Velocity Of Optokinetic Nystagmus Research Articles

前庭核中心に plaque 病変を認めた多発性硬化症2例における視運動性眼振所見の継時的検討

Electronystagmography (ENG) findings were chronologically studied through the clinical courses in two multiple sclerosis patients (1 male and 1 female, both 25 years of age). At the initial bout, they showed left facial palsy and horizontal gaze nystagmus. The MRI demonstrated a single plaque lesion around the left vestibular nuclei at the ponto-medullary junction in both cases. In ENG recordings of both cases, the slow phase velocities of optokinetic nystagmus (OKN) were severely attenuated bilaterally at onset. In contrast, the smooth pursuit was relatively preserved in both cases through their clinical courses. In several months activities of daily living had recovered to normal. In accordance with their recovery, the OKN finally improved to the normal level in both cases. The Present ENG studies showed a definite dissociation between eye movements of pursuit and optokinetic systems. In Cohen and Raphan's model, the slow phase eye velocity of OKN is comprised of two components: the “direct pathway” involving the flocculus, which is the mechanism responsible for the rapid rise in slow phase eye velocity and is also utilized in mediating ocular pursuit. The second component is the “indirect pathway” which is responsible for producing slow phase eye velocity during vestibular nystagmus, OKN, and optokinetic after-nystagmus (OKAN). A key element in the indirect pathway is velocity storage, which is closely related to the mechanism of the vestibular nuclei. Although the neural circuits that produce velocity storage remain unclear, our previous experimental studies demonstrated that microstimulation mainly in the central medial vestibular nuclei (MVN) of monkeys elicited horizontal nystagmus and after-nystagmus related to velocity storage. Furthermore, after microinjection of muscimol (a GABA-A agonist) into the stimulus effective sites in the MVN, the slow component of OKN, the dominant time constant of aVOR and OKAN transiently disappeared bilaterally. These findings suggested that the horizontal velocity storage is generated in the MVN. The results of our present ENG studies were quite coincident with those of our previous experimental studies. Consequently, in both cases in the present study, it was assumed that the “indirect pathway” was transiently disturbed by the plaque lesion around the VN. In addition, two important points were particularly emphasized. First, the neural networks related to the horizontal velocity storage should be situated at the restricted area of the MVN, mainly the central MVN. Second, a single unilateral vestibular lesion caused a deficit in the horizontal velocity storage in both directions, in a similar manner to the results of studies in the MVN on a single experimental lesion. In conclusion, the findings of the present study and previous studies suggest that the horizontal velocity storage is generated in similar neural circuits of the human vestibular nuclei.

脊髄小脳失調症3型 (Machado-Joseph 病) における神経耳科学的所見

In recent years, a definitive diagnosis of spinocerebellar ataxia type 3, also known as Machado-Joseph disease (SCA3/MJD), has become possible at an early stage with the development of a gene analysis method. We retrospectively investigated the otoneurological findings of 56 patients (male, 23 patients; female, 33 patients) who had been definitively diagnosed as having SCA3/MJD by gene information retrieval at Tokyo Metropolitan Neurological Hospital. In SCA3/MJD patients, the incidence of abnormal oto-neurological findings, e.g., upgaze palsy, gaze nystagmus, impaired optokinetic nystagmus (OKN), smooth pursuit, and saccade, reduced bilateral vestibulo-ocular reflex (VOR), and impaired visual suppression of VOR, was high. 12 of 56 patients had horizontal gaze palsy, so that those 12 cases were excluded from the later investigation. The reduced bilateral VOR performed by caloric response with cold and/or iced water was observed in 31 of 56 ears within six years of the disease; however, it was observed in all 32 ears of patients who had developed SCA3/MJD more than six years previously. Therefore, reduced bilateral VOR is considered to be a very useful biomarker of SCA3/MJD in clinical diagnosis, especially at six years or more since the onset of the disease. Moreover, the otoneurological findings in the markedly reduced VOR group (six patients) and normal VOR group (six patients) within six years after onset of the disease was investigated. In the markedly reduced VOR group, the incidence of upgaze palsy was higher, the impaired visual suppression of VOR was more advanced, and the mean maximum slow phase velocity of OKN was lower in comparison with the normal VOR group. It could indicate that the brainstem dysfunctions were more severe in the markedly reduced VOR group than in the normal VOR group. This may account for the fact that the bilateral VOR dysfunction in patients with SCA3/MJD may be due to a disorder in the central vestibular system originating from the VOR pathways.

