Slow-phase Response Research Articles

Perioperative vestibular assessment and testing

Vestibular disorders can be difficult to accurately diagnose and manage. A careful history and focused physical examination are typically adequate to establish a diagnosis and initiate medical treatment. Vestibular testing is an important component of the work-up, but it is particularly essential for patients being considered for surgical intervention for a vestibular disorder, where the testing can be used to more definitively confirm a suspected diagnosis and to determine baseline vestibular organ function. In this article, we will first briefly review key components of the history and physical examination of patients with vestibular complaints. We will then discuss the most commonly used vestibular tests and their role in the preoperative assessment of patients undergoing vestibular surgery, including nystagmography, caloric testing, rotary chair testing, video head impulse testing, and vestibular evoked myogenic potential testing.

The video head impulse test during post-rotatory nystagmus: physiology and clinical implications

The aim of this study was to test the effects of a sustained nystagmus on the head impulse response of the vestibulo-ocular reflex (VOR) in healthy subjects. VOR gain (slow-phase eye velocity/head velocity) was measured using video head impulse test goggles. Acting as a surrogate for a spontaneous nystagmus (SN), a post-rotatory nystagmus (PRN) was elicited after a sustained, constant-velocity rotation, and then head impulses were applied. 'Raw' VOR gain, uncorrected for PRN, in healthy subjects in response to head impulses with peak velocities in the range of 150°/s-250°/s was significantly increased (as reflected in an increase in the slope of the gain versus head velocity relationship) after inducing PRN with slow phases of nystagmus of high intensity (>30°/s) in the same but not in the opposite direction as the slow-phase response induced by the head impulses. The values of VOR gain themselves, however, remained in the normal range with slow-phase velocities of PRN < 30°/s. Finally, quick phases of PRN were suppressed during the first 20-160 ms of a head impulse; the time frame of suppression depended on the direction of PRN but not on the duration of the head impulse. Our results in normal subjects suggest that VOR gains measured using head impulses may have to be corrected for any superimposed SN when the slow-phase velocity of nystagmus is relatively high and the peak velocity of the head movements is relatively low. The suppression of quick phases during head impulses may help to improve steady fixation during rapid head movements.

Behavioral dissection of Drosophila larval phototaxis

A behavior generally comprises multiple processes. Analyzing these processes helps to reveal more characteristics of the behavior. In this report, light/dark choice-based Drosophila larval phototaxis is analyzed with a simplistic mathematical model to reveal a fast phase and a slow phase response that are involved. Larvae of the strain w1118, which is photophobic in phototaxis tests, prefer darkness to light in an immediate light/dark boundary passing test and demonstrate a significant reduction in motility in the dark condition during phototaxis tests. For tim01 larvae, which show neutral performance in phototaxis tests, larvae unexpectedly prefer light to darkness in the immediate light/dark boundary passing test and demonstrate no significant motility alteration in the dark condition. It is proposed that Drosophila larval phototaxis is determined by a fast phase immediate light/dark choice and an independent slow phase light/dark-induced motility alteration that follows.

Interaural Translational VOR: Suppression, Enhancement, and Cognitive Control

We investigated the influence of cognitive factors on the early response of the interaural translational vestibuloocular reflex (tVOR) in six normal subjects. Variables were prior knowledge of direction of head motion and the position of the fixation target relative to the head [head-fixed (HF) or space-fixed (SF)]. A manually driven device provided a step-like head translation (approximately 35 mm distance, peak acceleration, 0.6-1.3 g). Subjects looked at the SF or HF target located 15 cm in front of their heads in otherwise complete darkness. The testing paradigms were: random interleaving of SF and HF targets with unknown direction of head movement, known target location with random head direction (SFR or HFR), and known target location with known head direction (SFP or HFP). Timing was always unpredictable. A "gain" of the slow phase was calculated with respect to ideal performance (maintained fixation of the SF target, recorded/ideal eye velocity computed at time of peak head velocity). At such times, there were no significant differences in gain between HF and SF trials in the random condition; the average gain was approximately 36% of ideal. On the other hand, responses in the SFR and HFR conditions differed as early as 20 ms after the head began moving. Average gain was higher (0.43 +/- 0.11 vs. 0.34 +/- 0.14; means +/- SD, P < 0.05) for each subject in the SFR than the HFR condition. For SFP and HFP, the responses differed from the onset of head motion. Average slow-phase gain was higher (0.49 +/- 0.12 vs. 0.31 +/- 0.12, P < 0.02) for each subject in SFP than in HFP. The timing of corrective saccades during the tVOR was also influenced by cognitive factors. Visual error signals seemed to be more important for triggering saccades in HF trials, whereas preprogramming, probably based on labyrinthine information, seemed to be more important in SF trials. Simulations showed that the changes in slow-phase gain with cognition could be reproduced with simple parametric adjustments of the gain of activity from otolith afferents and suggest that higher-level cognitive control of the VOR could occur as early as the synapse of peripheral afferents on neurons in the vestibular nuclei, either directly from higher level centers or via the cerebellum. In sum, the tVOR-both in its slow-phase response and the saccadic corrections-is subject to "higher-level" cognitive influences including knowledge of where the line of sight must point during head motion and the impending direction of head motion.

