It has been shown that the superior division of the vestibular nerve is preferentially affected while the inferior division is spared in many cases of vestibular neuritis. Long-lasting horizontal rotational nystagmus, a positive result in the horizontal head impulse test (HIT), and a positive result of the caloric test are characteristics of vestibular neuritis. However, some other cases have been reported in which only the inferior vestibular nerve region is affected while the superior vestibular nerve region is spared. It should be noted that the examination findings may vary depending on the site of the lesion. The In regard to the?? clinical course of vestibular neuritis, abnormality in the HIT and subjective visual vertical (SVV) are often predictors of? early recovery. However, recovery of canal paresis in the caloric test is slower and the recovery rate in the caloric test is lower than that in the HIT and the SVV. Although some studies have indicated statistically significant beneficial effects of corticosteroid therapy on the outcomes of vestibular neuritis, it must be recognized that there is currently insufficient evidence to support the administration of corticosteroids to patients with vestibular neuritis. Taking into consideration the risk of adverse effects of steroid use, recommendations or decisions to treat patients with vestibular neuritis with corticosteroids should be discussed with each patient. To control the severe vertigo, nausea and vomiting in patients with vestibular neuritis in the acute stage, administration of vestibular suppressants and anti-emetics may be effective. These medications should be withdrawn as soon as possible because vestibular suppression may inhibit the process by which the brain compensates for vestibular imbalance. We consider that vestibular rehabilitation is effective for patients with vestibular neuritis who show persistent chronic disability for more than several weeks after the onset.
There have been several reports about the relation between acid-base imbalance or arterial blood gas abnormalities and the occurrence of vertigo, including Meniere' disease. In animal experiments, respiratory acidosis induced by CO2 inhalation or metabolic acidosis induced by injection of NH4Cl has been shown to cause attacks of vertigo in rabbits with hemilabyrinthectomy. In clinical studies, approximately half of the patients with dizziness have arterial blood gas abnormalities when their dizziness occurs. An increase of HCO3- is found in many patients with dizziness, and the frequency of attacks is higher in patients who have arterial blood gas abnormalities during the remission period. These patients are thought to have unilateral vestibular dysfunction, and it is suggested that arterial blood gas abnormalities cause temporary vestibular dehabituation that increases the frequency of dizziness. It has also been reported from a study that the middle ear pressure difference between both ears, which is larger during periods of dizziness or recurrent dizziness than at the time of remission, might be related to blood gas abnormalities in Meniere's disease. In the same study, a difference of more than 50 decapascals was significantly more common in the patient group with blood gas abnormalities. In addition, metabolic acidosis has been reported in patients with Meniere's disease, and the base excess and bicarbonate levels were also found to be beyond the normal range in Meniere's disease. Arterial blood gas abnormalities might develop for various reasons, including underlying diseases and middle ear pressure differences. The endolymph in the endolymphatic sac is acidic (pH6.6-7). It has been reported that carbonic anhydrase, vacuolar H+-ATPase, pendrin and aquaporin may participate in the acidification process or homeostasis. The role of acid-base disturbance or arterial blood gas abnormalities in dizziness, and the relation in acid-base balance between inner ear and arterial blood gas need to be investigated further.
The vestibulo-ocular reflex (VOR) is adaptable to adjustment of its performance in the event of visual-vestibular mismatch arising during head movements. In previous reports, an earth-fixed auditory target led to a VOR gain increase. On the other hand, there was no change in the VOR gain for a head-fixed auditory target. In the present report, we examined the changes of the VOR caused by adaptation to a rotating virtual sound source. The gain reduced in the post-adaptation phase when the sound rotated in the opposite direction to head rotation at the same velocity. There was no significant change in the VOR gain associated with adaptation to a sound source rotating the same direction as the head, but at twice the velocity. Adaptation of the VOR to auditory stimuli differed from that to visual stimuli. Our findings suggest that perception of the auditory location does not have any direct effect on the eye movements. Perception of auditory location, while it may influence eye movements through the visual motion perception system.
