Various factors are involved in the onset of motion sickness. As an investigation of one of those factors, the spatial orientation of experimental subjects was changed, and the relationship to the development of motion sickness was examined. For an objective study, it is necessary to establish an experimental model of motion sickness. Accordingly, artificial visual field information was created, and a computer capable of highspeed calculation was used to stimulate the experimental subjects with images undergoing temporal or spatial changes. Individual experimental subjects showed considerable variation in the development of motion sickness. Thus, it was important to perform the experiments on highly susceptible subjects. The results showed that, when for both time and space, the phase was asynchronized, motion sickness manifested at a high incidence. At the time motion sickness is manifested, there is always abnormal secretion of hypothalamus-pituitary-adrenal axis hormones and the development of symptoms of autonomic nervous system instability. For this reason, it can be surmised that there is involvement of emotions and the autonomic nervous system as a result of changes in spatial orientation. It can be thought that this is due to a state of asynchronization of the intrinsic information that leads to motor commands. In particular, information from an intrinsic model with unanticipated asynchronization of eye movement and head movement is important. The relationships among spatial orientation, head-eye movement, the memory process and emotion in the manifestation of motion sickness is discussed.

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We reviewed the hair cell pathology of genetic hearing loss and circling behavior and discussed possibility of gene therapy in human genetic inner ear disease through genetic inner ear disease animal models. First, we focused on the cytocauds containing pathological actin filaments in the vestibular type 1 hair cell of waltzing guinea pigs (WGP) and in auditory and vestibular hair cells of shaker-2 mice. The cytocaud, which seems like to be an actin filaments ladder, penetrates the basement membrane and runs along nerve fiber. One possible explanation is that hair cells detach from the basement membrane during development but do not in WGP and shaker-2 mice. However, the molecular signals that are required for detachment are unknown.
Furthermore, we tested the possibility of gene transudation in shaker-2 mice, the model of DFNB3, i.e. human deafness, in order to treat the hair cell pathology including cytocaud. Vestibular sensory epithelia of explant organ culture obtained from mouse pups at P1, P3, and P5 were transfected by adenovirus vector containing the bacterial lacZ in vitro and processed to detect the reporter gene expression. Vestibular hair cells can be transduced at all stages in shaker-2 mice. Our data demonstrate that differentiating hair cells in mouse explants can be virally transduced, suggesting that wild-type genes can be inserted into these cells to correct the phenotype. We need further investigations of gene therapy using animal in vivo data to discuss the possibility of clinical application for the genetic inner ear diseases.

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There is no report to our knowledge describing stabilographic investigation of idiopathic vertigo. We investigated each parameter of stabilography in 112 patients with idiopathic vertigo.
Stabilography was performed with eyes open and closed while standing with both feet together for 60 seconds using a stabilometer. The enveloped area, length/time, length/area, displacements in X- and Y- axes, Romberg ratio, power spectrum, velocity vectors, and standard deviation, kurtosis and skewness of amplitude histogram were measured. The velocity vectors, ranging 360 degrees, were divided into eight directions. Each was designated A-H from the anterior direction clockwise. We used age and gender matched data from 112 healthy subjects as a control group. Chi-square test was used for statistical analysis and p<0.01 was considered significant.
The positivity rate in the patients was significantly higher than that in the controls for length/time (p=0.0062), velocity vectors A (p<0.0001), B (p=0.0005), E (p<0.0001), and F (p=0.0067).
We found that the stabilogram in idiopathic vertigo patients tended to show anterior-posterior sway in good order. Our findings suggested that idiopathic vertigo is in part a functional and sensory abnormality without organic disease and has the potential to proceed to peripheral or central disease.

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Vertigo is thought to be a symptom which generally is hard to understand. There is no problem when there are some abnormal findings in equilibrium function tests, represented by characteristic nystagmus and CP. When encountering vertigo cases with rare abnormal findings, a short-term attack of vertigo and few objective findings, there are many patients for whom considerable effort is made on diagnosis and explanation. We investigated clinically the treatment of vertigo cases which showed no abnormal findings.
The subjects were 21 patients who were treated in former ENT clinic as unknown vertigo or vestibular disorder. Vertigo cases are classified into peripheral vertigo, central vertigo, functional vertigo and other vertigo. Vertigo can be classified into those types of vertigo based on the pattern of vertigo attack. It is indispensable in the treatment of vertigo to confirm the existence of nystagmus with the positional and positioning nystagmus test by Frenzel glasses and infrared CCD camera. Though a flow chart type diagnosis index is useful for vertigo, we must recognize the existence of serious pitfalls in it. The precise diagnosis of vertigo is essential for effective treatment of vertigo. The "diagnosis study" for vertigo contributes to further development and establishment for patients who suffer from intense vertigo.