Gaze Position Corrective Eye Movements in Normal Subjects and in Patients with Vestibular Deficits

Eye movements in response to high-acceleration head rotations (thrusts) in the horizontal plane from patients with unilateral (UVD) or bilateral vestibular loss (BVD) were recorded. The rapid, gaze-position corrections (GPCs) that appeared when vestibulo-ocular reflex (VOR) slow phases were undercompensatory were characterized. For comparison, eye movements from normal subjects who were asked to generate saccades in the direction opposite head rotation (in the same direction as slow phases) were recorded. This normal-subject model produced responses with spatial and temporal characteristics similar to those from GPCs in patients as follows: When head rotations were generated actively, compared with passively, gaze-position errors and corresponding GPCs were smaller and occurred earlier. During passively generated head thrusts, GPCs still occurred when head rotations were made in total darkness, though their accuracy decreased as the requirement for maintaining gaze on a specific location in space was relaxed. Time of onset of GPCs was not rigidly tied to head kinematics (peak velocity or peak acceleration). Speeds of GPCs, however, were lower than speeds of similar-sized, head-fixed saccades. Finally, during passive and active head thrusts in patients, sustained, high-frequency (20 to 30 Hz) oscillations that appeared as tiny saccades were occasionally observed, one immediately following the other, resembling a compensatory slow-phase response. Taken together, the results suggest that one strategy for overcoming a VOR deficit is to enlist the saccadic system to produce an oculomotor response that is required to compensate for head rotation. This response may come in the form of high-velocity GPCs or smaller-amplitude oscillations.

Abnormalities of optokinetic nystagmus in progressive supranuclear palsy

Objectives: To measure vertical and horizontal responses to optokinetic (OK) stimulation and investigate directional abnormalities of quick phases in progressive supranuclear palsy (PSP). Methods: Saccades and OK nystagmus were studied...

Vertical optokinetic nystagmus and saccades in normal human subjects.

Optokinetic stimulation induces nystagmus that can be used to test the saccadic and visual-tracking systems in some patients with voluntary gaze palsies. The purpose of this study was to characterize vertical optokinetic nystagmus (OKN) in normal human subjects, comparing the dynamic properties of the quick phases with voluntary saccades of similar size and measuring the slow-phase responses to visual stimuli with a range of spatial and temporal frequencies. Vertical OKN and saccades were recorded in 10 healthy adult subjects (age range, 24-54 years) using the magnetic search coil technique. The optokinetic (OK) stimulus subtended 72 degrees horizontally and 60 degrees vertically, consisted of black-and-white stripes with a spatial frequency of 0.04, 0.08, or 0.16 cyc/deg, and moved vertically at 10 to 50 deg/s. Vertical and horizontal saccades to visual targets separated by 1 degrees to 10 degrees were also elicited. Over 95% of quick phases were less than 10 degrees in amplitude; voluntary saccades of this amplitude range were slightly faster than quick phases of similar size. The amplitude-peak velocity relationships and amplitude-duration relationships of upward and downward fast movements (saccades or quick phases) were similar. Most vertical slow-phase OK responses showed greater gain for upward stimulus motion. OK gain decreased with increasing stimulus speed and increased spatial frequency, so that there was a general decrease in slow-phase velocity gain with increasing temporal frequency. In this study, the best OK responses were obtained using stripes with lower spatial frequencies and lower stripe speeds (0.4 cyc/deg at 10 deg/s). The dynamic properties of vertical quick phases of nystagmus are similar enough to those of voluntary saccades for OK stimulation to be used as a clinical test of the vertical saccadic system in individuals with voluntary gaze palsy.

Quinazolone-alkyl-carboxylic acid derivatives inhibit transmembrane Ca(2+) ion flux to (+)-(S)-alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid.