Isolating the Effects of Vection and Optokinetic Nystagmus on Optokinetic Rotation-Induced Motion Sickness

This study investigates isolated effects of vection and optokinetic nystagmus (OKN) on visually induced motion sickness (VIMS) provoked by rotating optokinetic drum patterns. VIMS was the subject of recent standardization activities, but the effects of OKN have not been studied in the absence ofvection. Experiment 1 suppressed OKN by eye fixation and examined VIMS severity (both ordinal and ratio scale) and time spent in saturated vection at four pattern rotating velocities of 0, 2, 14, and 34 degrees per second (dps). Experiment 2 suppressed vection by adding a peripheral visual field rotating in the opposite direction to the rotating patterns. VIMS severity and OKN slow-phase velocity were studied at four rotating velocities of 0, 30, 60, and 90 dps. Results from Experiment 1 indicated that VIMS severity increased as the pattern velocity increased from 0 dps to 34 dps. Results from Experiment 2 indicated that as the velocity of the rotating pattern increased, the slow-phase velocity of OKN and the severity of VIMS increased and peaked in the 60-dps condition. In both experiments, ratio-scaled nausea data significantly correlated with ordinal-scaled nausea ratings. VIMS can still occur in the absence of either vection or OKN. Interestingly, the profile of the summed results of the two experiments matches nicely with the profile reported by Hu et al. in which neither OKN nor vection were controlled. Potential applications include modeling and reduction of VIMS in computer gaming environments.

めまいを主訴とした交通外傷後低髄液圧症候群（脳脊髄液減少症）の２症例

We herein describe two patients with cerebrospinal fluid (CSF) leakage after whiplash injuries, mainly complaining of dizziness and vertigo. After automobile rear-end collisions with whiplash injuries but without head trauma, both patients immediately suffered from headache, vertigo, dizziness, nausea, neck pain and cervico-brachialgia. Neurological examinations were normal in both patients, except for neck tenderness. The RI cisternographies revealed the early filling of bladders within 2 hours and definite CSF leakages at the cervicothoracic junction in one of the patients and at the lumbar portion in the other. The magnetic resonance (MR) images depicted downward displacement of the cerebellar tonsils and the brain stem, and narrowing of the lateral ventricles, presenting an acquired Arnold-Chiari malformation. The patients were consequently diagnosed as having the intracranial hypotension (or CSF hypovolemia) syndrome and underwent several epidural blood patch (EBP) therapies. Transiently their various symptoms improved, but were soon exacerbated once more and have continued until the present. In the electronystagmography (ENG) studies, spontaneous downward nystagmus was observed in a patient in the dark. In the eye-tracking test (ETT), the smooth pursuit was relatively preserved with a saccade superimposed. The most striking finding was that of optokinetic nystagmus (OKN). In both patients, the slow phase velocity was saturated below 60 degrees and could not hold the steady state level in response to a higher stimulus velocity. The frequency of slow phase nystagmus was remarkably reduced. In Cohen & Raphan's model, the slow phase of OKN is supposed to be composed of two components; one is the "direct pathway" which is responsible for a rapid rise. The other is the "indirect pathway" which contains the velocity storage integrator and is responsible for a slower rise and maintaining the slow phase velocity to the steady state level. Our findings suggested the deterioration of both pathways in the slow phase velocity of OKN, that is dysfunctions of the vestibulo-cerebellar interactions. In conclusion, the dizziness and vertigo in the currently reported CSF hypovolemic patients were presumed to be derived from the severe damage especially to the cerebellum and the brain stem, caused by the downward sagging of the brain structures.

Spatial orientation of optokinetic nystagmus and ocular pursuit during orbital space flight.

