The effect of middle ear pressure treatment with the Meniett device and tympanic membrane massage (TMM) device for intractable vertigo in patients with Meniere's disease was reviewed. Pressure treatment with the Meniett device is induced after the ventilation tube is placed. Three double-blinded clinical trials and five long-term follow-up studies showed improvement in patients' vertigo. No complication were reported in the previous studies. The effect of the TMM device was reported to be similar to that of the Meniett device. Both the Meniett and TMM devices are minimally invasive treatments for middle ear pressure recommended as second-line treatment for intractable vertigo in patients with Meniere's disease.
Meniere's disease is characterized by intermittent episodes of vertigo lasting from minutes to hours, with fluctuating sensorineural hearing loss, tinnitus, and aural pressure. The primary histopathological correlate is endolymphatic hydrops. Several medical and surgical treatments have been offered to patients with Meniere's disease. It has been confirmed that no one effective treatment is available for these patients. According to the severity of the patients' symptoms, appropriate therapeutic strategies should be selected. If medical therapies including lifestyle change, diuretics, and local/systemic steroids have failed, then surgical approaches such as intratympanic gentamicin perfusion (GM), pressure pulse treatment with Meniett®, endolymphatic sac surgery (ESS) and vestibular neurectomy (VN) should be considered. Most reviews have reported relative good (80-100%) vertigo control rates with either GM, Meniett®, ESS, or VN, however, recurrence of vertigo has been noticed in certain cases. A combination of medical and surgical strategies should be recommended and the treatment algorithm for Meniere's disease indicated in “2011 Clinical practice guidelines for Meniere's disease” must be adopted.
We have recently encountered two cases of intractable Meniere's disease with a history of head trauma. Both patients underwent surgical treatments because conservative medical treatment had failed. As we supposed that they had developed a secondary endolymphatic hydrops associated with perilymphatic fistula, we first performed a simple mastoidectomy and opened the facial recess to carry out an exploratory tympanotomy. Next, we performed endolymphatic sac drainage and closed both oval and round windows with connective tissue whether we found an obvious fistula or not. One year-follow-up results showed complete relief from vertigo after the operation in both cases. It is suggested that relative increase in the endolymph pressure can become a cause of endolymphatic hydrops due to the decline of the perilymph pressure. In patients with Meniere's disease who have a history of trauma, we propose that it should be better to keep in mind the possibility of fistula-induced secondary hydrops.
The head impulse test (HIT) is a safe and quick way of assessing semicircular canal function in patients with peripheral vestibular loss at the bedside, first described in 1988. This test is practical even in sick patients and needs no equipment. The clinician identifies overt (=visible) catch-up saccades back to the target after passive head rotation as a clinical sign of canal paresis. However, it is known that some patients with absence of vestibular function do not make overt saccades, but instead make covert catch up saccades during the passive unpredictable head turn, which are extremely difficult for the clinician to detect with the naked eye. Recently, a new lightweight, nonslip, high-speed video-oculography system (vHIT; video head impulse test) has been developed that measures eye velocity during head rotations. This system is easy to use in a clinical setting, provides an objective measure of the vestibulo-ocular-reflex (VOR), and detects both overt and covert catch-up saccades in patients with vestibular loss.
The study was designed to determine whether a combination of spontaneous and head-shaking nystagmus and the head thrust test could be used in lieu of a caloric test for diagnosis of peripheral vestibular disorder. An analysis of vertigo/dizziness was conducted in 117 patients who visited our department between October 2009 and September 2011. Tests for spontaneous nystagmus, head-shaking nystagmus, head thrust, and electronystagmography including caloric testing were performed. Among the 117 patients, 83 patients were diagnosed as having peripheral disorders and 34 patients had non-peripheral disorders. The positive and negative predictive values for head thrust tests and spontaneous nystagmus were 73% and 85%, respectively, and a significant relationship was observed. Positive and negative predictive values were 80% and 55%, respectively, for canal paresis and spontaneous nystagmus. Of the 26 patients with positive results in head thrust tests, 25 (96%) had peripheral disorders. The positive results of the head thrust test in the peripheral group were significantly higher than that in non-peripheral group. Of the 24 patients with positive results for head-shaking nystagmus, 22 (93%) patients had peripheral disorders. The positive results of head-shaking nystagmus in the peripheral group were significantly higher than that in the non-peripheral group. Thirty-one (37%) of 83 patients with peripheral disorders were positive for head-shaking nystagmus and/or head thrust. On the other hand, of 34 patients with non-peripheral disorders, results were negative for 30 (88%) patients on the head-shaking nystagmus and head thrust tests. Negative results on these tests were more often observed in patients with non-peripheral disorders than in those with peripheral disorders. These results demonstrate that spontaneous nystagmus, head-shaking nystagmus, and head thrust tests are valid measurements and may be effectively used in combination for detection of vestibular disorders in patients with vertigo/dizziness.
We produced an interview sheet to assess for the presence of benign paroxysmal positional vertigo (BPPV), and to diagnose the subtype of BPPV and the affected ear when the diagnosis was BPPV. One hundred and thirty-seven patients, who were attending our clinic as outpatients with the chief complaint of dizziness, took the interview. We compared the result of the diagnosis from the examination for nystagmus with the result that we estimated from the answers to the interview sheet. In 37% (14 cases) of the patients who showed benign paroxysmal positional nystagmus (BPPN) the subtype of BPPV and the affected ear were diagnosed correctly based on the answers to the interview sheet, which was almost same result as a previous report (Higashi-Shingai K, et al. Acta Oto-laryngologica, 2011). We found that there was a problem when we presumed the diagnosis to be the horizontal canal type of BPPV with apogeotropic positional nystagmus and was clear that this is one point we should improve in the future. In addition, it is important to administer the Schellong test, and to examine for the presence or absence of a blood pressure regulation disorder when we suspect a diagnosis of BPPV although we cannot see BPPN.