Role of irregular otolith afferents in the steady-state nystagmus during off-vertical axis rotation

1992 ◽  
Vol 68 (5) ◽  
pp. 1895-1900 ◽  
Author(s):  
D. E. Angelaki ◽  
A. A. Perachio ◽  
M. J. Mustari ◽  
C. L. Strunk
Keyword(s):  
Steady State ◽  
Vertical Axis ◽  
Dynamic Responses ◽  
Velocity Storage ◽  
Slow Phase ◽  
Otolith Organs ◽  
Galvanic Stimulation ◽  
Storage Mechanism ◽  
Velocity Storage Mechanism ◽  
Ocular Nystagmus

1. During constant velocity off-vertical axis rotations (OVAR) in the dark a compensatory ocular nystagmus is present throughout rotation despite the lack of a maintained signal from the semicircular canals. Lesion experiments and canal plugging have attributed the steady-state ocular nystagmus during OVAR to inputs from the otolith organs and have demonstrated that it depends on an intact velocity storage mechanism. 2. To test whether irregularly discharging otolith afferents play a crucial role in the generation of the steady-state eye nystagmus during OVAR, we have used anodal (inhibitory) currents bilaterally to selectively and reversibly block irregular vestibular afferent discharge. During delivery of DC anodal currents (100 microA) bilaterally to both ears, the slow phase eye velocity of the steady-state nystagmus during OVAR was reduced or completely abolished. The disruption of the steady-state nystagmus was transient and lasted only during the period of galvanic stimulation. 3. To distinguish a possible effect of ablation of the background discharge rates of irregular vestibular afferents on the velocity storage mechanism from specific contributions of the dynamic responses from irregular otolith afferents to the circuit responsible for the generation of the steady-state nystagmus, bilateral DC anodal galvanic stimulation was applied during optokinetic nystagmus (OKN) and optokinetic afternystagmus (OKAN). No change in OKN and OKAN was observed.(ABSTRACT TRUNCATED AT 250 WORDS)

The Velocity Storage Mechanism of the Optokinetic Nystagmus Under Apparent Stimulus Movements in Squirrel Monkeys

1997 ◽  
Vol 7 (6) ◽  
pp. 441-451
Author(s):  
J. Kröller ◽  
F. Behrens ◽  
V.V. Marlinsky
Keyword(s):  
Steady State ◽  
Brain Stem ◽  
Apparent Movement ◽  
Squirrel Monkeys ◽  
Constant Light ◽  
Velocity Storage ◽  
Slow Phase ◽  
Stripe Pattern ◽  
Storage Mechanism ◽  
The Brain

Experiments in two awake untrained squirrel monkeys were performed to study the velocity storage mechanism during fast rise of OKN slow phase velocity. This was done by testing the monkey’s capability to perform OKN in response to a stationary-appearing stroboscopically illuminated stripe pattern of a horizontally rotating drum. Nystagmus was initially elicited during constant illumination lasting between 0.6 and 25 s. The periodicity of the stripe pattern was 2.37°. When after the constant light the flash illumination was switched on again, two types of behavior could occur, depending on the length of the constant light interval (CLI): 1) when the CLI was shorter than a threshold value of 6.2 seconds, the OKN ceased under the flash stimulation. Then a “post-OKN” occurred that increased with the length of the CLIs, indicating that the intermittently illuminated pattern did not provoke fixation suppression of OKN aftereffects. 2) when the CLI was above threshold, the OKN continued under the flash light: it will he called “apparent movement OKN.” The threshold CLI between the type 1 and the type 2 response did not depend on drum velocities between 21.5°/s and 71.3°/s. The average gain of the apparent movement OKN was 0.83 ± 0.04; gain and stability of slow phase eye movement velocity did not deviate systematically from the usually elicited OKN. OKAN after apparent movement OKN did not deviate from OKAN after constantly illuminated moving patterns. In response to the OKN initiation by a constantly illuminated pattern up to pattern velocities of 100°/s, the OKN steady state gain was reached within the first 2 or 3 nystagmus beats. We ascribe the increase of the post-OKN with CLI and the existence of a threshold constant light interval to activity-accumulation in the common velocity-to-position integrator (velocity storage) of the brain stem. Loading of the velocity storage takes place after the OKN gain has already reached the steady-state value. Apparent movement OKN could also be elicited in guinea pigs that lack an effective smooth pursuit system. We suggest that apparent movement OKN is produced by mechanisms located in the brain stem.

