This study shows that auditory brainstem response (ABR) can be used to measure the basilar membrane travelling wave velocity (TWV). TWV was calculated from the latency difference between wave V of the different derived ABRs and the cochlear location distance between the appropriate derived band center. frequency. The latency of wave V of derived ABR produced by six noise masked ABRs with the use of high pass filtered noises and the location of the corresponding cochlear partition (distance from the stapes footplate) were measured and five TWVs were estimated from these data. Ten subjects with normal hearing, seven patients with Ménière's disease and eight patients with sensori-neural hearing loss (SNHL) were examined. The TW V in the SNHL group was within normal limits at all frequencies, whereas the TWV at 8 kHz in the Meni6re group greatly exceeded that of the normal and SNHL group. This finding suggests that the measurement of basilar membrane TWV using derived ABR contributes to the diagnosis of Ménière's disease and the estimation of inner ear pathology.
Motion sickness was analyzed with questionnaires to 34 patients with stomach diseases. Fourteen of the patients had suffered from motion sickness. In three patients it had occurred after stomach distress. The results indicate that visceral afferents play a role in motion sickness. The patients were also questioned about dizziness. One had severe dizziness during episodes of stomach distress.
Caloric tests were performed in 38 normal volunteers and 63 patients with spinocerebellar degeneration (SCD). 1) Maximum slow phase velocity of caloric nystagmus in darkness (SPV-max), 2) visual suppression of caloric nystagmus (VS) and 3) tonic deviation of the eyes in darkness just before a light was put on for visual supression (D) were measured from electronystagmographic recordings. D was defined as positive when the eyes deviated to the side of cold water irrigation and negative when the eyes deviated to the opposite side. 1. Normal and SCD groups showed almost the same SPVmax value. 2. The SCD group showed a lower VS value than the norm-al group (p<0.005). 3. The mean value of D was positive in the SCD group, i.e. the eyes deviated to the side of cold water irrigation. In the normal group, it was also positive, but deviation was smaller than in the SCD group (p<0.025). 4. SCD patients with gaze nystagmus showed a lower VS value than patients wIthout gaze nystagmus (p<0.005). 5. Some SCD patients without gaze nystagmus showed a low VS value (≤ 30%).All of these patients showed a high D value (≥ 14°). 6. Although some normal subjects showed a high D value, they all showed a normal VS value. A large D could represent a poor VS in some of the SCD patients, because, aecording to Alexander's law : the slow phase velocity of vestibular nystagmus is less when the eyes are deviated to the side of the slow phase. The present study confirms that a low VS value definitely indicates impairment of the central vestibular system even if the eyes are deviated to the side of the slow phase.
In patients with peripheral vestibular disorders, spontaneous nystagmus is sometimes superimposed on smooth pursuit eye movements and reveals unilateral saccadic pursuit. To determine whether caloric nystagmus has an influence on smooth pursuit, we recorded horizontal eye tracking with cold water caloric stimulation in 12 normal subjects. We found that brisk caloric nystagmus was superimposed on smooth pursuit eye movements, and we measured slow phase velocity and fast phase velocity of the superimposed nystagmus. The influence was great when tracking was in the same direction as caloric nystagmus. We suggest that saccadic pursuit indicates not only central disorders but also peripheral vestibular lesions.
Patients subject to vertigo have been said to have autonomic nervous dysfunction, especially sympathetic hyperresponsiveness or parasympathetic hyporesponsiveness. Sympathetic nervous function in vertigo patients, in relation to antonomic nervous dysfunction, was examined by means of pulse wave velocity (PWV). In this study, 47 patients (12 with autonomic nervous dysfunction 12 with Ménière's disease, 8 with vertebrobasilar insufficiency and 15 others) were examined. R-R interval measurements on ECG were performed simultaneously to evaluate parasympathetic function. Autonomic nervous dysfunction, was confirmed in 24 patients. PWV, especially, reflects sympathetic nerve function, 13 patients (54.2 %) showed hyperresponse and 10 (41.7%) hyporesponse. In contrast, 18 (75 %) showed normal parasympathetic function. These results suggest that autonomic nervous dysfunction in patients with vertigo is mainly sympathetic dysfunction and that the measurement of PWV may be a useful diagnostic modality.
