It is very difficult to know exact caloric responses when spontaneous nystagmus is very strong. A method of determining caloric response was tested in 42 cases of acute vestibular dysfunction with strong spontaneous nystagmus. Caloric nystagmus was evoked by 20 ml of water at 5°C and recorded by electronystagmography. Spontaneous nystagmus was also recorded with eye open in darkness. The slow phase velocities of spontaneous nystagmus and caloric nystagmus were calculated. When the spontaneous nystagmus was in the same direction as the caloric nystagmus, the caloric response of this ear was expressed by subtracting the slow phase velocity of spontaneous nystagmus from the slow phase velocity of caloric nystagmus. When the spontaneous nystagmus was evoked in the other direction, the caloric response of this ear was expressed by adding the slow phase velocities of caloric nystagmus and spontaneous nystagmus.
Caloric tests should be performed frequently to determine the exact responses because of quick changes of spontaneous nystagmus and lesions.

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Twelve cases of benign paroxysmal positional vertigo after head injury were investigated clinically.
The age of the patients ranged from 7 to 71 years. In eight cases, vertigo occured in the critical position and in seven of these the position was on the side of the injury. Five patients had nystagmus in the critical position toward the side of injury.
Seven patients had positioning nystagmus when they moved from a sitting to a hanging position. Four of them had a critical position, and in three of these, the positioning nystagmus was toward the side of injury.
A close relationship was found among the side of injury, the critical position and the direction of nystagmus.

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The effect of methylcobalamin on vestibular compensation was investigated in 14 Hartley strain albino healthy male guinea pigs, weighing 600-850g. Four animals were controls, five were given intramuscular injections of methylcobalamin at a dose of 1000 μg/kg, and five at a dose of 2000 μg/kg.
Labyrinthectomy was performed by the injection of chloroform into the middle ear.
Changes of head deviation about the animal's longitudinal axis toward the eliminated labyrinth and ocular nystagmic beats were used to assess the compensation process.
Until 13 hours after labyrinthectomy the treated animals compensated significantly faster than the controls ; the effect was dose dependent.
It is concluded that methylcobalamin injection aids the recovery process after destruction of the peripheral labyrinth (vestibular compensation).
The possible mechanisms responsible for these results are discussed.

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A patient with superior oblique myokymia, a term introduced by Hoyt and Keane in 1970, is described. The lesion responsible for superior oblique myokymia is discussed on the basis of the results of Neurootological examinations and Magnetic Resonance Imaging (MRI).
A 55-year old woman consulted Gife University Hospital on November 28, 1985, complaining of abnormal eye movements.
Neurootological findings : Her left eye showed abnormal movements characterized by rapid (8-9 Hz), small amplitude, intorsional and vertical motility. These eye movements were seen best when she looked down and to the left. The diagnosis was superior oblique myokymia. Optokinetic nystagmus and visual suppression of caloric nystagmus were within normal limits.
Neuroradiological findings : MRI showed a lesion, suspected of being an arterio-venous malformation, which extended from the right cerebellar peduncle to the flocculus.
Ishikawa (1983) reported that the lesion responsible for superior oblique myokymia was the contralateral flocculus. MRI findings in our case supported his speculation. But the results of optokinetic nystagmus and visual suppression tests suggested that the function of the flocculus was not impaired. We speculate that the lesion did not affect the function of the flocculus or that it affected the part of the flocculus which was not related to optokinetic nystagmus and visual suppression of caloric nystagmus.

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Isolated paralysis of downward gaze is not very common. Only six cases have been reported with pathological anatomic findings since Andre-Thomas described the first case with autopsy.
A 47 year-old male with isolated paralysis of downward gaze was studied. In the neuro-otological examination, although doll's eye phenomenon of downward eye movement was preserved, neither optokinetic nystagmus nor smooth pursuit eye movement were present in the downward direction.
In the six cases that been described with autopsy, bilateral focal infarcts of the rostral mesencephalon were observed.
In this case, however, there were no abnormal findings in the rostral mesencephalon, though there were bilateral focal infarcts of the thalamus on CT scan. However, it is difficult to explain in the relationship between the isolated paralysis of downward gaze and the findings on the CT scan.

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Immunological mechanisms are considered to be among the causes of Meniere's disease. Immunological techniques have been used by many investigators to produce endolymphatic hydrops models, but these techniques have heretofore brought little success in producing models which simulate the idiopathic endolymphatic hydrops of Meniere's disease, where no inflammatory changes exist in the perilymphatic spaces. In this experiment, the immunological induction of this type of condition was attempted by injecting the antigen HRP into the endolymphatic sacs of 120 anesthetized guinea pigs which had been systematically sensitized to this antigen.
After a certain survival time, three tests were performed on these guinea pigs.
(1) Vestibular functions were checked by performing a swimming test on a group of 49 guinea pigs. A total of 20 displayed abnormal swimming pattenns ; of this number. 8 swam clockwise and 4 counterclockwise. In a group of 90 guinea pigs, only one case of spontaneous nystagmus was observed.
(2) Auditory functions were measured by electrocochleography. It was found that the action potential thresholds were elevated in guinea pigs with severe endolymphatic hydrops.
(3) After the completion of these tests histopathological studies were performed ; 78 of the 120 guinea pigs in the test group showed endolymphatic hydrops ; 75 of these displayed no inflammatory changes in the perilymphatic spaces. The endolymphatic sacs of the guinea pigs were packed with soft granulation tissue induced by the immunological mechanism; disturbances in the absorption of endolymph due to this tissue are felt to be the cause of the hydrops.
These results were compared with the histopathological findings obtained in another group of guinea pigs in which the antigen had been injected into the stylomastoid forman. A small number displayed mild endolymphatic hydrops, but considerable precipitation in the scala vestibuli was present.

