In order to identify the origin of the mossy fibers which convey the visual input to the cerebellar flocculus, tracer experiments with the method of retrograde axonal transport of horse-radish peroxidase (HRP) and electrophysiological experiments of plotting the stimulation threshold curve and destroying of the brain stem were performed in cats. Following careful electrophoretic introduction of HRP into the flocculus, labeled neurons with HRP were detected in (1) the dorsal cap of the contralateral inferior olive to the injection site, (2) the bilateral vestibular nuclei, (3) the bilateral perihypoglossal complex, (4) the ipsilateral lateral reticular nucleus, and (5) the bilateral pontine tegmental reticular nucleus (Bechterew) NRT. These findings were consistent with those in the previous reports. In the present experiments, however, labeled neurons were found only in the medial part of the NRT, but not in the lateral part such as the processus tegmentosus lateralis. Furthermore, a larger number of labeled neurons was counted in the contralateral NRT compared with the ipsilateral NRT. No labeled neuron could be detected in the pontine nuclei or the accessory optic tract nucleus. Electrical stimulation (pulse width 0.05msec) of the NRT induced the evoked potentials in the flocculus. The threshold current for the evoked potential was lowest in the NRT (lower than 100μA). After electrolytic destruction of the NRT by the passing of positve DC current (1mA, 20sec), the component attributed to the mossy fiber activation of the visually induced potentials in the flocculus decreased markedly in its amplitude. These above-mentioned findings suggest strogly that the NRT may project to the flocculus and that this pathway may be at least part of the relay nuclei of the visual input from the retina to the flocculus.
Effects of ocular fixation upon caloric nystagmus have been used as a routine test. Percentage reduction in slow-phase velocity of caloric nystagmus induced by ocular fixation, however, varies depending upon the test condition employed. In the present experiment, we standardized the effects of ocular fixation upon caloric nystagmus in 58 normal individuals. The electronystagmographic test was performed in total darkness. The caloric stimulus was 50ml water, most often 30°C or 44°C, sometimes 20°C, for an irrigation period of 20 sec, with about 7-minute intervals. Subjects were requested to fix their gaze upon a spot on the ceiling about 3m away during the maximum intensity of slow-phase velocity for 10 sec. The amount of reduction of slow-phase velocity induced by ocular fixation was obtained during the first half of the 10-sec period and compared with the control period. The percentage reduction in slow-phase velocity induced by ocular fixation did not depend upon the temperature of the water applied as a caloric stimulus. The mean percentage reduction in slow-phase velocity induced was about 82±12%. On the basis of these results, fixation-suppression of caloric nystagmus was studied in 669 consecutive cases. An analysis of caloric nystagmus with failure of fixation-suppression (FFS) made it possible to classify patterns of FFS into three types. Together with the recent anatomical and physiological data, the underlying neuroanatomical substrates responsible for the FFS was discussed.
Loss of visual suppression (VS) of caloric nystagmus was produced after creating flocculus destruction. The flocculus receives visual signals through a climbing fiber pathway and also through a mossy fiber pathway. In the previous report, we stated that the inferior olive as a source of the climbing fiber might be unrelated to the immediate modification of the vestibuloocular reflex by visual stimuli. A mossy fiber pathway presumably via the superior colliculus is a likely candidate for visual suppression of caloric nystagmus. A very recent anatomical and physiological experiment has revealed that the nucleus pontis (NP) and the nucleus reticularis tegmenti pontis (NRT) project mossy fibers to the flocculus. In the present experiment, major concerns were to ascertain whether NP or NRT is the prefloccular relay nucleus responsible for the VS of caloric nystagmus. To achieve this goal, the VS of caloric nystagmus and optokinetic nystagmus (OKN) were investigated after making lesions in NP or NRT in 27 cats. After making the NP lesions, the VS of caloric nystagmus was revealed and OKN was normal in all the cats with the NP lesion. After making the NRT lesion, loss of VS was observed toward the side opposite to the lesion and OKN showed directional preponderence to the lesion site. These experimental findings are quite compatible with the fact that the early component of the field potentials in the flocculus induced by strobe flashes decreased markedly after making a lesion in the contralateral NRT. Together with the anatomical evidence that the superior colliculus sends its fibers to the NRT, the mossy fiber pathway via NRT is believed to be the final relay nuclei responsible for the VS of caloric nystagmus.