Cutaneous temperature changes and subjective sensations concomitant with repeated caloric and metopic cooling stimuli were studied quantitatively in order to observe the adaptation of the vestibular autonomic reflex system and the somatic autonomic system response. The subjects were 17 healthy adults. Stimuli were applied three times at intervals of 6 minutes. The caloric stimulus consisted of exposing the right ear at 50°C for 60 seconds, while the metopic cooling stimulus consisted of applying an ice pack to the metopic region for 30 seconds. Subjective sensation was quantified during caloric stimulation by scoring vertigo and nausea on a six-grade scale and emesis on a two-grade scale. These scores were then totaled. During metopic cooling, stimulation by scoring cold sensations in the metopic region was on a six-grade scale. When caloric stimulation was applied, lowered sensory scores were associated with significantly decreased cutaneous temperature variation and slow-phase velocity. Conversely, no significant changes in either cutaneous temperature variations or sensory scores were recognized when metopic cooling stimulation was applied. These results indicate that the loci of central adaptation mechanisms, including the vomiting centers, are largely involved as sites responsible for adaptation in the vestibular autonomic reflex system.
Two patients with upbeat nystagmus in the primary position of gaze were studied neuro-otologically. The nystagmus appeared with oscillopsia and body imbalance in gait and standing. These symptoms appeared during malnutrition caused by the loss of appetite. One patient was alcoholic and the other had a psychiatric disorder. Nutritional encephalopathy was diagnosed in both patients. 1) Upbeat nystagmus was observed during forward, downward, right and left gaze. It did not behave in accordance with Alexander's law. Pursuit eye movement in the upward direction was saccadic, and the velocity of saccadic eye movement in the downward direction decreased. Vertical optokinetic nystagmus could not be elicited. Disturbance of horizontal eye movements was observed in pursuit eye movement and optokinetic nystagmus. 2) The position and velocity of the head and eyes during vertical head oscillation with fixation on an earth-fixed visual target were recorded with a microcomputer and a specially designed program. The velocity of upward eye movements was faster than that of downward eye movements, suggesting a disturbance of the integration mechanism from position signal to velocity signal in visual and vestibular pursuit eye movement. We concluded that a disturbance of the neural integrator in the prepositus hypoglossi nuclei was probably responsible for upbeat nystagmus in these patients.
Electrooculographically, torsion of the head with closed eyes elicits a transient saccadic deviation (TSD) of about 26° directed to the head torsion. The velocity of TSD was measured in active and passive head torsions and compared with the velocities of sacades between two targets with 10° and 20° visual angles in 11 normal adults (aged 25 to 49 years). The mean velocities of TSDs in active and passive maneuvers were 130°/sec and 160°/sec, respectively not a significant difference. The maximum velocities of TSDs were similar to those of saccades shown with 10° visual angle (around 200°/sec). According to the confidence limit and frequency distribution of the velocities of TSDs, the minimum value was thought to be 100°/sec, below which it might suggest a lowered alertness of the parapontine reticular formation (P PRF). In conclusion, the velocity of TSD may be a valuable indicator of the funct ion of PPRF.
Positional nystagmus of the direction changing type, especially nystagmus towards the side of the upper ear in the lateral head position, is considered to appear in patients with disorders of the central nervous system. However, it might also occur in patients with peripheral vestibular disturbances. The pathogenesis of nystagmus directed towards the upper ear side remains obscure because controversial results have been reported in several papers. This paper discribes two patients with positional nystagmus directed towards the upper ear side, which was provoked after a short latency in both lateral head positions and disppeared within a few days. In both patients neurological and neurootological examinations indicated the presence of peripheral vestibular disorders. A fragment of statoconia adhering temporarily to the cupula of the lateral semicircular canal might be the cause of the nystagmus in our two patients.