We designed a new dynamic equilibrium examination on a stabilometer, involving lifting up of only the heels alternately, two steps per second, over a total of 120 steps, guided by an electric metronome operating at 120 BPM (beats per minute), with the eyes open and closed. The total locus length (L) and the environed area (A) were measured. This unique stepping test was named the “Foulage test” and we suggested demonstrated in two previous studies that FT (=120 A/L) is useful for quantitative measurement of the body sway. To ascertain the usefulness of FT as a useful dynamic equilibrium parameter, we examined 20 patients of Meniere's disease and one with delayed hydrops, and compared the FT at the first examination carried out at the onset of a severe vertigo attack with that at the last examination, improved to normal condition. The FT decreased significantly in the ‘eyes closed’ condition (p<0.01 Wilcoxon's test). With the eyes open, it did not improve entirely, but in 11 patients with nystagmus, it decreased significantly (p<0.05). The dynamic Romberg rate (closed-eye FT/ open-eye FT) also decreased (p<0.01). After a severe vertigo attack, three conceptual periods are suggested based on a combination of the FT values obtained with the eyes open or closed. During the first period, the open-eye FT is abnormally high, therefore, the dynamic Romberg rate is not unexpectedly high even if the closed-eye FT is higher. It seemed to be paradoxical as a severe labyrinthine disorder. During the subsequent 2nd period, the open-eye FT improves to normal, while the closed-eye FT still remains high, so that the dynamic Romberg rate is high. The closed-eye-FT decreases progressively each day and this period is maintained for about one month. During the final 3rd period, both the FT values are normal and the dynamic Romberg rate is low. This study suggested that the Foulage test can be useful for quantitative determination of the body sway in patients of Ménière's disease and delayed hydrops quantitatively and is also useful to follow up the course after a vertigo attack.
Many researchers have reported the effects of paroxetine chloride on vertigo patients, but most of the analyses have been based on subjective evaluations. In this study, we attempted to determine whether paroxetine chloride might decrease the frequency of vertigo attacks and resolve the hearing impairment in patients with Meniere's disease. The subjects were 7 females with Meniere's disease treated with paroxetine chloride, seen from January 2006 to September 2009. The patients ranged in age from 25 to 58 years. The mean duration of treatment was 22.4 (±27.6) months. The patients' psychiatric diagnoses were as follows: depression (1 case), panic disorder (3 cases), adjustment disorder (1 case), and insomnia (1 case was unspecified). The course of the vertigo attack and hearing impairment could be tracked in 7 cases and 9 ears (5 cases), respectively. The mean frequency of the vertigo attacks decreased significantly from 1.5 (±1.4) prior to treatment to 0.71 (±1.1) by 3 months of treatment and 0.14 (±0.41) by 6 months of treatment. The mean hearing level was 19.2 (±3.6) dB before the treatment and 20.6 (±8.6) dB after the treatment. These results suggest that paroxetine chloride can improve the frequency of vertigo attacks, but not the hearing impairment, in patients with Meniere's disease.
Downbeat nystagmus (DBN) is commonly caused by central lesions, e.g., vestibulo-cerebellar and brainstem lesions, and there are few reports on DBN caused by peripheral lesions. We report two cases of Meniere's disease who presented with DBN and fluctuating low-tone sensorineural hearing loss. Case 1: a 55-year-old female. The patient was admitted to our hospital in September 20XX because of a vertigo attack. She exhibited rightward horizontal nystagmus in the supine position, however, the positioning test triggered DBN, which changed later to rightward horizontal nystagmus. There were no apparent neurological or neuro-otological abnormalities. Two days later, pure-tone audiometry showed low-tone sensorinueral hearing loss in the left ear. Magnetic resonance imaging (MRI) revealed no abnormal findings. Although steroid and isosorbide administrations were not effective, the symptoms resolved completely with the administration of diazepam. Case 2: A 26-year-old female. In August 20XX, the patient consulted a neighborhood clinic for hearing loss and tinnitus in the left ear. She presented with a history of repeated hearing loss and positional DBN and was referred to our hospital for further examination. Pure-tone audiometry showed low-tone hearing loss. The positional and positioning tests triggered DBN. There were no abnormal findings on neuro-otological and MRI examinations. Isosorbide administration improved the hearing loss and nystagmus. Thus, we encountered two cases of Meniere's disease presenting with DBN. The positional DBN in both cases was suspected to be caused by endolymphatic hydrops in the saccule and anterior semicircular canal.