The method and objective of the analysis of equilibrium dysfunction based on the indices of gravitudinal fluctuations as well as the expression of the body sway in mathematical values have contributed in the diagnosis of the location of disturbance and the classification of diseases. The power spectrum analysis of deviation is one of the analytical methods which have gained much popularity in practice in recent years. We have recently conducted a power spectrum analysis of body sway velocity. It was not possible to analyze the directional component of a body sway by this method, but observation of sways in terms of velocity was possible. Formerly, it was difficult to analyse the high frequency of the body sway in terms of the power spectrum : however, by converting the body sway into the velocity power spectrum, the analysis of the high frequency body sway could be easily be performed. We used this method for the analysis of 19 cases of spinocerebellar degeneration, seven cases of Parkinson's disease, 22 cases of hemiplegia, and eight cases of Meniere's disease. For basic data, tetanic stimulation of lower limb muscles was given by connecting plate electrodes to the tibial nerves bilaterally below the knees to induce body movements. In this experiment, a peak was observed which coincided with the loaded frequency in the sway velocity power spectrum. It was discovered also in this experiment that the velocity component of body sway in the normal person was a noise which was inversely proportional to the Feurier's frequency, which is said to be Schottky effect (by Johnson 1925, 1/f noise). When various neurological diseases was analysed using this method, a distinct finding was observed at higher frequencies, i.e. a deviation in the slope of the spectrum from that of the 1/f noise. How a method like this can be utilized for the analysis of body movements was discussed.
Cross-correlation analysis between the head movement and the movement of the center of gravity was performed to obtain basic data on normal subjects. A recording apparatus to determine the head movement consists of an industrial television set which picks up the movement of a light-emitting diode on the helmet which the standing subject is wearing and transmits the movement in terms of voltage to a preamplifier connected to a wave control unit and finally to an X-Y recorder. A system for recording the movement of the center of gravity consists of a straingauge-platform on which the subject stands and the movement in voltage is transmitted to a preamplifier and to an X-Y recorder. The information obtained from the head and the center of gravity can at the same time be fed into a data recorder, which separately stores the data on anteroposterior and lateral displacements on magnetic tape. The data recorded on the tape were fed into a processor for cross-correlation analysis. Three types of cross-correlograms were classified according to the characteristics shown in the correlograms which were obtained from normal subjects standing with eyes open and with eyes closed. The type A correlogram revealed a random and sine wave process of about 0.3Hz with the eyes open and 0.5Hz with them closed. Type B showed a random and sine wave process of 0.3Hz with the eyes open and 1.0Hz superimposed on 0.3Hz wave with the eyes closed. Type C was a random and sine wave process of about 0.6Hz with the eyes open and 0.3Hz with them closed.
The current of the galvanic test is supposed to stimulate the vestibular system, but the exact location of stimulation has not been identified. Electrocochleography can determine the cochlear or retrocochlear hearing impairment due to the SP change and the threshold of AP and CM can be compared. Patients with sensory hearing impairment and canal paresis were examined by electrocochleography (transtympanic method) and the galvanic body sway test (GBST, monopolar and monoaural method). The following results were obtained. 1) Five of the eight patients with the cochlear type of hearing impairment showed a normal threshold of GBST (under 1mA), and all six patinets with the cochlear nerve type showed an abnormal threshold (1.1mA to 2mA) or no response with 2mA. 2) Two patients with the lesions in the brain stem, which could not be recognized N2 to N5 waves in Brain Stem Response, showed an abnormal GBST. 3) Eight patients who showed canal paresis and had diminished caloric nystagmus showed a normal GBST even when there was retrocochlear hearing impairment. 4) Eleven patients showed too marked cochlear damage CM to speculate the damage of the cochlear nerve (AP). The results of their GBST were normal in six and abnormal in five cases. According to these results, the stimulus site of GBST is speculated to be the vestibular nerve, proximal to Scarpa's ganglion, and the sites of the lesion causing hearing impairment and canal paresis are suspected to be almost the same.
