Endolymph which fills the scala media is an unusual extracellular fluid in that its composition is reminiscent of intracellular fluid such as its high potassium concentration. This characteristic ion homeostasis is important for the production of the endocochlear DC potential which is the main driving force for sensory transduction. Imbalance of ion homeostasis in the inner ear is therefore closely-linked to the pathophysiological mechanism of hearing impairment and balance disorder. Moreover, it is very important to study the physiology of ion channels in the inner ear. Ion channel measuring methods have been established electro-physiologically and recently developed using molecular physiology and molecular genetics. The ion channel's function can be measured as the result of `ion flux' by ion selective electrodes, a vibrating probe and the Ussing chamber. In this paper, ion transport models are introduced and useful ion measuring methods are explained.
It is known that oxidative stress plays some role in inner ear diseases, such as sensorineural hearing loss due to aging. Free radicals are produced as a result of oxidative stress, such as reactive oxygen species (ROS) and nitric oxide. Radical scavengers and antioxidants play a role in the protection against oxidative stress. Although some basic data have indicated a relationship between oxidative stress and endolymphatic hydrops, no clinical data have been published from patients. Diacron reactive oxygen metabolites (d-ROM) were measured by the Free Radical Analytical system 4 (FRAS4) from the blood of 39 patients. The subjects consisted of 16 controls, 13 patients with Ménière's disease, and 10 patients with benign paroxysmal positional vertigo. The d-ROM value of the controls was 307.3±42.5U Carr, compared with 350.1±50.5U Carr in BPPV and 352.2±71.5U Carr in Ménière's disease subjects. Although no statistically significant differences were seen among the groups, patients with BPPV and Ménière's disease had slightly higher values than the controls, suggesting that free radicals were being produced in patients with both Ménière's disease and benign paroxysmal positional vertigo. It may be useful to control dizziness or vertigo by reducing free radicals as a product of oxidative stress, and controlling oxidative stress may be a valuable approach in the treatment of patients with dizziness due to Ménière's disease or benign paroxysmal positional vertigo.
Although many patients with both episodic vertigo and migraine have been reported, we have few opportunities to observe pathological nystagmus during an attack in these patients. We report herein on two cases with migraine associated vertigo (MAV) in which neuro-otological findings could be observed at the acute stage of vertigo. The first patient was a 46-year-old woman, with migraine without aura. She visited our clinic complaining of an episodic dizzy feeling with a migrainous headache and phonophobia. On the first examination, she did not show nystagmus or disequilibrium. Four months later, she had further acute vertigo attacks, during which she showed right beating spontaneous nystagmus lasting for 3 hours. Her vertigo attack and headache are currently well-controlled with lomerizine. The second case was a 47-year-old woman who visited our clinic complaining of vertigo accompanied by a migrainous headache and left tinnitus. On the first examination, there were no remarkable findings except for 35% canal paresis of the left ear on caloric testing. Later, she showed direction fixed spontaneous nystagmus during a vertigo attack lasting for a few days. This patient's vertigo attack and headache have also been well-controlled with lomerizine. These cases showed that patients with MAV could have acute asymmetrical disorders of the vestibular system. The lesion site was considered to be in the peripheral vestibular system at least in the second case. However, the actual pathophysiology of MAV remains unclear.
We examined the effects of powerful sound stimuli on postural stability in normal humans. Sound stimuli consisted of pure tone of 500 Hz, 105 dB HL for 5 sec duration, which were applied to the right ear. Each subject was studied under 4 different conditions: eyes open, eyes closed, head rotated 90 degree to the right and head rotated 90 degree to the left. Positive responses were observed in more than 85% of the subjects. Preponderance of response direction was indefinite under most conditions in subjects. Mono-phase postural responses were most elicited, but poly-phase responses were frequently observed in this experiment. In order to prove the vestibular-evoked responses, postural responses of patients with absent vestibular function and deaf patients have to be examined. Reproducibility and habituation of responses also will be examined in a future experiment.
