Practica Oto-Rhino-Laryngologica
Online ISSN : 1884-4545
Print ISSN : 0032-6313
ISSN-L : 0032-6313
Volume 75, Issue 9special
Displaying 1-7 of 7 articles from this issue
  • Toshi Naito
    1982 Volume 75 Issue 9special Pages 1895-1901
    Published: September 15, 1982
    Released on J-STAGE: November 04, 2011
    JOURNAL FREE ACCESS
    In 1861 Prosper Ménière first reported a new and epoch-making theory that human vertigo can be caused by inner ear disturbance.
    The probable factors which might have led him to this excellent theory can be recapitulated as follows. (1) First of all, we must consider him to be a genius endowed with excellent power of inspiration and insight. (2) Because he was a doctor in the Institute for Deafness for a long time, he saw many patients suffering from deafness and tinnitus combined with vertigo. (3) His senior doctor in the institute, J. M. Itard, had also been interested in this disease and had often told him about it, which aroused and fortified his interest in it. Itard, however, had no idea that the cause of vertigo lay in the inner ear. (4) Ménière's was an excellent, particularly attentive and thoughtful observer of patients. (5) He knew well and was extremely interested in Prof. Flourens's experiment on pigeons showing ataxia from inner ear destruction. (6) His excellent power of speculation could connect human vertigo with this pigeon ataxia. (7) Through the kindness of a doctor friend, he fortunately encountered an autopsy case of a patient suffering from vertigo and could discover the pathological change—bleeding—in the inner ear, which was unaccompanied by any changes in the brain.
    One of the most remarkable topics in Menièrology is that his apparently lost tomb and descendants have recently been discovered in Paris. Mme. Baroness Menière is the 5th generation of the Ménière's family. It is admirable that 5 members of the Ménière's family including him received the medal of “la légion d'honneur”.
    Although the existence of endolymphatic hydrops in the inner ear has been confirmed since the first reports of Yamakawa and Hallpike in 1938, the real cause of this disease still remains obscure.
    We speculate that its real cause is not a simple one, but a compound of several factors which form a serial or/and parallel pattern.
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  • Takashi Tokita
    1982 Volume 75 Issue 9special Pages 1902-1913
    Published: September 15, 1982
    Released on J-STAGE: November 04, 2011
    JOURNAL FREE ACCESS
    Peculiarities of labyrinthine equilibrium disturbance were studied.
    1) Long-term observation of equilibrium disturbance in patients with bilateral loss of labyrinthine excitability indicated that equilibrium disturbances continuing more than 5 years after the incidence of the loss of labyrinthine excitability were disturbances of body balance in standing and walking in the dark and disturbances in visual fixation during walking and running (jumbling phenomenon). The results indicated that the most important role of the vestibulo-spinal reflexes is the righting reflexes which aid in maintaining standing posture and that the vestibulo-ocular reflexes in humans play an active part in visual fixation during movements with periodic head motion. From this point of view, we attempted to analyse the body sway appearing in the upright standing posture of these patients and to study the transfer function of the vestibulo-ocular system in humans.
    2) The feature of the standing sway in these patients was forward and backward sway consisting of about 0.4Hz and a component faster than 0.4Hz. We considered that the sway was induced because of the increase in the spinal reflexes caused by the loss of labyrinthine control of the antigravity muscular tonus and due to loss of labyrinthine head-righting movement which indicates a frequency-dependent gain enhancement.
    3) The Bode plots of the transfer function of the vestibulo-ocular system obtained from a pendular rotation test in the dark showed frequency-dependent gain enhancement at the rate of 5dB/decade in a frequency range of 0.3 to 5Hz. This indicates that the vestibulo-ocular system plays an important role in visual fixation during rapid head movement. We considered that the deficit of this vestibulo-ocular function causes the jumbling phenomenon.
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  • Jun-Ichi Suzuki
    1982 Volume 75 Issue 9special Pages 1914-1921
    Published: September 15, 1982
    Released on J-STAGE: November 04, 2011
    JOURNAL FREE ACCESS
    Vertigo and loss of balance are frequently encountered in primary care. Neurotology can contribute to the primary care of vertigo and loss of balance by organizing a battery of tests to establish diagnosis. The tests are classified into the following five: 1) neurotological tests, mostly for brainstem functions, 2) tests for visual fixation on a target, stationary or tracking; 3) examinations of nystagmus without visual fixation but with postitional and positioning procedures; 4) auditory examinations; and 5) caloric tests. The diagnostic significance and clinical evaluation of these tests are presented with comments. These tests and other clinical examinations should give conclusions in diagnosing vertigo and/or loss-of-balance in the following categories: 1) the existence, degree and nature, 2) the location, and 3) the cause of the lesion.