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We have been using the head up tilt test (hereafter referred to as HUT) to examine vasovagal reflex (VVR). However, some questions remain as to "What is the difference between the Schellong test (ST) and HUT?" and "Why is VVR not induced in ST?" Our previous investigation suggested that VVR is readily induced in HUT because the heart rate increases sharply immediately after sitting up (or rising) in HUT. However, this reason remains uncertain. We suspected that the tension of the muscles of the lower limbs and peripheral blood retention might have some effects on the occurrence of VVR. We therefore performed the following three orthostatic tests.
The study subjects were seven normal volunteers who had neither vertigo nor heart disease, with a mean age of 41 years.
We performed the following three orthostatic tests for the 7 volunteers, and measured the heart rate and blood pressure while the volunteers were being kept at rest in a supine position, immediately after they sat up (or rose), and while they were being kept in a sitting (or standing) position.
1. ST
2. HUT
3. HUT with volunteers with elastic bandage applied th the lower limbs
There was no significant difference in blood pressure and heart rate at rest among the above three tests. In HUT, heart rates immediately after sitting up (or rising) were significantly higher than heart rates measured at rest (P<0.01). However, there was no singificant difference between heart rate measured at rest and that measured immediately after sitting up (or rising) in either HUT or ST, if HUT was performed with volunteers with elastic bandage applied to their lower limbs. Among the above three tests, increase in heart rate was the largest with HUT.
The tension of the muscle in the lower limbs reduced peripheral blood retention and maintained adequate circulatory blood in a sitting-up (or rising) position. We consider that peripheral blood retention occurs in HUT because of low muscle tension and is associated with a sharp increase in heart rate, readily resulting in VVR.

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We reported a 15-years old male with vertigo, left tinnitus and left hearing loss due to a cyst of the left cerebellopontine angle. Chief complaint of the patient was recurrent attacks of vertigo, fluctuated left tinnitus and left hearing loss. A cystic lesion 5.0×5.0 mm in size was found in the left cerebellopontine angle by head MR images (MRI). The results of physiological tests, auditory evoked brainstem response (ABR), short increment sensitivity index test (SISI test) and stapedial reflex (SR) reviewed labyrinthine deafness. Smooth pursuit eye movement test (ETT) and opto kinetic nystagmus test (OKN) did not show any central abnormal findings.
The cyst of the cerebellopontine angle was assumed to compress the vestibulocochlear nerve or labyrinthine artery in this case.

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Nineteen patients (12 males and 7 females, average age 61 years) of acute vertigo with cerebrovascular lesion were investigated retrospectively. All patients were finally diagnosed as vascular lesions in the posterior fossa, cerebellum or brainstem, 17 patients with infarction and 2 with hemorrhage. Of 19 patients, 11 were initially suspected of peripheral lesions and other 8 of central lesions.
Twelve of 19 patients initially visited emergency unit of our institute and 12 patients visited Neuro-otology clinic initially or from the emergency unit, and 15 patients were admitted to Neuro-otology ward. Most patients who were initially suspected of peripherallesions visited emergency unit and were admitted to Neuro-otology ward directly.
Neurological and neuro-otological symptoms and signs were slight at initial visit or on admission among patients initially suspected of peripheral lesions, though all patients were diagnosed as central lesion within a few days (mode 2 days).
Diagnosis of central lesion were made mainly based on neurological, neurootological and MRI findings, and CT scans were not so useful except in patients with hemorrhage. Of neuro-otological examinations, the nystagmus test, eye movement tests and qualitative tests for pursuit and optokinetic nystagmus were most effective in the diagnosis of central lesion.

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This is a review of the various surgical approaches to Meniere's disease to date. At present, endolymphatic sac surgery is used to improve labyrinthine function, and intratympanic gentamicin (GM) therapy to reduce this function. Also used are intracranial division of the vestibular portion of the auditory nerve, and labyrinthine destruction (i.e., labyrinthectomy).
In 1996, the Karolinska Hospital in Stockholm, based on its results, reported its policy the use of the following three surgical treatments for vertigo: (1) endolymphatic sac surgery; (2) intratympanic gentamicin (GM) therapy; and (3) intracranial division of the vestibular portion of the auditory nerve.
However, there has been no uniformity to date among the various ways to perform the surgery.