On Earth, eye velocity of horizontal optokinetic nystagmus (OKN) orients to gravito-inertial acceleration (GIA), the sum of linear accelerations acting on the head and body. We determined whether adaptation to micro-gravity altered this orientation and whether ocular pursuit exhibited similar properties. Eye movements of four astronauts were recorded with three-dimensional video-oculography. Optokinetic stimuli were stripes moving horizontally, vertically, and obliquely at 30 degrees/s. Ocular pursuit was produced by a spot moving horizontally or vertically at 20 degrees/s. Subjects were either stationary or were centrifuged during OKN with 1 or 0.5 g of interaural or dorsoventral centripetal linear acceleration. Average eye position during OKN (the beating field) moved into the quick-phase direction by 10 degrees during lateral and upward field movement in all conditions. The beating field did not shift up during downward OKN on Earth, but there was a strong upward movement of the beating field (9 degrees) during downward OKN in the absence of gravity; this likely represents an adaptation to the lack of a vertical 1-g bias in-flight. The horizontal OKN velocity axis tilted 9 degrees in the roll plane toward the GIA during interaural centrifugation, both on Earth and in space. During oblique OKN, the velocity vector tilted towards the GIA in the roll plane when there was a disparity between the direction of stripe motion and the GIA, but not when the two were aligned. In contrast, dorsoventral acceleration tilted the horizontal OKN velocity vector 6 degrees in pitch away from the GIA. Roll tilts of the horizontal OKN velocity vector toward the GIA during interaural centrifugation are consistent with the orientation properties of velocity storage, but pitch tilts away from the GIA when centrifuged while supine are not. We speculate that visual suppression during OKN may have caused the velocity vector to tilt away from the GIA during dorsoventral centrifugation. Vertical OKN and ocular pursuit did not exhibit orientation toward the GIA in any condition. Static full-body roll tilts and centrifugation generating an equivalent interaural acceleration produced the same tilts in the horizontal OKN velocity before and after flight. Thus, the magnitude of tilt in OKN velocity was dependent on the magnitude of interaural linear acceleration, rather than the tilt of the GIA with regard to the head. These results favor a 'filter' model of spatial orientation in which orienting eye movements are proportional to the magnitude of low frequency interaural linear acceleration, rather than models that postulate an internal representation of gravity as the basis for spatial orientation.

Effects on the optokinetic system of midline lesions in the pretectum of monkeys

The nucleus of the optic tract (NOT), an important visuo-motor relay between the retina and preoculomotor structures, is responsible for mediating horizontal optokinetic nystagmus (OKN) in monkeys, cats, rabbits and rats. In addition to its projection to the vestibular nuclei, the NOT has a prominent projection to the contralateral NOT via the posterior commissure. In order to evaluate the role of the commissural fibers between the NOTs in OKN, we cut the posterior commissure in three Macaca fuscata. The animals viewed the OKN stripes under three conditions: right eye viewing, left eye viewing, and both eyes viewing. OKN was recorded in response to counter-clockwise and clockwise stimulation at stimulus velocities of 30 degrees/s, 60 degrees/s and 90 degrees/s. After control data were gathered, the posterior commissure was transected with an operating knife. Before the animal was sacrificed, biocytin, an anterograde tracer, was injected into the left NOT in order to confirm that all of the commissural fibers had been cut. Although the midline lesions decreased the initial rapid rise and steady state OKN slow-phase velocity in all three animals, there were no directional differences observed during monocular clockwise or counter-clockwise visual stimulation to either eye. In two of the three animals, there were no significant differences in the time-constants of optokinetic after nystagmus (OKAN) after the lesion. In the remaining animal, the time-constants decreased at stimulus velocities of 30 degrees/s and 60 degrees/s. In conclusion, gain reduction in the rapid rise and steady state slow-phase velocity of OKN can be explained by removal of an excitatory signal mediated by commissural fibers to inhibitory interneurons in the contralateral NOT. However, interrupting the commissural fibers had no effect on the velocity storage mechanism, because the time-constants of OKAN mostly remained largely unchanged by the lesion.