Comparison of the kinetics of the inward Ca(2+) ion flux to (S)-alpha-Amino-3-hydroxy-5-methylisoxazole-4-propionic acid [(S)-AMPA] in cerebrocortical homogenates and that of the previously reported transmembrane Na(+) ion influx mediated by an AMPA receptor in hippocampal homogenates established that the agonist-induced opening of the AMPA receptor channels occurs in two kinetically distinguishable phases. Here we report that the 2-methyl-4-oxo-3H-quinazoline-3-acetic acid (Q1) inhibits the major slow-phase response specifically, whereas the acetyl piperidine derivative (Q5) is a more potent inhibitor of the fast-phase response. Both the quinazolone-3-propionic acid (Q2) and the quinazolone-3-acetic acid methyl ester (Q3) enhanced the slow-phase response to (S)-AMPA. The information provided by docking different Q1, Q2, and Q5 models at the ligand-binding core of iGluRs were used to define agonistic and antagonistic modes of interactions. Based on the effects of quinazolone-3-alkyl-carboxylic acid derivatives on specific [(3)H]Glu binding and kinetically distinguishable Ca(2+) ion permeability responses to (S)-AMPA and molecular modeling, the fast- and the slow-phase (S)-AMPA-elicited Ca(2+) ion fluxes were corresponded to different subunit compositions and degrees of S1S2 bridging interaction relative to substitution of kainate thereupon. Substitutions of agonists and antagonists into the iGluR2 S1S2 ligand binding core induced different modes of domain-domain bridging.

Vestibular catch-up saccades in labyrinthine deficiency.

During rapid head rotations, saccades ipsiversive with compensatory vestibulo-ocular reflex (VOR) slow phases may augment the deficient VOR and assist gaze stabilization in space. The present experiments compared these vestibular catch-up saccades (VCUSs) with visually and memory-guided saccades. To characterize VCUSs and their relationship to deficiency of the initial VOR, we delivered random, whole-body transients of 1000 and 2800 degrees/s2 peak yaw acceleration around four different eccentric vertical axes in eight unilaterally and one bilaterally vestibulopathic subjects, as well as nine age-matched normal subjects. Eye and head movements were sampled at 1200 Hz using magnetic search coils. Subjects fixed targets at either 500 or 15 cm distance immediately before unpredictable onset of rotation in darkness. Under all testing conditions, normal subjects exhibited only compensatory vestibular slow phases and occasional anticompensatory quick phases. This behavior was also typical of unilaterally vestibulopathic subjects rotated contralesionally. When rotated ipsilesionally, however, vestibulopathic subjects had deficient slow-phase VOR gain with prolonged latency, and six of the nine exhibited saccadic movements in the compensatory direction (VCUSs). Higher head accelerations preferentially evoked VCUSs, but there were no preferred combinations of target distances and eccentric rotation axes. Peak velocities and durations of VCUSs increased with saccade amplitude. The latency distribution for VCUSs peaked around 70 ms, substantially shorter than reported for either visually guided express saccades or vestibular memory contingent saccades. The latency of each VCUS was highly correlated with the gaze error prior to that VCUS. The amplitude of VCUSs was calibrated to gaze position error, such that VCUSs reduced gaze error by an average of 37%. Thus when VOR slow-phase responses cannot compensate fully for head rotation, vestibular gaze position error can nevertheless calibrate the programming of VCUSs to augment the deficient VOR, much like catch-up saccades substitute for deficient visual pursuit.

Adaptation of primate vestibuloocular reflex to altered peripheral vestibular inputs. I. Frequency-specific recovery of horizontal VOR after inactivation of the lateral semicircular canals.

1. The adaptive plasticity of the vestibuloocular reflex (VOR) following a selective lesion of the peripheral vestibular organs was investigated in rhesus monkeys whose lateral semicircular canals were inactivated by plugging of the canal lumen in both ears. Gain and phase of horizontal, vertical, and torsional slow-phase eye velocity were determined from three-dimensional eye movement recordings obtained acutely after the plugging operation, as well as in regular intervals up to 10 mo later. 2. Acutely after plugging, horizontal VOR was minimal during yaw rotation with gains of < 0.1 at all frequencies. Horizontal VOR gain gradually increased over time, reaching gains of 0.4-0.5 for yaw oscillations at 1.1 Hz approximately 5 mo after lateral canal inactivation. This response recovery was strongly frequency dependent: horizontal VOR gains were largest at the highest frequency tested and progressively decreased for lower frequencies. Below approximately 0.1 Hz, no consistent horizontal VOR could be elicited even 10 mo after plugging. 3. The frequency-dependent changes in gain paralleled changes in horizontal VOR phase. Below approximately 0.1-0.05 Hz large phase leads were present, similarly as in semicircular canal primary afferents. Smaller phase leads were also present at higher frequencies, particularly at 1.1 Hz (the highest frequency tested). 4. Consistent with the afferent-like dynamics of the adapted horizontal VOR, per- and postrotatory horizontal responses to constant-velocity yaw rotations were short lasting. Time constants of the slow-phase eye velocity envelope of the horizontal postrotatory nystagmus were approximately 2 s. Nonetheless, a consistent horizontal optokinetic afternystagmus was evoked in plugged animals. 5. A torsional component that was absent in intact animals was consistently present during yaw rotation acutely after lateral canal inactivation and remained approximately constant thereafter. The frequency response characteristics of this torsional component resembled those of the adapted horizontal slow-phase responses: gain decreased and large phase leads were introduced at frequencies below approximately 0.05-0.1 Hz. Torsional responses elicited by roll oscillations in supine position, on the other hand, were indistinguishable in their dynamics from intact animals. No consistent vertical nystagmus was elicited during yaw rotation. 6. Our results show that there is a slow, frequency-specific recovery of horizontal VOR after selective inactivation of the lateral semicircular canals. Both the spatial organization and the dynamic properties of the adapted VOR responses are distinctly different from responses in intact animals, suggesting complex changes in the underlying vestibuloocular circuitry.