A 42-year-old male complained of tremor of the hands and titubation. Neurological and neurotological examinations revealed 1) tremor of the hands, 2) truncal ataxia, 3) mild cerebellar ataxia of the extremities, 4) mild limitation of eye movement to the right, 5) geotropic positional nystagmus, 6) down-beat positioning nystagmus, 7) impairment of horizontal eye movements including smooth pursuit, optokinetic nystagmus (OKN) and vestibulo-ocular reflex (VOR) and 8) absence of stapedial reflex. Among the negative findings, 9) there were no signs of damage of the paramedian pontine reticular formation of the left side, medial longitudinal fasciculus or the abducens nerve, 10) vertical ocular movements were not impaired, 11) pure tone audiometry and auditory brainstem response were normal and 12) the facial muscles were not palsied. T2-weighted images of NMR-CT in the coronary plane revealed a horseshoe-shaped high-signal region extending bilaterally in the central area of the pons. A diagnosis of central pontine myelinolysis (CPM) was made from the clinical course and the NMR-CT findings, but the serum electrolytes were not abnormal. An alcoholic history and malnutrition might have contributed to the development of C PM in this patient. The finding that OKN and VOR were impaired only in the horizontal direction and not in the vertical direction indicates that the vertical eye movement system connecting with the vestibular nucleus (VN) is independent of the horizontal system connecting with the VN.
A 65 year-old male patient had been treated for Late cortical cerebellar atrophy (LCCA) for 7 years. His neuro-otological findings and a review of the literature on LCCA are presented in this paper. In 1985, this patient was found to have down-beat nystagmus and gaze nystagmus. Electronystagmography (ENG) showed a very abnormal pattern. His eye tracking test (ETT) showed saccadic pursuit, no optokinetic nystagmus and no visual suppression. The neuro-otological findings suggested a cerebellar lesion, although he had no neurological abnormality. In 1986, trunkal ataxia and speech disturbance appeared. MRI showed atrophy of the vermis. These findings led us to the clinical diagnosis of LCCA. It was interesting that the neuro-otological findings preceded the neurological signs. Probably the oculomotor system and the equilibrium system of this patient with LCCA are degenerating separately.
The jugular bulb is the upper part of internal jugular vein in the temporal bone. Occasionally, the jugular bulb may be high. The relationship between a high jugular bulb and various inner ear diseases has been discussed by several authors. A high jugular bulb with jugular bulb diverticulum is an extremely rare condition which is thought to affect inner ear. We describe a patient with a high jugular bulb and a jugular bulb diverticulum and discuss the relationship between this condition and inner ear disorders. A 32-year-old woman had had recurrent vertigo attacks and right tinnitus for 4 years. She did not notice any hearing impairment. She suffered a severe vertigo attack starting September 19, 1991 and was admitted to Otowa Hospital on September 27. Equilibrium function was essentially normal. Pure tone audiogram (on the right) revealed low tone sensori-neural hearing loss. The acoustic brainstem response was almost symmetrical and there was no inter-peak-latency prolongation. A right plain x-ray (Schüller) showed an ordinary sigmoid sinus plate, but CT scan revealed a high jugular bulb on the right. MR angiography demonstrated a high jugular bulb and also a jugular bulb diverticulum.
A 55-year-old female was admitted to hospital after the acute onset of vertigo similar to thet of Meniere's disease. She also complained of nausea, vomiting, left tinnitus, left hearing loss and diplopia. A right Horner's syndrome, pain and temperature loss over the right side of the face and left trunk and limbs were noted. However, she had no limb ataxia or dysarthria. Magnetic resonance imaging (MRI) demonstrated a right inferior cerebellar infarction. Ocular motor abnormalities were : skew deviation, mixed horizontal-torsional nystagmus toward the left, and upbeating vertical nystagmus. In addition, in the positional nystagmus with the right-side (damaged side) down, vertical nystagmus was directed upward, and with the left-sidedown, anticlockwise torsional nystagmus of large amplitude appeared accompanied by an intense sensation of vertigo. We attribute the nystagmus to an imbalance of central projections from the anterior and posterior semicircular canals and the otolith receptors that mediate ocular counter-roll.