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  • Tadashi Fukuda
    1982 Volume 75 Issue 9special Pages 1923-1924
    Published: September 15, 1982
    Released on J-STAGE: November 04, 2011
    JOURNAL FREE ACCESS
    Postures, which appear in a momentary and well-balanced state between gravity and anti-gravity forces while in motion, were discussed, using as examples various styles in the performance of Kabuki and postures in sports. The author emphasized that the investigation of these styles and postures are helpful in understanding the physiological meaning of a momentary standstill while in motion, i. e., Ma which composes the beauty of Japanese arts.
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  • Manabi Hinoki
    1982 Volume 75 Issue 9special Pages 1925-1942
    Published: September 15, 1982
    Released on J-STAGE: November 04, 2011
    JOURNAL FREE ACCESS
    The author devised a new type of examination for the detection of olfactory vertigo. A subject is required to inhale the vapor of a liquid-form of garlic. The resulting changes in the eye and body equilibrium functions are then examined using various equilibrium tests. This examination was termed “Equilibrium test for olfactory vertigo’. Ten normal subjects and 35 with cranio-cervical injury were the subjects examined herein.
    The results obtained were as follows:
    1) In normal subjects, neither vertigo nor ataxia was induced when the above equilibrium test was carried out.
    2) In traumatized patients, an increase in the degrees of vertigo and ataxia was observed when the same equilibrium test was carried out.
    The following results were noted:
    1) The equilibrium test was positive in patients who complained of hyperosmia.
    2) Patients giving a positive sign in the equilibrium test had hypersensitivity to adrenaline and an increase in ataxia when this drug was administered. Furthermore, the ataxia induced by garlic tended to be similar to that induced by adrenaline.
    3) A positive sign of the equilibrium test was more marked in patients with cerebellar ataxia than in those without this ataxia. Among the former patients, the development of olfaction-related ataxia became increasingly evident when the cerebellar dysfunction advanced.
    4) Cloxazolam, a minor tranquilizer of the Benzodiazepine group, produced beneficial effects on the vertigo due to olfaction, except in patients with both olfactory vertigo and cerebellar ataxia.
    5) Similarity was found between the neural elements related to the development of both types of vertigo, i. e. olfactory and psychosomatic, although the former type of vertigo was not always accompanied by the latter.
    6) Patients who showed increased disequilibrium in the equilibrium test for olfactory vertigo using Alinamin (liquid-form of garlic) tended to develop reduced disequilibrium when examined by the same test using a musk-like substance.
    This tendency was significantly evident in patients giving a positive result in the adrenaline test (Hinoki 1971).
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  • Eiji Sakata
    1982 Volume 75 Issue 9special Pages 1943-1972
    Published: September 15, 1982
    Released on J-STAGE: November 04, 2011
    JOURNAL FREE ACCESS
    Over the years, a number of eminent researchers have indicated that once we begin a study of nystagmus we literally fall into a labyrinth and eventually we reach a point wherein we are at a loss as to what to do. This statement is obviously a negative approach, but it cannot be denied that such a view has created obstacles in the development of current neurotology. There are various reasons underlying this viewpoint, and one may be that previously, researchers approached the study of nystagmus by observing patients with multiple sclerosis.
    Confusion generally results from the fact that multiple sclerosis lesions appear randomly and are distributed throughout most of the nervous system. Current otological research approaches the study of nystagmus from the basis of the peripheral labyrinth which, in turn, exerts a definite influence on ocular movements. Research on nystagmus has steadily advanced from the labyrinth to retro-labyrinthine structures and currently includes the central nervous system. This report is accompanied by a discussion of the relationships between eye movements and lesions located in the mesencephalon, pons, medulla, dorsal portion of the brain stem, the brain stem in general, the hemispheric portion of the cerebellum, cerebellar vermis and cerebral hemispheres. General disorders of the CNS and the labyrinth are also considered.
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  • Setsuko Takemori
    1982 Volume 75 Issue 9special Pages 1973-1978
    Published: September 15, 1982
    Released on J-STAGE: November 04, 2011
    JOURNAL FREE ACCESS
    The visual suppression test is one of the visual fixation tests. It is carried out by recording caloric nystagmus by electro-oculography (EOG), and the maximum slow phase velocity of caloric nystagmus in darkness is compared with the slow phase velocity in the light with the eyes open. Visual suppression of the slow phase velocity of caloric nystagmus is 66±11% in normal subjects. Visual suppression in normal subjects is not influenced by the temperature of the water used for the caloric test and not changed by the background illumination in the light. Visual suppression is stronger when the target is closer to the eyes of the subjects. Visual suppression increased when the subjects have been examined repeatedly. The following abnormalities have been diagnosed by this test.
    1. Reduced visual suppression (visual suppression, 40%-10%): flocculus and nodulus lesions on the side of the lesion.
    2. Abolished visual suppression with the augmentation of caloric nystagmus in light (visual suppression, under 10%): pontine lesions.
    3. Reduced or abolished visual suppression with the augmentation of caloric nystagmus in light (visual suppression, under 40%): lower parietal lobe lesions.
    4. Increased visual suppression (visual suppression, over 75%): compensation after unilateral sudden loss of inner ear function.
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