Neural mechanisms of gaze, vertical and rotatory nystagmus are reviewed. For all eye movements, eye velocity is an oculomotor parameter. Eye velocity signals are transformed by a neural integrator in the brain stem to obtain the eye position signal. A lesion of neural integrator leads to gaze-evoked nystagmus. Vertical nystagmus arises from a lesional or functional tone imbalance, which is due to disruption of the central vestibulo-ocular reflex pathway in the pitch plane. Downbeat nystagmus is caused by lesions between the vestibular nuclei or flocculus. Upbeat nystagmus is caused by lesions in the brachium conjunctivum, the ventral tegmental pathway and the prepositus hypoglossal nucleus. Rotatory nystagmus involves an epicodic ocular tilt reaction, which is a clinical sign of an imbalance of the central vestibulo-ocular reflex in the roll plane. Unilateral infarction of the brain stem leads to rotatory nystagmus.
To evaluate dynamic postural control, the Body Tracking Test (BTT) was developed. This paper investigated gain for both the target and tracking. The subject standing on the stabilometer was asked to track a moving optical target that was displayed on a screen by his/ her bodily movement. Then, stabilometric data was recorded and computer-analyzed. The horizontal or vertical span of the target was 15cm. An optical target moved in a horizontal or vertical manner. The movement of the optical target was programmed by controlled triangular waves and the optical target speed was approximately 0.1 Hz. The sampling time was 50 mseconds for a total of 60 seconds. The subject stood erect on the stabilometer with feet together and the display screen was placed at eye level. Healthy young adult volunteers were examined under this system. Overall, there were 87 subjects, (male 49, female 38). Mean age was 27.6 (21-37 years). We established 7 scales to determine the gain for target and tracking. Scale 1 is 1.4, Scale 2 is 1.6, Scale 3 is 1.8, Scale 4 is 2.0, Scale 5 is 2.2, Scale 6 is 2.4, Scale 7 is 2.6. Total distance of the bodily movements was adjusted by body weight. To compare the result of each scale, the total distance of bodily movements was divided by total target movement. This ratio was called the "Index of BTT movement". In the horizontal body tracking test, the minimal index was Scale 3, and a gain of 1.8 was thought to be the best score for tracking. In the vertical body tracking test, the minimal index was Scale 2, and a gain of 1.6 was thought to be the best score for tracking.
Since Rask-Andersen and Stahle reported the existence of macrophages and lymphocytes in the endolymphatic sac in 1979, the endolymphatic sac has been thought to play an important role in inner ear immune reactions. However, in the inner ear, especially in the cochlea, the first defensive mechanism in which macrophages and natural killer cells play a significant role before specific immune reactions start remain unknown. As asialoGM1 is one of the surface markers of cells with natural killer activity as well as macrophages in mice and rats, we investigated the localization of asialoGM1-positive cells in murine cochlea using immunohistochemical techniques. As a result, only a few asialoGM1-positive cells were recognized on the wall of the scala tympani by light microscopy, and transmission electron microscopy revealed that these asialoGM1-positive cells were macrophages. These cells appeared to be round or flat, and were scattered primarily at the basal turn of the cochlea and near the collecting venule. This result suggests that these cells play a defensive role against pathogens entering the cochlea, but its function is not very powerful.
A passive impulsive head rotation test was performed to evaluate the affected side of the labyrinth. A device reported by Tokita (1993) was used to record head and eye movements. Displacements and velocities of head and eye movements were respectively recorded by terrestrial magnetism sensor and an electronystagmographic technique. To examine vestibulo-ocular response (VOR), passive impulsive head rotations to the right and left at irregular intervals were performed repeatedly similar to the maneuver reported by Halmagyi et al (1993). From the record, latency and VOR gain ratio (VOR gain on the affected side rotation/VOR gain on the healthy side rotation) at 40ms and 80ms after onset of head rotation were measured. Twenty-two patients with unilateral vestibular disorders were examined in this manner. The affected side of the labyrinth was determined by caloric test. Seventeen patients showed VOR gain ratios less than 0.8 indicating hyporeaction of the affected labyrinth. Three patients including one with a slight canal paresis on caloric test showed ratios within 1±0.2. Two patients including one with a prolonged course showed ratios greater than 1.2. Examination of the VOR gain ratio on passive impulsive head rotation was a useful rotation test to evaluate the affected side of the labyrinth.