Caloric nystagmus and voluntary and reflex optokinetic nystagmus (OKN) were examined in 13 elderly Japanese. The caloric test was performed with 5 ml of 20°C water, and the visual suppression test was done at the same time.In the OKN test, an Ohm-type rotating cylinder was rotated 2°/sec for 90 sec. Caloric nystagmus and OKN were analyzed with a computer and a specially designed program. In the caloric test, maximum slow phase and rapid phase velocity were evaluated. In OKN, the ocular ability to catch and follow the stripes was evaluated qualitatively from the relation between stripe movements and nystagmus waves. The number of nystagmus beats, average eye speed of the slow phase for 10 sec and average eye speed of the rapid phase for 2 degrees of amplitude were calculated quantitatively. These results were compared with those of normal younger subjects in their twenties and thirties. 1. In the caloric test, maximum slow phase velocity was decreased in only 1 person according to Uemura's criteria or in 2 persons according Midorikawa's criteria. Visual suppression was within the normal range of younger subjects, in all persons. 2. In voluntary OKN, 10 of the 13 elderly persons showed saccadic eye movements in stripe pursuit and 3 showed dysmetria in catching the stripe qualitatively. Only 1 person had a decrease in number of beats, 8 persons had decreased eyespeed of the slow phase at over 20/sec-60/sec and 3 persons had decreased eyespeed of the rapid phase quantitatively in comparison with the normal younger subjects. In reflex OKN, only a few abnormalities were revealed by qualitative and quantitative analysis. 3. The eyespeed of the rapid phase of voluntary OKN in the eledrly was significantly slower than in the younger subjects, but there was no significant difference in the eyespeed of caloric and reflex OKN.
1. Twelve ballet dancers with various levels of dancing experience and skill were examined with the visual suppression test using post-rotatory nystagmus (PRVST) and caloric stimulation (CVST). 2. The PRVST results showed a suppression rate of 80.7 %, higher than in untrained subjects. The CVST results showed a suppression rate of 80.1%, similar to that in untrained subjects. 3. A correlation between the PRVST and CVST suppression rates and length of dancing experience showed that the suppression rate increased as the level of experience and skill rose. 4. However, the CVST suppression rates in the two groups with fewer than 3 years and with 3 to 10 years of experience were close to those of untrained subjects. This is different from the PRVST supperssion rates. 5. These results indicated that the PRVST and CVST tests can aid in the clinical and quantitative assessment of the functions of the central nervous system in the visual-vestibular interaction in ballet dancers. It is also possible that we have examined the function of the vestibulo-cerebellum in a state that can be thought to be the habituation of visual-vestibular interaction. 6. It may also be possible to use the suppression rates of PRVST and CV ST to determine the approximate level of a dancer's experience and skill.
In order to determine whether thermography is useful for diagnosing abnormal autonomic nervous function (ANF) in patients with vertigo, we tested 51 patients with this procedure. Hand skin temperatures were measured bilaterally before and after ice water immersion. R-R intervals on ECG (R-R) and pulse wave velocity (PWV) were also measured to examine ANF. Thermography results were correlated with the test results, and a final diagnosis of ANF was determined. In this study, 16 patients (31 %) showed abnormal thermal findings; a useful parameter was found to be the rate of recovery of the average skin temperature. However 14 patients (27 %) with normal thermography findings were finally diagnosed as having abnormal ANF on the basis of the results of R-R and/or PWV measurements. Thus, thermography may be an abjunct diagnostic modality.