Analysis of Optokinetic Nystagmus in Patients with Lesions on the Left Unilateral Parietal Lobe or the Entire Left Hemisphere

Optokinetic nystagmus (OKN) was studied by computer analysis in nine patients with lesions on the left unilateral parietal lobe (group A) and in five patients with lesions on the entire left hemisphere (group B), as confirmed by CAT or MRI scans. OKN stimulation and recordings were evaluated based on the optokinetic pattern (OKP). In group A, there was no directional preponderance. However, in group B, the Electronystagmography recordings showed typical asymmetry of OKP. This asymmetry was revealed by a low amplitude and a significantly impaired slow-phase eye velocity of the right OKP. Asymmetry of OKP resulted from the impaired slow-phase eye velocity of the contralateral OKN to the damaged hemisphere because of a slight change in fast-phase eye velocity.

Open-Loop and Closed-Loop Optokinetic Nystagmus (OKN) in Myasthenia Gravis and Nonmyasthenic Subjects

Optokinetic nystagmus (OKN) eye movements of myasthenia gravis (MG) and nonmyasthenic ocular palsies, and normal subjects were examined under closed-loop and open-loop conditions. The open-loop OKN condition was achieved by adding the signal of eye-movement velocity of OKN to the computer-generated signal controlling the stimulus grating moving. The OKN was recorded by means of electromagnetic search scleral coil technique. In MG patients, the open-loop gains of OKN increased significantly after the intramuscular injection of an acetylcholinesterase inhibitor, neostigmine, while the closed-loop OKN gains were not significantly changed. Both the closed-loop and open-loop OKN gains of normal subjects and nonmyasthenic patients were not increased for the administration of neostigmine. The experimental results indicated that the open-loop OKN gain could be sensitive to reflect the changes of the function of neuromuscular junction in MG patients.

サルにおける両側視索核間の投射遮断による視運動性眼振に及ぼす影響について

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.

Eye movement deficits following ibotenic acid lesions of the nucleus prepositus hypoglossi in monkeys II. Pursuit, vestibular, and optokinetic responses.

The eyes are moved by a combination of neural commands that code eye velocity and eye position. The eye position signal is supposed to be derived from velocity-coded command signals by mathematical integration via a single oculomotor neural integrator. For horizontal eye movements, the neural integrator is thought to reside in the rostral nucleus prepositus hypoglossi (nph) and project directly to the abducens nuclei. In a previous study, permanent, serial ibotenic acid lesions of the nph in three rhesus macaques compromised the neural integrator for fixation but saccades were not affected. In the present study, to determine further whether the nph is the neural substrate for a single oculomotor neural integrator, the effects of those lesions on smooth pursuit, the vestibulo-ocular reflex (VOR), vestibular nystagmus (VN), and optokinetic nystagmus (OKN) are documented. The lesions were correlated with long-lasting deficits in eye movements, indicated most clearly by the animals' inability to maintain steady gaze in the dark. However, smooth pursuit and sinusoidal VOR in the dark, like the saccades in the previous study, were affected minimally. The gain of horizontal smooth pursuit (eye movement/target movement) decreased slightly (<25%) and phase lead increased slightly for all frequencies (0.3-1.0 Hz, +/-10 degrees target tracking), most noticeably for higher frequencies (0.8-0.7 and approximately 20 degrees for 1.0-Hz tracking). Vertical smooth pursuit was not affected significantly. Surprisingly, horizontal sinusoidal VOR gain and phase also were not affected significantly. Lesions had complex effects on both VN and OKN. The plateau of per- and postrotatory VN was shortened substantially ( approximately 50%), whereas the initial response and the time constant of decay decreased slightly. The initial OKN response also decreased slightly, and the charging phase was prolonged transiently then recovered to below normal levels like the VN time constant. Maximum steady-state, slow eye velocity of OKN decreased progressively by approximately 30% over the course of the lesions. These results support the previous conclusion that the oculomotor neural integrator is not a single neural entity and that the mathematical integrative function for different oculomotor subsystems is most likely distributed among a number of nuclei. They also show that the nph apparently is not involved in integrating smooth pursuit signals and that lesions of the nph can fractionate the VOR and nystagmic responses to adequate stimuli.