The vestibulo-ocular reflex (VOR) generates smooth eye movements that are compensatory for head movements to ensure gaze stabilization during head rotations. The VOR is under adaptive control that corrects VOR performance when visual-vestibular mismatch arises during head movement. During normal visual-vestibular interaction, cooperation between the VOR and vision results in stabilization of the retinal image. Adaptive VOR recalibration occurs when a visual-vestibular mismatch arises through the manipulation of visual feedback during head movement or by lesion-induced modification of vestibular input. Considering how important VOR is in stabilizing gaze, one could predict that when VOR is lost, patients would be severely disabled by retinal image movement due to head movement. To compensate for vestibular deficits, the vestibular system uses other substitutes such as visual and somatosensory information for the lost vestibular signals. To investigate the contribution of somatosensory signal to the VOR, especially the semicircular-ocular reflex (ScOR), we examined the plasticity of the ScOR using vestibular-somatosensory interaction and the effect of the adaptive plasticity of the ScOR by somatosensory stimulation. We demonstrated a reasonably consistent effect on adaptation of ScOR gain using a somatosensory stimulation paradigm. Our data suggest that the ScOR and somatosensory signals share common neural pathways in such a way that a change in the synaptic efficacy of one pathway is accompanied by a change in the other. The role of a neural storage system that receives input from both the semicircular canals and the somatosensory system to maintain a spatial orientation is discussed.
We compared the influences of auditory and visual targets on the vestibulo-ocular reflex (VOR) in healthy adults, to investigate auditory, visual, and vestibular modality integration in location perception. Under head fixed target conditions, VOR gains with visual target decreased, compared with VOR gain in darkness. VOR gains with auditory target were as big as those in darkness. On the other hand, in earth fixed conditions, VOR gains increased and phase delay decreased with both visual and auditory target. These findings suggest that auditory stimuli with relative motion have an influence on the vestibule-ocular system.
Some patients have different vertiginous symptoms such as faintness, rotatory sensation or swaying sensation when rising to the standing position. These symptoms, hereafter referred to as orthostatic vertigo (OV), are believed to occur due to hypoperfusion of the brain with the orthostatic decrease in blood pressure (BP). However, it is unclear whether the orthostatic decrease in blood pressure is directly involved in the onset of OV. Therefore, we studied the influence of the orthostatic change in BP on OV. All 780 subjects in the present study had orthostatic changes in their BP examined, including 239 cases with OV and 541 cases without OV. Orthostatic hypotension (OH) was defined as a systolic BP decrease of more than 20 mmHg when standing. In subjects with a BP of 140 mmHg and over before standing, the orthostatic decrease in BP was more than 20 mmHg in cases with OV, significantly different from those without OV. In the case of a BP over 160 mmHg, subjects with OV showed a severe OH greater than 30 mmHg. In contrast, when the BP was under 140 mmHg, OH was not detected even in those subjects with OV. Under 110 mmHg BP, there was no difference of orthostatic decrease in blood pressure between in cases with OV and those without OV. These results suggest that it is necessary to consider the BP before standing when assessing the incidence of OV due to OH.
This study aimed to investigate vestibular evoked myogenic potential (VEMP) latencies in patients with acoustic neuromas (ANs), and to clarify the change in the 3 parameters: origin nerve, localization, and tumor size. The VEMPs of 119 patients with ANs confirmed surgically were recorded. We used the peak latencies of the first positive-negative peak of the VEMP, P13-N23, for the evaluation. VEMPs were absent in 49 (41%) of patients with ANs. Both patients with superior and inferior neuromas had a significantly prolonged p13 and n23. Patients with ANs of 11∼20mm in size had a significantly prolonged p13. Patients with ANs present in both the internal auditory meatus and the cerebropontine (CP) angle had a significantly prolonged p13 and n23. These results suggest that it is impossible to predict the origin nerve of a tumor from the results of the VEMP. We hypothesized that the latency prolongation is caused not only by the tumor size but also by the tumor localization.