Afternystagmus, the concept of which has not yet been clearly defined, may be interpreted as a phenomenon which fits in phase II, or the reversal phase, of experimentally-induced nystagmus such as rotational or postrotational nystagmus or caloric nystagmus, in addition to optokinetic afternystagmus and its reversal phase and headshaking (after-) nystagmus including the reversal phase. A feature common to these phases of nystagmus may be the appearance of a temporary nystagmic reaction following, either immediately or after a definite interval of time (“latent period”), the elimination of an optokinetic stimulus or a physical vestibular stimulus that induces deviation of the cupula and then following the subsequent disappearance of excitement of the peripheral sensory organs, i.e., optic organ and vestibular labyrinth, that respond to these stimuli. Afternystagmus in this sense has never been generalized and the phenomenon may not actually be so simple. A panel discussion of this phenomenon and the neural mechanisms involved was held at the 51st Annual Meeting of the Japan Society for Equilibrium Research, which opened in Maebashi, Gunma prefecture on November 7, 1992
Optokinetic afternystagmus in rhesus monkeys is ususlly very active and lasts long enough for detailed analysis possible. During the course of optokinetic afternystagmus (OKAN), the axis of eyeball rotation was found to gradually change its direction in space, presumably according to a “rule.” During the course of caloric nystagmus, the axis of eyeball rotation also appeared to change the direction. Caloric afternystagmus changed its intensity with different head positions. Postrotatory and headshaking nystagmus are also under investigation. More discoveries are expected with the use of computerized three dimensional recording of eye movements. Data concerning “afternystagmus” are definitely accumulating. New concepts are required to explain the new findings.
Recent advances in vestibular physiology have led to a better appreciation of the pathophysiological significance and the clinical diagnostic implications of various types of “afternystagmus”. Afternystagmus will be defined here as a nystagmus that appears after or outlasts any stimulus that leads to a real (e.g. actual body rotation) or perceived (e.g. the feeling of self motion associated with full field optokinetic stimulation) sense of body rotation. We will first briefly review types of afternystagmus that are shown by normal subjects, and then concentrate upon an analysis of two prototypical types of “pathological” afternystagmus that can appear in patients : headshaking induced nystagmus (HSN) and periodic alternating nystagmus (PAN).
Optokinetic after-nystagmus (OKAN), which is often neglected today, is based on various pathological eye movements and occurs roughly between spontaneous and provoked nystagmus on the one hand and experimental nystagmus on the other. OKAN is not induced through an intense stimulus like caloric or rotatory nystagmus, however, so that it is of additional clinical importance besides its usefulness in the determination of subtle differences between the two sides. In this report the reaction modes of OKAN have been classified and summarized and its clinical significance is described. 1) Bárány R : Physiologie und Pathologie des Bongengansapparates beim Menschen. pp 107-142, Franz Deuticke, Leipzig and Vienna, 1907 2) Brandt T, Dichgans J, Buchele W : Motion habituation : inverted self-motion perception and optokinetic after-nystagmus. Exp. Brain Res 21 : 337-352, 1979 3) Sakata E, Nagashima C : Diagnostic evaluation of optokinetic after-nystagmus (OKAN). Otolaryngol (Tokyo) 42 : 589-596, 1970 4) Itoh A, Ohtsu K, Sakata E : Diagnostic contribution of optokinetic after nystagmus (OKAN) Eguilibrium Res 43 : 243-255, 1984
The influences of otolith input on both horizontal OKN and subsequent OKAN were examined with the use of a large-field optokinetic stimulation with constant acceleration combined with a static change of position using a tilting-bed. Eight subjects faced a f 1.5m dome-screen at a distance of 1.15m, and were tilted on their sides from an upright position to 45 and 90°. OK stimuli (4°/s2uniform, for 0 to 80°/sover 20s, or to 160°/s) were projected onto the screen 4times at each tilt position. The stimulus profile was followed immediately by 60s of darkness for OKAN recording. Pursuit tracking was examined by means of a spot oscillation in a 20° sinusoidal wave at frequencies between 0.2 and 1.0Hz. The amplitude gains were almost equal in the 5 positions. On the other hand, the slow phase optokinetic break-off point was highest in the upright position and was decreased in all the other tilt positions. Both the OKAN duration and the time-constant of its slow phase decay decreased with tilt. We conclude that otolith inputs influence OKN generation, and affect retinal nystagmus to a much greater extent than foveal nystagmus.