We present a 41-year-old male with vertigo due to orthostatic hypotension caused by diabetic neuropathy. Autonomic function test showed no increase in either plasma noradrenaline or sympathetic activity in response to standing up. During head up tilting, vertebral blood flow measured by Doppler flowmeter decreased with a decrease in blood pressure and asymmetrical vertebral blood flow was evident. Head up tilting also induced nystagmus and vertigo. After the patient was treated for orthostatic hypotension by L-threo-3, 4-dihydroxyphenylserine, a precursor of noradrenaline, neither asymmetrical vertebral blood flow nor nystagmus were observed during head up tilt. It is suggested that asymmetrical vertebral blood flow induced by sympathetic dysfunction causes asymmetrical excitability of the vestibular system, resulting in nystagmus and vertigo.
We studied horizontal optokinetic nystagmus (OKN) and horizontal optokinetic afternystagmus (OKAN) in five normal human subjects. The cylinder was rotated with an equal velocity of 40°/sec, 60°/sec, 70°/sec, 80°/sec, 90°/sec, 100°/sec. In a dark room, illumination was switched on for 30 sec and then turned off. Eye movements were analyzed by computer. We examined the relationship among averaged retinal slip velocity (RSV, drum velocity minus averaged slow-phase velocity of OKN), slow phase velocity of the first OKAN, duration of OKAN and time constant of the decay of slow phase velocity of OKAN. We supposed that the most effective RSV for OKAN ranged from 20°/sec to 40°/sec. We also found that fixation of a small target during optokinetic stimulation almost completely prevented the development of OKAN. We speculated that the target image across the fovea (retinal slip on the fovea) was very important for generation of OKAN.
The normal ranges and normal patterns of optokinetic after-nystagmus (OKAN) were investigated in 147 normal subjects aged 20-78 (mean 42.0 years). Histograms of the duration of the first phase of OKAN were similar to Poisson's distribution. Hyporesponse less than 10 sec, middle response between 10 and 60 sec, and hyper-response above 60 sec were observed in 44.9%, 44.2% and 10.9% of all subjects, respectively. Combinations of the first phase of OKAN towards the sides were classified into 6 groups with 2 subgroups. An asymmetric pattern of OKAN to the right or left appeared in 61.8% of 147 cases. Bilateral hypo-responses also appeared in normal subjects with normal canal function or normal caloric test. The second phase of OKAN was observed in 9 subjects, but a third phase was not detected.
To test vertical semicircular canal function, we developed a new and convenient type of rotation-chair, in which subjects sat with their heads and backs tilting backward 60°and with their heads rolling laterally 45°. A CCD camera and infrared video system was used to record eye movement in the dark. Normal subjects were rotated with an acceleration of 2°/sec2 until the angular velocity reached 60°/sec. The rotation was then stopped with a deceleration of 100°/sec2 after per-rotation nystagmus subsided. The maximal slow phase eye velocity (MSPEV) of vertical components of vertical semicircular canal (VSCC)-induced post-rotatory nystagmus (PRN) were analysed. Subjects were first rotated with laterally rolling head angles of 30°, 45° and 60°to examine the optimal angle for stimulating VSCC. MSPEV of posterior semicircular canal (PSCC)-induced PRN was largest with a head angle of 60°. While MSPEV of anterior semicircular canal (ASCC)-induced PRN did not vary with the laterally rolling head angle. MSPEV of the vertical components of VSCC-induced PRN was then compared with that of the horizontal components of lateral semicircular canal (LSCC)-induced PRN. MSPEV of both PSCC- and ASCC-induced PRN were significantly smaller than that of LSCC-induced PRN. MSPEV of ASCC-induced PRN was slightly smaller than that of PSCC-induced PRN, though individual differences varied widely. However, there were very small leftright differences in MSPEV of both PSCC- and ASCC-induced PRN. Therefore, it is suggested that our PRN function test involving VSCC can diagnose vestibular diseases.
Using an infrared CCD camera and electronystagmography, we observed positional nystagmus in 36 patients with peripheral positional vertigo. Patients were classified into two categories; (a) the lateral type (n=18): horizontal nystagmus occurs in the lateral position and (b) the sagittal type (n=18): rotatory nystagmus occurs in the headhanging position. In the lateral type, we performed the rolling procedure for 15 patients, and in the sagittal type, we performed the canalith repositioning procedure (CRP). The direction of positional nystagmus reversed in six patients (40%) with the lateral type after the rolling procedure, and 1 patient showed spontaneous change in the direction of positional nystagmus without any procedure. Therefore, we cannot discriminate between peripheral and central origin by the direction of positional nystagmus alone. Soon after CRP, 7 patients (39%) showed the disappearance of positional nystagmus and 3 patients (17%) showed a reverse in the nystagmus direction. In sixteen patients (89%) with the sagittal type, CRP was effective. The free-floating particles theory explains the immediate change of positional nystagmus and the usefulness of CRP. We suggest that lesions in the lateral type involve the lateral semicircular canal, and that in the sagittal type involves the posterior semicircular canal.