Search

It has been shown that the nucleus of the optic tract (NOT) is an important visuomotor relay between the retina and preoculomotor structures, and is responsible for mediating horizontal optokinetic nystagmus (OKN) in monkeys, cats, rabbits, and rats. The details between the NOT and the vestibular nucleus in the brain stem concerning the morphology of fibers-of-passage and axon terminals have been disclosed in cats and monkeys. One is that they project to the contralateral NOT via the posterior commissure. In order to evaluate the role of the commissural fibers between the NOTs, the posterior commissure was cut in the present experient. Three fuscata monkeys (M17, M19, M22) were used. A magnetic search coil was sutured to the right eye to record eye position. Several bolts were embedded and secured with dental acrylic cement to fasten the animal's head during experiments. The animal was mounted on a turn table covered by an OKN screen, onto which OKN stripes were projected from above. The animals viewed the OKN stripes under three conditions: right eye viewing, left eye viewing, and bilateral eye viewing. OKN was recorded in response to counter clockwise (CCW) and clockwise (CW) stimulation at stimulus velocities of 30°/s, 60°/s, and 90°/s. After the control experiment was completed, the posterior commissure was transected by an operator knife. After follow-up studies were completed, an anterograde tracer was injected in the left NOT to ascertain the complete block between NOTs. Rapid rise (RR) and steady state (SS) of slow-phase OKN velocity and time-constants (TC) of optokinetic afternystagmus (OKAN) were measured. In three aniamis, OKN gains elicited with monocular viewing were approximately equal to the those of binocularly-evoked OKN before and after surgery. In the three monkeys, the commissurectomy decreased RR and SS to both sides during the three weeks immediately after surgery. In M22, TC showed the tendency to decrease by only 30°/s and 60°/s after surgery. There were no significant differences in TCs of other experiments.In conclusion, gain reduction in RR and SS can be explained by decrease of inhibiting the resting rate in NOT, which is conducted via commissural fibers. This was caused by interruption due to a middle-line lesions. Furthermore, interrupting the commissural fibers has nothing to do with the velocity storage mechanism.

We report a patient with vertigo and sudden hearing loss due to acute disseminated encephalomyelitis (ADEM).A 17-year-old male complained of sudden hearing loss in the right ear and dizziness subsequent to symptoms resembling those of a common cold. To his recall, he had never manifested any previous neurological disturbances. Audiometric testing revealed severe sensorineural hearing loss in his right ear and mild sensorineural hearing loss in his left ear. In addition, a short increment sensitivity index (SISI) test was positive bilaterally. Neuro-otological examinations revealed horizontal-rotating nystagmus and upbeat nystagmus on positional and/or positioning nystagmus tests. Although pursuit eye movement was normal, the optokinetic nystagmus was impaired and fast-phase velocity of the nystagmus was reduced. Caloric tests revealed severe hypofunction bilaterally. MRI showed patchy high-intensity areas in the pons, left frontal lobe, left superior frontal gyrus, and left parietal lobe on T2-weighted and FLAIR (fluid attenuated inversion recovery) images.Based on the history, physical examinations, laboratory tests, and MRI findings for this patient, he was diagnosed as having ADEM with bilateral inner ear lesions. This patient was considered to be an unusual case of ADEM complicated with cochlear and vestibular signs. To our knowledge, such a case has not been previously reported.

In order to clarify the diagnostic significance of eye tracking tests (ETT), optokinetic nystagmus tests (OKN), and visual suppression test (VST) on routine ENG tests, we investigated the findings of ETT, OKN, and VST in 1, 225 patients who complained of vertigo and dizziness, and in 440 of the patients, we compared these findings with MRI abnormalities.Abnormal results of ETT, OKN, and VST were seen in 433 patients (35.1%), 399 patients (32.6%), and 128 patients (10.5%), respectively. All tests showed impairment in 66 patients (5.4%). Both ETT and OKN abnormalities with normal VST were observed in 173 patients (14.1%), while 356 patients (29.1%) had abnormal findings for ETT, OKN, or VST. In the patients who had severely impaired ETT, OKN, or VST, there was a significantly higher proportion of infratentorial lesions on MRI than in the other patients. In the patients with abnormalities on both ETT and OKN, infratentorial le-sions were more frequently found by MRI, and the patients who had abnormalities on all tests had the highest incidence (61.7%) of infratentorial lesions on MRI.We conclude that the evaluation of ETT, OKN, and VST abnormalities should be quite useful in the diagnosis of infratentorial lesions.

A 56-year-old man complained of a hearing loss and tinnitus in his right ear after short intense exposure to a high level of sound. Although he had no complaints of vertigo or dizziness, his neuro-otological examination revealed apogeotropic direction changing type of positional nystagmus. An audiogram showed right high-frequency sensorineural hearing loss. An eye tracking test (ETT) and an optokinetic nystagmus (OKN) test showed no abnormalities. A caloric test showed normal responses in both ear sides. One week after the exposure to a high level of sound, the positional nystagmus completely disappeared.Apogeotropic direction changing type of positional nystagmus is generally considered to be a phenomenon observed in patients with central vestibular lesion. However, physical examination and laboratory tests of this patient suggested that he suffered from only a peripheral vestibular impairment. From these results, apogeotropic direction changing type of positional nystagmus observed in this patient resulted from an impair-ment of the peripheral vestibular system.

A patient with acute hearing loss and vertigo due to infarction involving the anterior--inferior cerebellar artery (AICA) is reported.A 64-year-old female complained of sudden-onset, severe, unilateral hearing loss and vertigo without any other neurological deficits. Neuro-otological examinations revealed a horizontal, spontaneous, positional, and gaze nystagmus toward the right. Pursuit eye movement and optokinetic nystagmus were unilaterally impaired and ABR showed the absence of waves II-IV and prolonged I-V interpeak latency difference. Based on finding of neuro-otological examination, brain stem lesion was suspected and neuroradiological examinations were performed. MRI showed a pontine infarction in the AICA area and angiography demonstrated stenosis of the right AICA thus the patient was diagnosed as having AICA syndrome.The clinical signs of AICA syndrome are occasionally similar to those of inner ear disorders. In such cases, neuro-otological examinations such as ENG and ABR are clinically useful in distinguishing AICA syndrome from inner ear diseases.

In the present study, the values of parameters, such as peak velocity and amplitude of the fast phase of optokinetic nystagmus (OKN), were measured quantitatively in 5 normal subjects by a microcomputer, and the effects of several methodological factors on nystagmus parameters were investigated.1) The relationship between peak velocities and amplitude of the fast phase of OKN could be obtained from a bestfit exponential equation, i. e., velocity=K (1-exp [-amplitude/L]), where K is the asymptotic maximum velocity and L is a curvature parameter.2) Analog filters with highcutoff frequencies affected the computation of peak velocities of the fast phase of OKN. The results showed that the analog filter should be about 10Hz or higher.3) Sampling frequencies influenced the velocity of the fast phase of OKN, and it was shown that the analog data should be digitized at a rate of 200 samples/sec or more.4) It was recognized that the value of the velocity at each amplitude obtained from a best-fit exponenntial equation could be used as an index for the evaluation of the fast phase of OKN.

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.