This study included 209 patients with vertigo of various causes who underwent both manually rotated vestibulo-ocular reflex (VOR) testing and bithermal air caloric testing at our hospital from January 2009 to July 2012. The VOR directional predominance (VOR-DP%) values in the 79 patients with greater than 30% caloric canal paresis (CP) were significantly higher than those in the 43 normal subjects. On the other hand, the VOR-DP% values in 81% of patients with CP were within normal limits, as those in the 43 normal subjects varied widely (the normal range is considered to be wide). In all of the vertiginous cases, the VOR-DP% values showed only a slight correlation with the CP% values. However, the VOR-DP% was well-correlated with the CP% in patients with vestibular neuritis, Hunt syndrome and sudden deafness with vertigo, especially in the acute stage within 2 weeks of the onset. The VOR-DP% values in these latter patients with vestibular neuritis, Hunt syndrome and sudden deafness with vertigo decreased with time, regardless of the presence or absence of recovery from CP. Manually rotated VOR testing is thought to be one of the useful tools in daily clinical practice, that allows estimation of both peripheral vestibular function and the degree of recovery from imbalance in patients with acute unilateral peripheral vestibular deficit.
Vestibular evoked myogenic potentials (VEMPs) recorded by surface electrodes have been used clinically to assess vestibular function. Cervical vestibular evoked myogenic potentials (cVEMPs), which are recorded from the sternocleidomastoid muscles (SCMs) in response to air-conducted sound (ACS) and bone-conducted vibrations (BCV) have been used to evaluate the functions of the saccule and the inferior vestibular nerve, since physiological and clinical studies have shown that cVEMPs recorded in response to air-conducted sound reflect the functions of the saccular afferents. Ocular vestibular evoked myogenic potentials (oVEMPs), which are recorded from beneath the eyes in response to ACS and BCV, have been considered to represent the vestibular functions mediated by the crossed-otolith ocular pathway. Recent clinical studies have suggested that both oVEMPs in response to ACS, and oVEMPs in response to BCV reflect the functions of the utricle and the superior vestibular nerve. In this paper, I shall explain how cVEMPs to ACS and BCV and oVEMPs to ACS and BCV should be recorded, and how to use these vestibular tests in clinical practice.
In humans, intense air- and bone-conducted sound has been reported to evoke cervical vestibular evoked myogenic potentials (cVEMP) on the sternocleidomastoid muscle. In addition, these stimuli can evoke ocular vestibular evoked myogenic potentials (oVEMP) on the extraocular muscles. In this study, basic studies into the cVEMP and oVEMP were reviewed. First, the sensitivity of primary vestibular afferents in the internal auditory meatus was investigated. These studies suggested that irregular primary otoliths afferent from both utricular and saccular maculae might respond to both air- and bone-conducted sound. Second, the differences between utricle and saccule-activated neural circuitry in both vestibulo-ocular reflex (VOR) and vestibulocollic reflex (VCR) systems were evaluated. These studies described that utricular afferents have a strong projection to the VOR system, whereas the saccular afferents have a strong projection to the VCR system. Third, identifying the appropriate animal models for both cVEMP and oVEMP was also important to resolve the questions about the neural pathways underlying these responses.
Two decades have passed since the first publication of vestibular evoked myogenic potentials (VEMP). Now, cervical VEMP and ocular VEMP are accepted widely for the examination of the saccular organs and utricular organs, respectively. Can a new disease concept be developed using VEMP testing? In a previous study, it was reported that 6 out of 18 patients with undiagnosed dizziness showed abnormal cVEMP. Dizziness with a sensation of falling was related to the abnormal results. Another author study reported that 9 out of 10 subjects with lateral tilt sensation showed abnormal oVEMP. Thus, disequilibrium in the sagittal plane and horizontal plane is probably caused by otolith disorders and can be diagnosed only by VEMP testing. The lesion site of vestibular neuritis had been believed to be in the superior vestibular nerve. However, there are some reports about cases of acute-onset disequlibrium who showed inferior vestibular verve lesions. They showed abnormal cVEMP and normal results on caloric testing, thus the etiology was suggested to be inferior vestibular neuritis. The disease could be diagnosed only by VEMP testing. A positive result of diuretic-loading VEMP testing was observed in patients with Meniere's disease; a positive result was also obtained in some cases without the typical symptoms of Meniere's disease. They complained of recurrent tinnitus, aural fullness and severe disequilibrium or the sensation of falling downward or backward. The etiology was suggested to be saccular endolymphatic hydrops that could only be diagnosed by VEMP testing. As mentioned above, VEMP testing was useful to diagnose the etiology of disequilibrium caused by otolith dysfunction or superior vestibular nerve disorders. Therefore, the answer to the question, “Can new disease concept be developed using VEMP testing?” is “yes”.