Electronystagmograms of the eye tracking test, that is, eye tracking patterns were quantitatively assessed in 63 subjects. Abnormal findings consisted in remarkable irregularities of eye speed. These irregularities appeared in the form of spikes on electronystagmograms at the time constant of 0.03 sec. We measured the height of the spike by taking 40°/sec as a unit, and summed up the units of spikes appearing for 9 seconds to obtain the total index. The total indices ranged from zero (normal) to the forties (markedly abnormal). These numerals showed the level of abnormality of the eye tracking pattern more accurately than visual analysis, the method of determination in current use.
Three hundred and forty-six patients who complained of dizziness were examined neurotologically to clarify the etiology and to locate the lesion. 1. About 50% of the patients with dizziness have psychogenic problems confirmed on the Cornell Medical Index. Some of them needed further psychological examination and treatment. 2. The remaining 50% of patients with dizziness showed unilateral or bilateral hypo or afunction on the caloric test. One should differentiate whether the lesion is located in the inner ear or in the vestibular nerve. 1) When the spontaneous nystagmus was recorded by ENG with eyes open in darkness : Although spontaneous nystagmus did not appear on the eye speed recording of the eye tracking test in the case of inner ear lesions, it appeared on the eye speed recording of the eye tracking test in such vestibular nerve lesions as vestibular neuronitis, Hunt syndrome, etc. 2) Selective diagnosis of the inner ear lesion. In the caloric test the lateral semicircular canal function is evaluated. When the eyes were closed, the eye ball moved upwards and was adducted. The upward movement of the eye ball was maintained during the eye closure, but it suddenly or gradually turned down when the lesion was in the anterior semi-circular canal. Thus, the anterior semi-circular canal lesion can be diagnosed when the DC-recording shows turning down of the eye ball which had initially moved upwards.
Preoperative electronystagmography (ENG) recordings were done in 100 patients with chronic otitis media to detect vestibulocular disturbance associated with this condition. ENG recordings were performed under five conditions : gazing, eyes closed, eyes covered and performance of mental calculation with eyes closed and eyes covered. The optokinetic pattern test (OKP) and eye tracking test (ETT) were also done. The rate of appearance of spontaneous nystagmus in these 100 patients was compared with the rate of appearance of the 100 normal individuals in the report of Kaga et al. Both slow phase velocity (degree/second) and frequency (number/second) were measured on ENG recordings and also compared with the normal results. The relation between the rate of appearance of the spontaneous nystagmus with the following clinical signs and symptoms were investigated : 1) vertigo, 2) otorrhea, 3) unilateral, or bilateral chronic otitis media, 4) history of operation, 5) cholesteatoma and 6) bone conduction abnormalities. Spontaneous nystagmus was found in 67% of the patients with chronic otitis media. Both slow phase velocity and frequency of spontaneous nystagmus of the patients were remarkably larger than that of the normal individuals in each of the above conditions. Significant difference was seen with respect to the following : vertigo, bone conduction abnormalities and unilateral cholesteatoma. The direction of the spontaneous nystagmus in patients with unilateral chronic otitis media with otorrhea was contralateral to the lesion rather than ipsilateral. Six patients showed abnormal optokinetic patterns and they also had abnormal results on the eye tracking test.