Effect of body positions in human optokinetic nystagmus and optokinetic after nystagmus

We determined whether whole body tilt would shift the axis of optokinetic nystagmus (OKN) and optokinetic-after nystagmus (OKAN) induced by full-field rotation at 35 degrees/sec. Fifteen normal people were positioned upright or tilted 30 degrees, 60 degrees or 90 degrees to both sides. Stripes of 5 degrees were projected on a 10-foot dome around the subject's yaw axis. Each trial lasted 45 sec. The lights were then extinguished, and the subject remained in darkness for 30 sec, while after nystagmus (OKAN) was recorded. Horizontal and vertical eye movements were recorded by video-oculography at 60 Hz. Eye position and velocity data were stored on optic disk cartridge by use of the data acquisition system. A. OKAN: For the subject in the upright position, the OKN velocity vector was aligned with both gravity and the subject's yaw axis with two minor exceptions. When the subject was tilted, a vertical OKN component (VOKN) appeared in a majority of subjects. For all 15 subjects, the mean angle of the OKN velocity vector regravity (Vectorg) was 22.6 +/- 7.2 degrees at 30 degrees tilted position. The Vectorg were 48.5 +/- 10.3 degrees at 60 degrees tilted position, and 76.4 +/- 12.6 degrees at 90 degrees tilted position. This represented shifts of the OKN velocity vector from the body axis of 7.4 degrees, 11.5 degrees and 13.6 degrees, respectively. The horizontal OKN (HOKN) gain remained unchanged in different positions. B. OKAN: The duration of HOKAN and initial slow phase velocity (SPV) of HOKAN decreased as the body position increased from upright to 30 degrees, 60 degrees and 90 degrees tilted position, respectively. The incidence and initial SPV of VOKAN and Re-Body did not change as the body position increased from upright to 30 degrees, 60 degrees and 90 degrees tilted position, respectively. Thus, VOKN was observed during HOKN as subjects were tilted and tended to vector to gravity, but VOKAN was not always observed during horizontal OKAN when subjects were tilted.

On the Optokinetic Response During Step-Wise Changes in Stimulus Velocity in Squirrel Monkeys

In two awake untrained squirrel monkeys the horizontal optokinetic nystagmus (OKN) was studied. The goal was to quantify the buildup of the slow-phase eye movement velocity during the first two seconds and the eye movements after OKN interruption by a stationary surround. We intended to uncover possible effects of a "charged' velocity storage on eye movements at a stationary surround. Using an optokinetic drum, a paradigm was designed to create sudden changes of the pattern (within 5 ms) between appearing to be stationary or rotating. Velocity steps from zero to 14 to 73 degrees/s and back to zero could be achieved. OKN onset: 201 velocity trajectories were analyzed. The mean latency between the onset of pattern movement and the onset of slow-phase eye movements was 82.8 +/- 16.5 ms. Over a limited period the initial increase in slow-phase velocity could be approximated by a straight line. The slope was on average 103 +/- 67 degrees/s2 and did not show a significant dependency on pattern movement velocity. Eye movement velocity at the end of the linear part increased linearly with drum velocity; the slope was 0.59. After the linear range, the slow-phase velocity increased further but at slower accelerations and usually reached the final gain within the two seconds. The initial linear acceleration component is an open-loop reflex response and we conclude that closing the loop happens when about 60% of the stimulus velocity is reached. OKN-offset: The influence of a fully charged OKN velocity storage mechanism on eye movements after a sudden exposure of a stationary surround was studied in 23 trials. After OKN interruption the velocity decay commenced after an interval of 83.5 +/- 16.6 ms. On average the slope of the consecutive linear velocity decay was -195.4 +/- 83.6 degrees/s2. During 5.8 +/- 0.98 s the OKN still had some impact on the fixating eye movements. We conclude that this time represents the time for velocity storage discharging. An active process seems to control the impact of velocity storage on eye movements.

水平性視運動性後眼振の検討 Ｒｅｔｉｎａｌ Ｓｌｉｐ速度との関係

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.