Spatial orientation of postrotatory nystagmus during static roll tilt in cats

2002 ◽  
Vol 12 (1) ◽  
pp. 15-23
Author(s):  
Keiko Yasuda ◽  
Hiroaki Fushiki ◽  
Rinnosuke Wada ◽  
Yukio Watanabe
Keyword(s):  
Spatial Orientation ◽  
Vertical Axis ◽  
Longitudinal Axis ◽  
Velocity Storage ◽  
Slow Phase ◽  
Storage Mechanism ◽  
Spatial Disorientation ◽  
Acceleration And Deceleration ◽  
Eye Velocity ◽  
Roll Tilt

While the stimulation of otolith inputs reduces the duration of postrotatory nystagmus (PRN), there is still room for dialogue about the effect of static tilt on the orientation of PRN. We studied one possible influence of static roll tilt on the spatial orientation of PRN in cats. The animal was rotated about an earth-vertical axis (EVA) at a constant velocity of 100 deg/s with an acceleration and deceleration of 120 deg / s 2 . Within two seconds after stopping EVA rotation, the animal was passively tilted at 45 deg/s about its longitudinal axis by as much as ± 90 deg in steps of 15 deg. Eye movements were measured with magnetic search coils. The angle of the PRN plane and its slow phase eye velocity were measured. The time constant of PRN decreased with an increase in roll tilt. The PRN plane remained earth horizontal within a range of ± 30 deg roll tilt. Beyond this range, the velocity of PRN decreased too rapidly to measure any change in orientation. Our results indicate a spatially limited and temporally short interaction of the semicircular canal and otolith signals in the velocity storage mechanism of cat PRN. Our data, along with previous studies, suggest that different species show different solutions to the problem of the imbalance and spatial disorientation during contradictory stimuli.

Characteristics of Nystagmus Evoked by Electrical Stimulation of The Uvular/Nodular Lobules of the Cerebellum in Monkey

1992 ◽  
Vol 2 (3) ◽  
pp. 235-245
Author(s):  
S.J. Heinen ◽  
D.K. Oh ◽  
E.L. Keller
Keyword(s):  
Electrical Stimulation ◽  
Velocity Storage ◽  
Large Field ◽  
Slow Phase ◽  
Stimulus Pulse ◽  
Storage Mechanism ◽  
Velocity Storage Mechanism ◽  
Stimulus Offset ◽  
Eye Velocity ◽  
Stimulation Of

Electrical stimulation in the monkey vestibulocerebellum has previously been shown to produce ocular nystagmus, but large stimulating current values were used. Using long duration (⩽10-second) stimulus pulse trains and low current values (<50 μA), we studied the nystagmus evoked by microstimulation in the uvular/nodular regions of the cerebellum. In doing this, we found quantitative differences in the nystagmus evoked from these two regions. Stimulation of the nodulus typically produced a vigorous nystagmus with a contralateral slow phase and a prolonged afternystagmus in the same direction. In contrast, stimulation of the uvula typically produced a regular ipsilateral nystagmus pattern with a very short, if any, afternystagmus in the same direction. In addition, at some stimulation sites in the uvula we observed an adaptation in the slow phase eye velocity during the time that the stimulation remained on. This effect could result in a secondary nystagmus, with a slow phase velocity direction opposite to that first evoked by the stimulation, followed by a prolonged afternystagmus in the direction of the secondary nystagmus at stimulus offset. The nystagmus evoked by these cerebellar stimulations differs from both natural nystagmus produced by large field visual motion and from the nystagmus produced by electrical stimulation of the nucleus of the optic tract. The nystagmus produced by uvular and nodular stimulation shows a shorter latency and a more rapid slow phase eye velocity buildup. The uvula stimulations also showed a much shorter afternystagmus. Also, the same nystagmus was evoked whether the animal was in a lighted or dark surround. These characteristics and recent single-unit recording studies in the uvula seem to suggest that the uvula acts not as a direct input to the velocity storage mechanism, but instead perhaps as part of an internal regulator for balance between the bilateral vestibular nuclei which are normally part of the nystagmus response. On the other hand, the nodulus, with its prolonged afternystagmus in the same direction as the evoked nystagmus, may be involved as a part of the velocity storage mechanism.