Seventy-two cases of positional vertigo of the benign paroxysmal type were analysed with respect to several clinical findings, especially the characteristic rotatory nystagmus in the positional and positioning tests. The results of the analysis were as follows. (1) This disease is much more common in the fourth to sixth decades of life than the others. The sex distribution was 26 males and 46 females or a male to female ratio of 1 : 1.7. (2) The evidence of otitis media, hypertension or head injury was demostrated 31% of the 72 cases. (3) In 10 patients, gaze nystagmus was seen and of these, two patients had nystagmus in both directions. (4) In many cases, there was close correlation between the direction of the rotatory nystagmus, the affected ear and the undermost ear in critical position. (5) Within four weeks after the onset of the symptom, the positional or positioning nystagmus could almost always be detected with the rotatory element, latent period, decrescendo and fatigability. But these nystagmus were absent in about 50% of the patients examined four weeks after onset. The detection rate of the positional nystagmus decreased more markedly than that of the positioning nystgmus. Although the criteria for the diagnosis of this disease should be strict, at present rather common cases which can not satisfy the criteria are not so rare. For this reason, we concluded that it is important to detect the characteristic rotatory nystagmus in the p sitional and positioning tests within four weeks after the onset of this condition.
A patient with Ménière's disease whose younger brother and two children had positional vertigo of benign paroxysmal type is presented. The family history and other reports on paroxysmal vertigo suggest the possibility that paroxysmal vertigo may be inherited in some cases. To evaluate the relationship between paroxysmal vertigo and heredity, we studied the association between paroxysmal vertigo (Ménière's disease, P.V.B.P) and HLA (Human Leucocyte Antigens). Twenty-eight patients were typed for HLA-A, B or C locus by the lymphocyte toxcitity test. HLA-Bw16 was found in 27.8 per cent of the Ménière's disease cases (N=18) as compared to 9.3 per cent in the controls (N=215) and the relative risk was 3.75 (P<0.05).
A case of the one and a half syndrome appearing in pons bleeding is reported. A 65-year-old male patient had been suffering from hypertension for ten years, who noticed sudden vertigo while delivering a lecture. After this attack, the patient showed the characteristic abnormal eye movement : namely the left eye showed no horizontal eye movement; however the right eye moved only to the right with monocular nystagmus in the right lateral gaze. Upward gaze, downward gaze and convergence were normal. This trait of abnormal eye movement was explained by Fisher as lesions of PPRF & MLF. This lesion was confirmed by the CT scanner. The extent of the lesion was discussed on the basis of the results of neurotological and neurological examinations.
Follow-up study of the vestibular neuronitis was made comparing the findings of the computed galvanic body-sway test. The computed galvanographs, which were obtained from patients with vestibular neuronitis, showed a peculiar “slow and sluggish pattern”. In the process of the illness, this slow and sluggish pattern changed its appearance and came to resemble the pattern obtained from the opposite healthy side. Improvement of the abnormal pattern was observed in seven patients (observation period : 6 months to 6 years, averaged 33 months). Three other patients (observation period : one month to one year, averaged 5.3 months) showed no marked change in the pattern. These findings suggested that there is some possibility of recovery of the conductibility of the vestibular nerve which was affected by vestibular neuronitis.
A case of convergence nystagmus after head trauma caused by traffic accident is reported and the literature is reviewed. A 23-year-old man was referred to our clinic for examination of equilibrium disturbance which developed after head traum which had occurred four years earlier. The definite and characteristic finding in the ENG test was a peculiar nystagmus on convergence gaze. The oculomotor function was seemingly within normal limits. From the neurootological findings some relatively localized lesion in the upper midbrain which was due to brain-stem concussion, slight bleeding and secondary degeneration was suspected.
A 32-year-old male with acute, left-sided petrositis rapidly developed ipsilateral pontine angle symptoms, i.e. paralyses of the fifth to eighth cranial nerves, lateral gaze nystagmus and disturbances of horizontal optokinetic nystagmus and horizontal smooth pursuit eye movement. Because the cranial nerve disturbance was more marked in the seventh and eighth cranial nerves than in the fifth and sixth nerves this case was considered to be a rare paralabyrinthitis type as opposed to the more common apicitis type. It was inferred that inflammation extended into the internal acoustic meatus causing the development of the disturbance of the seventh and eighth nerves. Also, localized pachymeningitis at this region and compression of the brain stem due to an extradural abscess was considered to be responsible for the development of the abnormal eye movement including lateral gaze nystagmus. The causative organism was proteus inconstans B and the patient recovered in about one month's time with adequate antibiotic treatment (Bactramin).