ヒトの視運動性眼振に対する視連動訓練効果と機構の検討

We investigated the mechanism by which repetitive optic stimulation affects optokinetic responses. Eleven persons, physically healthy, took part in this study. The subjects were stimulated optokinetically to the right. The angular velocity of the Ohm type drum was 50 deg/sec, and the duration of the stimulation was 30 seconds. This stimulation was successively applied 5 times a day over a period of 3 weeks. Optokinetic nystagmus (OKN) was recorded with electronystagmography and analyzed with a computer. Before and during this trial, we did 2 tests every week. First, the drum was rotated with an angular acceleration of 2 deg/sec2, and optokinetic adaptation limit (OAL) was estimated. Next, the drum was rotated with an equal velocity of 40, 60 and 80 deg/sec. The initial rapid rise (IR), the maximum steady state slow phase velocity (SS) and the time constant of optokinetic afternystagmus (TC) were calculated. These items were evaluated with stimulation towards the right only in 5 subjects and with stimulation towards both the right and the left in 6 subjects.Optokinetic training produced the following results : OAL increased significantly on stimulation towards the right, but did not increase on stimulation towards the left. SS increased significantly at a velocity of 60 and 80 deg/sec in both directions. IR increased significantly on stimulation toards the right, and increased slightly on stimulation towards the left. TC decreased on stimulation towards the right. We conclude that the increase of the slow phase velocity of OKN was due mainly to the enhanced function of the pursuit system, but other factors also had a role in training effects.

Role of the dorsolateral pontine nucleus in two components of optokinetic nystagmus (OKN).

The anatomical features of the dorsolateral pontine nucleus (DLPN) implicate a role of the nucleus in the generation of smooth-pursuit eye movements. The DLPN receives convergent inputs from a variety of parieto-occipital cortical visual areas and projects its fibers to the flocculus and vermal lobules VI and VII. In addition to cortical afferent fibers, the DLPN receives descending fibers from the nucleus of the optic tract which is indicated as the first subcortical optokinetic nystagmus (OKN) relay. DLPN units respond not only to a discrete visual spot but also to large-field OKN stimuli. On the basis of the above anatomical and physiological features, OKN was investigated in 2 alert monkeys whose DLPN was physiologically identified and into which reversible lidocaine was injected. The present findings showed that a rapid rise in OKN velocity was reduced in both monkeys, whose lesions included the uppermost rostral part of the nucleus in the one monkey and the entire nucleus in the other, whereas optokinetic after-nystagmus velocity was affected only in the latter. Taken together with physiological data, the DLPN possibly shares the domain of low selectivity speed selection in OKN and does not play a main role in the generation of OKN.

Optokinetic-vestibular interaction in patients with increased gain of the vestibulo-ocular reflex.

We studied optokinetic nystagmus (OKN), optokinetic afternystagmus (OKAN) and visual-vestibular interaction in five patients with markedly elevated vestibulo-ocular reflex (VOR) gain due to cerebellar atrophy. All had impaired smooth pursuit, decreased initial slow phase velocity of OKN, and impaired ability to suppress the VOR with real or imagined targets. OKN slow phase velocity gradually built up over 25-45 s, reaching normal values for low stimulus velocities (< or = 30 deg/s). Initial velocity of OKAN was increased, but the rate of decay of OKAN was normal. These findings can be explained by models that include separate velocity storage and variable gain elements shared by the vestibular and optokinetic systems.

OKN and OKAN induced by stripe and random dot patterns

The velocity storage mechanism in optokinetic nystagmus (OKN) was studied in 50 healthy adults. We used stepwise stimulations generated by projecting stripe and numerous random dot patterns on a screen at 20, 40, 60 and 80 deg/sec. The slow-phase OKN velocity followed stripe and random dot patterns almost immediately after the onset of the stimuli at 20 deg/sec. On the other hand, it tended to gradually increase after the onset of stimuli at 60 or 80 deg/sec. This gradual increase in slow-phase eye velocity has also been observed in several animal species, such as the monkey and cat. The slow-phase velocity of the first OKAN beat was higher with the random dot pattern than with the stripe pattern regardless of stimulation velocity. The above findings indicate that OKN in man is mediated through direct and also indirect pathways as observed in animals. With random dot pattern stimulation, particularly, the indirect pathway seems to perform an important role in generating OKN and OKAN.