Suppression of Optokinetic Velocity Storage in Humans by Static Tilt in Roll

1991 ◽  
Vol 1 (4) ◽  
pp. 347-355 ◽  
Author(s):  
S.H. Lafortune ◽  
D.J. Ireland ◽  
R.M. Jell
Keyword(s):  
Exponential Model ◽  
Velocity Storage ◽  
Slow Phase ◽  
Indirect Pathway ◽  
Otolith Organ ◽  
Storage Mechanism ◽  
3 Dimensional ◽  
Double Exponential ◽  
Double Exponential Model ◽  
Anterior Posterior

The effects of static tilts about the roll (anterior-posterior) axis on human horizontal optokinetic afternystagmus (HOKAN) were examined. Static tilts in roll, with subjects lying on their left side, produced significant tilt-dependent HOKAN suppression. Only the slow (indirect pathway) component time constant (1/D) of the double exponential model for human HOKAN decreased with angle of roll tilt. The effect was direction specific in that suppression occurred only following a leftward-going stimulus. These findings provide further support for the postulate that otolith-organ-mediated activity can couple to the horizontal velocity storage mechanism in humans. A slight trend towards a tilt-dependent reduction of coefficient A (initial slow phase velocity of fast component decay) was revealed, suggesting the possibility that otolith-organ-mediated activity could couple to direct (pursuit-mediated?) pathways as well. No horizontal-to-vertical cross-coupling occurred, indicating that this aspect of the 3-dimensional model for velocity storage proposed by Raphan & Cohen (1988) may not completely apply to humans.

Multisensory Integration in the Human Vestibular Velocity Storage Mechanism?

1991 ◽  
Vol 111 (sup481) ◽  
pp. 311-314
Author(s):  
Ralph Jell ◽  
Sylviane Lafortune ◽  
Gang Wei ◽  
Desmond Ireland
Keyword(s):  
Multisensory Integration ◽  
Velocity Storage ◽  
Storage Mechanism ◽  
Velocity Storage Mechanism

scholarly journals Effect of the Stimulus Duration on the Adaptation of the Optokinetic Afternystagmus

2021 ◽  
Vol 12 ◽  
Author(s):  
Jan Gygli ◽  
Fausto Romano ◽  
Christopher J. Bockisch ◽  
Nina Feddermann-Demont ◽  
Dominik Straumann ◽  
...  
Keyword(s):  
Stimulus Duration ◽  
Velocity Storage ◽  
Slow Phase ◽  
Velocity Signal ◽  
Storage Mechanism ◽  
Central Processing ◽  
Optokinetic Afternystagmus ◽  
Vestibulo Ocular Reflex ◽  
The One ◽  
Rigorous Model

Observing a rotating visual pattern covering a large portion of the visual field induces optokinetic nystagmus (OKN). If the lights are suddenly switched off, optokinetic afternystagmus (OKAN) occurs. OKAN is hypothesized to originate in the velocity storage mechanism (VSM), a central processing network involved in multi-sensory integration. During a sustained visual rotation, the VSM builds up a velocity signal. After the lights are turned off, the VSM discharges slowly, with OKAN as the neurophysiological correlate. It has been reported that the initial afternystagmus in the direction of the preceding stimulus (OKAN-I) can be followed by a reversed one (OKAN-II), which increases with stimulus duration up to 15 min. In 11 healthy adults, we investigated OKAN following optokinetic stimulus lasting 30 s, 3-, 5-, and 10-min. Analysis of slow-phase cumulative eye position and velocity found OKAN-II in only 5/11 participants. Those participants presented it in over 70% of their trials with longer durations, but only in 10% of their 30 s trials. While this confirms that OKAN-II manifests predominantly after sustained stimuli, it suggests that its occurrence is subject-specific. We also did not observe further increases with stimulus duration. Conversely, OKAN-II onset occurred later as stimulus duration increased (p = 0.02), while OKAN-II occurrence and peak velocity did not differ between the three longest stimuli. Previous studies on OKAN-I, used negative saturation models to account for OKAN-II. As these approaches have no foundation in the OKAN-II literature, we evaluated if a simplified version of a rigorous model of OKAN adaptation could be used in humans. Slow-phase velocity following the trials with 3-, 5-, and 10-min stimuli was fitted with a sum of two decreasing exponential functions with opposite signs (one for OKAN-I and one for OKAN-II). The model assumes separate mechanisms for OKAN-I, representing VSM discharge, and OKAN-II, described as a slower adaptation phenomenon. Although the fit was qualitatively imperfect, this is not surprising given the limited reliability of OKAN in humans. The estimated adaptation time constant seems comparable to the one describing the reversal of the vestibulo-ocular reflex during sustained rotation, suggesting a possible shared adaptive mechanism.

Sign in / Sign up

Export Citation Format

Share Document