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The origins of afferent connections to quick eye movement-related pause neurons (PN) in cats were investigated with the use of retrograde transport of horseradish peroxidase with wheat germ agglutinin (WGA-HRP). After injected WGA-HRP into the PN region, HRP-labeled cells were found in the nucleus prepositus hypoglossi, descending vestibular nucleus, medial vestibular nucleus, lateral vestibular neucleus, gigantocellular reticular nucleus, parvocellular reticular nucleus, nucleus reticularis pontis caudalis, nucleus reticularis pontis oralis, nucleus reticularis tegmenti pontis, locus ceruleus, dorsal raphe nucleus and superior colliculus.

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Our previous studies concerning the cat's y-group were reviewed. Anatomical experiments using retro-grade axonal transport of horseradish peroxidase demonstrated projections from the cerebellar floccular caudal-zone to the y-group. Electric stimulation of the y-group produced the upward eye movement, while destruction eliminated the downward eye movement elicited by electric stimulation of the caudal-zone. The neuronal pathway mediating the downward eye movement was then investigated with the use of systematic microstimulation techniques. It was found that target neurons of caudal-zone inhibition project to the oculomotor neurons innervating the contralaterai rectus muscles and the ipsilateral inferior oblique muscles via 'crossing ventral tegmental tract'. Differences in the neuronal connections between the dorsal (DY) and ventral (VY) subdivisions of the y-group were then investigated. It was found that 1) target neurons were located in the DY, and about half of these neurons received vestibular nerve inputs polysynaptically; 2) in the VY, on the other hand, most neurons received monosynaptic vestibular nerve inputs, and some of these neurons projected to the flocculus.

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A case of atypical acoustic neurinoma is presented. The initial symptom was sudden deafness. This was followed by hearing threshold fluctuation.
The tumor was an internal type with a cystic lesion. These two factors caused various symptoms and made the precise diagnosis difficult.
The necessity of taking atypical acoustic neurinomas into consideration, detailed history taking and neuro-otological findings are discussed.

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In the previous report, we described the cause of the corneo-retinal potential increase after the optokinetic pattern test. We speculated that the rise of retinal activity in response to optokinetic stimulation leads to an increase of the potential. The present study is intended to confirm this speculation.
Two optokinetic stimulus conditions were employed in this experiment. First, subjects fix their eyes on the stationary target during optokinetic stimulation without following black stripes. This induces mainly retinal stimulation (condition A). Next, subjects follow black moving stripes in the usual optokinetic test (condition B), which cause mainly foveal stimulation during low drum steed. Stimulus speeds of 30, 45, 60, and 90°/sec constant angular velocities were used.
The corneo-retinal potential increased in condition A after all four stimulus speeds. In condition B, however, the potential did not increase after 30°/sec constant angular velocity stimulation.
These data support the idea that the increase of corneoretinal potential after optokinetic stimulation is due to the rise of retinal cell activity.

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The anterior semicircular canals of bull frogs were isolated, and the cupula was removed from the crista and the sensory cilia on the crista were depressed toward the canal side by a glass micropipette. Seven points on the crista were selected for stimulation. Decremental time constants of the anterior ampullary nerve action potentials were measured. The longer time constants were measured at the lateral points of stimulation which progressively shortened towards the central point. The overall values of the time constant were significantly shorter than those of the posterior semicircular canal. This indicates that the anterior semicircular canal has a larger number of phasic receptors than the posterior canal.

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There are two distinct excitatory projections to the medial rectus (MR) motoneuron pool from the posterior brain stem in the cat. First, abducens internuclear neurons send their axons into the contralateral medial longitudinal fasciculus to terminate upon MR motoneurons. Secondly, the ascending tract of Deiters' (ATD) also terminates upon MR motoneurons.
We studied the effects of a unilateral ATD lesion on the horizontal eye movements evoked by optokinetic and vestivular stimuli. ENGs were recorded prior to and after the lesion was induced in the fully alert cat. The eye velocity on the side of the lesion during the slow and fast phases was compared with that of the intact side. The lesion to the ATD was confirmed histologically and physiologically.
The lesion of the right ATD resulted in the following: (1) During clockwise OKN stimulation (optokinetic rotation to the right), the slow phase eye velocity on the side of the lesion was slower than that of the intact side, while the fast phase eye velocity was not affected. (2) During counterclockwise stimulation, neither the slow nor fast phase eye velocity of either side was affected. (3) During caloric stimulation, slow and fast phase eye velocity was not changed. On the basis of these data, we concluded that ATD was one of the final pathways mediating the visual signals responsible for OKN.

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Slow eye movement induced by a vestibulo-ocular reflex was enhanced or inhibited in various postures of rabbits. A tonic neck reflex functions to help pursuit eye movement in both active and passive postures.

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