Afternystagmus is defined as nystagmus which persists after the cessation of stimulation of the vestibular system. Optokinetic afternystagmus (OKAN) starts when the lights for OKN are turned off. The start of caloric afternystagmus cannot be determined because the end of thermal stimulation of the inner ear cannot be determined. However, the reversal phase of caloric nystagmus (caloric second phase) is analogous to the second phase of OKAN and head shaking nystagmus II. This paper concentrates on the caloric second phase as caloric afternystagmus. Clinically applied mild thermal stimulation to the external ear rarely induces caloric second phase in normal human subjects or in patients with otogenic vertigo. In rhesus monkeys, as well as in some patients with cerebellar lesions, it elicits an active second phase of caloric nystagmus. Three dimensional eye movement recordings in rhesus monkeys revealed that the caloric second phase was inclined to move in the space horizontal plane indifferent of head positions; the torsional nystagmus was prominent in the supine and in the prone positions, vertical nystagmus was prominent in the side position, and horizontal nystagmus was prominent in the upright position. As a pure expression of “velocity storage”, yaw OKAN in the tilted position was reported to be not pure yaw nystagmus but nystagmus which was shifted in the space horizontal plane. Therefore, the second phase of caloric nystagmus is thought to be an expression of velocity storage. Horizontal caloric second phase was recorded by ENG in all 29 normal subjects when they were brought to the sitting position. These facts suggest that the testing of caloric second phase in the sitting position may give information on velocity storage in human subjects.
We developed a new type of rotatory chair system to examine vertical semicircular canal-stimulative postrotatory nystagmus in normal ears. The subjects sat on the rotatory chair with their heads and backs tilting backward 60 from the vertical line, and their heads at 30°, 45°, or 60°to the plane of rotation. The rotation was performed with an initial acceleration of 10°/sec 2 for 10 sec and a terminal acceleration of 100° or 180°/sec 2 following a period of constant velocity for 20 sec in each position with either clockwise or counter-clockwise rotation. In this position, we were able to examine isolated excitatory single canals for all four of the vertical semicircular canals. The postrotatory nystagmus was analyzed with an infrared video recording system. There were no remarkable differences in the maximum slow phase eye velocity and the duration of postrotatory nystagmus between terminal acceleration of 100°/sec 2 and that of 180°/sec 2. Moreover, there were no obvious differences in the balance of nystagmic reactions, after stimulative rotation for the anterior or posterior semicircular canal, between the left and the right sides. However, the degree of postrotatory nystagmic reaction in each posterior semicircular canal was usually much more than that in each anterior semicircular canal in most normal subjects.
The characteristics of postrotatory nystagmus primary and second phase (PRN I and PRN II), and optokinetic after nystagmus (OKAN) were investigated. The slow phase velocity time course of both PRN I and OKAN were approximated by the exponential function : V = VIexp (-T/TC) where V is slow phase velocity time course, VI, initial velocity, T, time from the initiation of after nystagmus, and TC, a time constant. VI and TC were calculated by the least square method. The slow phase velocity time course of PRN I and OKAN were well approximated by the exponential function. Although the TC of both. PRN I and OKAN increased with the increase of stimulating velocity, the increase of TC reached a plateau in high velocity stimulation. From these results we concluded that PRN I and OKAN are similar responses involved in the velocity storage mechanism. PRN II was observed in only 4 (38%) of 11 healthy subjects, but in 23 (78 %) of 28 patients with vertigo or dizziness. In 18 (78 %) of the 23, it was observed only in a unilateral direction. The duration of PRN II was in negative correlation with PRN I in the same stimulation. These results sugest that PRN II is a subliminal vestibular asymmetry developed by vestibular stimulation as head shaking nystagmus.
Head shaking nystagmus (HSN) is a pathological afternystagmus. It has been known that HSN manifests itself mainly on the basis of vestibular asymmetry. We analyzed 94 patients with vertigo of peripheral origin for the most part, in whom both bithermal caloric and horizontal head shaking stimulations were performed at the initial clinical examination. All patients had a follow-up period of at least two months with repeated head shaking tests. All nystagmus was observed with Frenzel's spectacles in darkness. The main results obtained are as follows : 1. Horizontal HSN reflects very well caloric canal paresis, but it is also subject to the influence of various factors other than canal paresis, such as presumably the directional preponderance of the vestibular system or latent spontaneous nystagmus. 2. Horizontal HSN may reverse its direction in the course of months. This occurs especially in endolymphatic hydrops, as in Meniere's disease, or in recurrent vestibular vertigo, occasionally also in patients with central lesions.