Pharmacological study of the chicken's monocular optokinetic nystagmus: Involvement of the ON retinal channel evidenced by the glutamatergic separation of ON and OFF pathways

The chicken's monocular optokinetic nystagmus (OKN), recorded by the magnetic search coil technique, displays a directional asymmetry, the temporal-nasal (T-N) stimulation being more efficient than the nasal-temporal (N-T) one to evoke the reflex. The intravitreal administration of APB, a glutamate agonist which selectively blocks the ON retinal channel strongly reduced the eye monocular OKN; it also induced spontaneous eye movements in the T-N direction. The intravitreal injection of PDA another glutamate analog, which reduces the OFF channel, while increasing the activity of the ON channel, induced a large increase in OKN velocity gain, especially for a N-T stimulation at the lowest drum speeds. These results indicate the main involvement of the ON retinal channel in the OKN genesis and the inhibitory effect of the OFF channel upon this oculomotor reflex.

Optokinetic nystagmus and afternystagmus in human beings: relationship to nonlinear processing of information about retinal slip

In four normal human subjects we measured eye movements during full-field optokinetic stimulation (10-220 deg/s) and determined the relationship among retinal-slip velocity (drum velocity minus slow-phase eye velocity), the slow-phase velocity of optokinetic nystagmus (OKN) and the initial value of the slow-phase velocity of optokinetic afternystagmus (OKAN) measured in darkness. OKN and OKAN were maximum (63-84 and 11-19 deg/s, respectively) when retinal slip ranged from 30-100 deg/s. For higher values of retinal slip, OKN and OKAN fell (in 3 subjects) or reached a plateau (in the fourth). The amplitude of OKAN in human beings was much less than that reported in monkeys. The shape, however, of the curve relating retinal slip to the amplitude of OKAN was similar to that of monkeys. Furthermore, in both cases the curve resembles that obtained by plotting the results of experimental recordings of neural discharge in the nucleus of the optic tract as a function of retinal slip. These results imply that the processing of visual information for generation of OKAN is similar in monkeys and human beings but that the gain of the system is much less in human beings. We also found that fixation of a small target during optokinetic stimulation nearly completely prevented the development of OKAN while fixation of a small target for short periods after optokinetic stimulation did not alter the pattern of decay of OKAN. Thus, fixation may actively prevent the coupling of visual information into the velocity-storage mechanism.

Effects of lesions of the nucleus of the optic tract on optokinetic nystagmus and after-nystagmus in the monkey

1. The nucleus of the optic tract (NOT) and the dorsal terminal nucleus (DTN) of the accessory optic system were lesioned electrolytically or with kainic acid in rhesus monkeys. When lesions involved NOT and DTN, peak velocities of optokinetic nystagmus (OKN) with slow phases toward the side of the lesion were reduced, and optokinetic after-nystagmus (OKAN) was reduced or abolished. The jump in slow phase eye velocity at the onset of OKN was smaller in most animals, but was not lost. Initially, there was spontaneous nystagmus with contralateral slow phases. OKN and OKAN with contralateral slow phases were unaffected. 2. Damage to adjacent regions had no effect on OKN or OKAN with two exceptions: 1. A vascular lesion in the MRF, medial to NOT and adjacent to the central gray matter, caused a transient loss of the initial jump in OKN. The slow rise in slow phase velocity was prolonged, but the gain of OKAN was unaffected. There was no effect after a kainic acid lesion in this region in another animal. 2. Lesions of the fiber tract in the pulvinar that inputs to the brachium of the superior colliculus caused a transient reduction in the buildup and peak velocity of OKN and OKAN. 3. In terms of a previous model (Cohen et al. 1977; Waespe et al. 1983), the findings suggest that the indirect pathway that activates the velocity storage integrator in the vestibular system to produce the slow rise in ipsilateral OKN and OKAN, lies in NOT and DTN. Activity for the rapid rise in OKN, carried in the direct pathway, is probably transmitted to the pontine nuclei and flocculus via an anatomically separate fiber pathway that lies in the MRF. A fiber tract in the pulvinar that inputs to the brachium of the superior colliculus appears to carry activity related to retinal slip from the visual cortex to NOT and DTN.