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This study was designed to investigate retrospectively the long-term prognosis of vertigo and hearing impairment in Meniere's disease. The results of mostly conservative treatments against vertigo and hearing impairment were evaluated in 39 patients with typical Meniere's disease on the basis of AAO-HNS's 1995 Guideline.
The total number of vertigo attacks and the worst mean value of 4 frequency hearing levels were examined for 6 months after four periods, which were the first visit to our hospital, and 2 yrs, 10 yrs and 20 yrs later.
The mean values from the worst mean of 4 frequency hearing levels for 6 months since the first visit day, and 2 yrs, 10 yrs and 20 yrs later, were 43 dB, 46 dB, 55 dB and 76 dB, respectively. Stage classification for 6 months since the first visit showed that stage 1 (less than 25 dB), stage 2 (26-40 dB), stage 3 (41-70 dB) and stage 4 (more than 71 dB) were 24%, 16%, 50% and 10%, respectively. In the time course of 2 yrs the rate of stage 1 decreased to 16%. The rate of the stage 4 increased from 10% to 27% 10 yrs later and to 67% 20 yrs later.
The mean worst hearing levels showed 14% improved (improved more than 10 dB) and 35% worsened (worsened more than 10 dB) hearing at 2 yrs later. The rate of improved hearing decreased to 9% and that of worsened hearing increased to 50% 10 yrs later. Comparison of the rate of vertigo attacks for 6 months between the first visit and 2 yrs later revealed 63% at class A (completely controlled) and 83% at class A plus B (improved). At 10 yrs later, 60% was class A and 80% class A plus B. Vertigo attack completely disappeared in all four stages 20 yrs later It was considered important for the prevention of progressive non-recovery hearing loss to provide adequate therapy for Meniere's disease within 2 yrs after the patient's first visit.

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Endolymphatic sac surgery for Meniere's disease was criticized by Thomsen et al. in 1981 using a double-blind, placebo-controlled study. They concluded that the effect of endolymphatic sac surgery was placebo. However, Welling et al. pointed out recently that Thomsen et al. used an inappropriate statistical analysis in that paper, and reevaluated the effect of endolymphatic sac surgery in 2000. In order to reevaluate endolymphatic sac surgery, we studied the long-term results of vertigo and hearing after endolymphatic sac surgery. Endolymphatic sac surgery controlled vertigo in 70-80% of patients. Concerning hearing endolymphatic sac surgery maintained the preoperative hearing level to at least 6 years after surgery; however, the hearing level deteriorated gradually after 7 years, likely to return to the "natural history" of Meniere's disease. It was concluded that endolymphatic sac surgery was effective in controlling vertigo and maintaining the hearing level, and that it did not have a placebo effect.

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In our regular otolaryngology practice, we encounter patients with Meniere's disease exacerbated by stress. We counsel such patients on the behavioral and lifestyle changes they can make to improve their disease condition. We conducted a study investigating the effect of our counseling program on the hearing level of patients with Meniere's disease. The subjects were 37 Meniere's disease patients who underwent counseling and drug treatment and 29 Meniere's disease patients who underwent only drug treatment. The counseling focused on helping patients recognize their own behaviors that produce stress, helping patients learn to relax, helping patients incorporate sweat-producting exercise into their routines, and helping them remove sources of stress if possible. The content of the counseling differed slightly on a case-by-case basis. After 1 year, audiograms were obtained from all patients in each group, and these audiograms were compared with those obtained before the study began. The change after 1 year was then compared between groups. In the group that underwent counseling, audiograms improved in 29 patients (78.4%), did not change in 5 (13.5%), and worsened in 3 (8.1%). In the drug treatment group, audiograms improved in 16 patients (52.2%), did not change in 11 (37.9%), and worsened in 2 (6.9%). Thus, the counseling was shown to be effective in improving the hearing level of patients with Meniere's disease influenced by stress. Counseling has not been established as a treatment strategy for Meniere's disease, but at present, drug regimens and surgery are the only other options. According to our findings, we recommend counseling along with drug therapy in keeping with the patient's lifestyle to improve the hearing ability of those with Meniere's disease.

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It is well known that Ménière's disease is related to stress and mental illness. However, the details of this fact are not well documented. By conducting clinical analysis and basic experiments, we intend to clarify this fact.
It is important to differentiate physical and mental disorders when evaluating patients. We divided the patients into three groups, a physical disorder group, a mental disorder group, and a physical and mental disorders group. In the last group, both disorders influence each other. The three groups are being managed with different treatment strategies.
Most otorhinolaryngologists are not familiar with mental management. Under the supervision of psychologists and psychiatrists, we have managed the patients with medications and group psychotherapies. Although our experiences are still limited, we believe psychological analysis and management of Ménière's disease are important.

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The aim of this survey was to determine some of the factors connected to the disturbance of social activity of patients suffering from Meniere's disease. The clinical course of 43 cases with classical Meniere's disease were analyzed for a period of twenty to fifty years. According to the grade of bilateral hearing impairment or damaged social activity, these cases were classified into three groups:
A: 15 cases with persistent bilateral profound hearing loss
B: 11 cases with difficulty of social activity due to repeated attacks of vertigo for a long time
C: 17 cases without severe loss of hearing or damaged social activity despite longstanding symptoms
These clinical records were carefully analyzed and compared between Groups A and C or Groups B and C. As a result, the author found several points suggesting methods of prevention of severe damage of social activities, as follows:
1. Continuous, careful observation, even during the stable periods, to find small, unrecognized fluctuation of hearing in the low-tone range, followed by medical checks and continuous treatment.
2. During the acive stage, the application of "time series analysis" of the daily recording of the aural, general and environmental conditions to find the precipitating factor.
3. To accomplish these activities, a well organized medical care system, including the patient's self-monitoring and tele-medical communication between patients and doctors.

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