The nucleus of the optic tract (NOT) is a visuopreoculomotor relay point responsible for optokinetic nystagmus (OKN). 1) In the present experiment, the effect of NOT lesions on both the rapid and the slow rise of OKN and optokinetic after-nystagmus (OKAN) was examined in 6 fuscata monkeys. In 3 monkeys with total NOT lesions no slow rise OKN velocity or OKAN was produced towards the side of the lesion. In one of the remaining 3 monkeys with partial NOT lesions, a slow rise in OKN and OKAN slow phase velocity were selectively reduced towards the side of the lesion. In all monkeys except for one which had marked spontaneus nystagmus, the peak velocity of vestibular nystagmus was not affected after NOT lesions. These findings indicate that the dynamics of the charge of the velocity storage mechanism is influenced separately by NOT lesions : OKN and OKAN are abolished, but vestibular nystagmus remains unaffected. 2) To investigate how OKN signals descend and converge on the vestibular nucleus, biocytin was used as an anterograde tracer. The pretectofugal fibers comprised of the following three pathways : 1 The NOT-contralateral NOT. 2 The NOT-the nucleus reticularis tegmenti pontis. 3 The NOT-the inferior olive, dorsal cap. The labeled fibers descended along the medial lemniscus to the medulla with axons branching out to the dorsolateral pontine nucleus, lateral part of the nucleus reticularis tegmenti pontis, nucleus prepositus hypoglossi, medial vestibular nucleus and finally the dorsal cap of the inferior olive ipsilateral to the injection site. The NOT efferent fibers terminated in the medial vestibular nucleus which could serve to drive the storage mechanisms.
The oculomotor system uses both vestibular and visual information to stabilize images on the retina. Together, they maintain the angle of gaze when either the individual or the visual surroundings are moving. By modelling consistent with experimental data, it has been suggested that several mathematical integrations are necessary to produce the adequate gaze signal in the CNS. The velocity storage integrator holds or stores activity related to slow phase eye velocity, which is utilized in generating OKN and OKAN, and it is also responsible for producing the dominant time constant of vestibular nystagmus. Recent studies have shown that the velocity storage system has a three-dimensional structure dependent on gravity (cross-coupling). The neural circuits, however, underlying the velocity storage are still unknown. Recently, we recorded single units in the vestibular nuclei (VN) and the nucleus prepositus hypoglossi (PPH) and stimulated these sites electrically to determine the location of the neural structures associated with the various integrators. Our data suggest that there are two different integrators in the rostral medulla. One is the velocity storage integrator, which appears to lie in the VN. The other is the velocity-to-position integrator, probably closely associated with the PPH.
Questions about the characteristics of after nystagmus were raised and discussed. 1. Why is the behavior of OKN and OKAN so different in different animal species, especially between humans and monkeys ? 2. Steady firing from the labyrinth is essential for generating OKAN. The elimination of OKAN may not be welcomed from the physiological point of view. Is vestibular neurectomy for treating Meniere disease etc. therefore not recommended ? 3. The flocculus plays an important role in the generation of high speed OKAN. Is OKAN less prominent in patients with cerebellar lesions, including flocculus, than in normal subjects ? 4. Horizontal OKAN is greatly reduced under 0 G conditions created by parabolic flight. Is OKAN reduced under microgravity conditions in space ? 5. In monkeys, the velocity storage mechanism may be related to generation of the first phase of caloric nystagmus. There is some difference of caloric nystagmus direction between monkeys and human subjects, in supine and prone positions, especially in the direction of the torsional component. Is this phenomenon interpreted as species difference ? 6. The same vestibular nucleus neurons share pathways of generations of OKAN and post rotatory nystgamus. Can we conclude that the time constant of these two types of nystagmus is similar ?