative to the surgery. This method should be consider in every patient with the unilateral Meniere's disease, who had not responded to the conventional treatment.
The etiopathogenesis of Meniere's disease has remained controversial since the early 1900s. Many investigators have studied the molecular and cellular pathology of the inner ear in patients with this disorder. Three basic pathologic mechanisms have emerged; fibrosis of the endolymphatic sac and vestibular epithelia, altered glycoprotein metabolism, and immune-mediated inner ear disease. This article reviews the current understanding of these three basic pathologic processes.
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32 patients with Meniere's disease (MD) were examined audiologically in the trial of diagnostic potential of otoacoustic emission (OAE) method. Two classes of OAE were registered: delayed evoked otoacoustic emission (DEOAE) and otoacoustic emission at the frequency of the distortion product (DPOAE). DEOAE in MD patients is recordable in tonal hearing reduction to 50 dB, DPOAE--to 65 dB. Amplitude of both these otoacoustic emissions in normal ear (hearing tonal threshold under 20 dB) of MD patients was significantly less than in control patients with normal hearing. OAE can be added to diagnostic tools for examining structures of the internal ear in MD.
Understanding the pathogenesis of Meniere's disease can result from studying its natural history; however, a marvelous opportunity for this understanding exists in surgical revisions of endolymphatic sac enhancement. In addition to avoiding destructive procedures, revision of endolymphatic sac enhancement has restored health to many patients. The procedures and findings from such revisions, which are briefly described in this article, have provided the best opportunity for the author to understand and observe the pathogenesis of Meniere's disease.
Among 22 patients with Meniere's disease treated with ultrasonic irradiation, only eight showed extinguished caloric reaction. Long-term therapeutic effect had been obtained in all the patients, Histological examination of the lateral semicircular canal and the crista ampullaris from five patients previously treated with ultrasound for Meniere's disease showed the following changes: (1) In the subepithelial tissue in crista ampullairs no signs of degeneration were found. The nerve fibres were normal. (2) The sensory cells with nerve-endings and supporting cells also appeared normal. (3) The secretory cells showed pronounced cellular vacuolization and increased intercellular space. (4) The lateral semicircular canal was completely obliterated with destruction of the membranous canal. It is concluded that the therapeutic effect may be due to the creation of an endolymphatic fistula.