Automatic recognition of fast and slow phases in nystagmic eye movements using a neural network

This paper presents an algorithm for the automatic classification of fast and slow phases during nystagmic eye movements, using a neural network. When a patient is presented with a nonstationary visual field, the resulting eye movements may be used to determine valuable clinical information about patients with vertigo and balance disorders. When the nonstationary visual field is induced by sinusoidally rotating the patient in a chair, the eye movements—collectively referred to as nystagmus—typically consist of short, high-velocity movements (fast phases) which are in the direction of the stimulus and longer, low-velocity movements (slow phases) which are in the direction opposite to that of the stimulus. The slow phases are produced to compensate for the moving visual field. By extrapolating over the fast-phase segments, the slow-phase segments can be pieced together to form a slow-phase response. When the stimulus is sinusoidal, the slow phase response is also sinusoidal and the magnitude and phase relationships between the stimulus and response may be used to help identify the source of the patient's disorder. Thus, the ability to accurately reconstruct the response from the slow-phase segments is extremely important. This, in turn, necessitates the ability to accurately determine the locations of the fast and slow phases of nystagmus. For the neural network used here, the optimal input feature set and number of hidden units are determined, along with the necessary preprocessing of the network inputs and the postprocessing of the network output data. It is also shown that an effective error-correction algorithm can be applied to the outputs of the neural network to improve its classification ability. Finally, results are presented for the performance of the network on independent sets of test data. The classifications obtained from the neural network when applied to the test data are much more accurate than those obtained using two current classifiers: an algorithm proposed by Wall and Black and an algorithm proposed by Jell, Turnipseed and Guedry

Transient analysis of vestibular nystagmus

The significance of a nystagmus-dependent, transient component in the overall slow-phase response of the vestibulo-ocular reflex (VOR) is brought into focus. First, a simulated example is presented that shows how this transient component can bias current algorithms for the estimation of VOR parameters. Second, new algorithms are proposed that are able to estimate VOR parameters regardless of the presence of transients. Third, the new algorithms are applied to experimental data, and the results are compared with those from current algorithms. The results clearly show that the transient component can significantly alter the apparent VOR time constant, particularly when the reflex has been lesioned. The algorithms open new areas of research on the possible role of nystagmus in enhancing the compensatory function of the VOR.

Response of the electrochromic dye, merocyanine 540, to membrane potential in rat liver mitochondria

Merocyanine binds extensively to rat liver mitochondria in spite of the presence of a sulfonic acid group which would suggest only limited penetration through the membrane. Passive binding shows both tight and weak binding components and is dependent on salt concentration and ionic strength in accord with the Gouy-Chapman theory. The binding of merocyanine to mitochondria is accompanied by both a fluorescence enhancement and a spectral shift. Induction of an electrical field by either respiration or K+ diffusion potential results in a partial reversal of the spectral shift seen on dye binding. At low temperature, the merocyanine spectral response to an electrical field is biphasic, consisting of a fast phase with a t1/2 of less than 1 sec at 15 degrees C and a slower phase which may vary considerably in rate and extent with conditions. The spectral shift during the two phases appears similar, but differ in sensitivity to ionic strength and temperature. The spectral shift during the fast phase at 15 degrees C indicates that the major component is a decrease in bound monomer and an increase in the aqueous dimer, indicating an "on-off" mechanism. It is suggested that the fast and slow phases of the merocyanine response may be due to two different populations of dye, possibly located at the outer and inner surfaces, respectively, of the mitochondrial membrane. The electrophoretic movement of the dye located in the membrane interior would result in the temperature-sensitive slow phase response. Demonstration of the proportionality of the fast phase response to the magnitude of the membrane potential suggests the usefulness of merocyanine in studies with mitochondrial systems.

Adaptive plasticity in the gaze stabilizing synergy of slow and saccadic eye movements

When a normal human subject is briefly turned in total darkness while trying to "look" at a spatially fixed target, the vestibulo-ocular reflex (VOR) produces slow-phase compensatory eye movements tending to hold the eyes on target. However, slow-phase compensation per se is generally inadequate in these circumstances. Nevertheless it has recently been found, that even in the dark, this inadequacy tends to be corrected by supplementary saccades usually acting in the compensatory direction. The present study further investigates this phenomenon by measuring the respective contributions of saccadic, slow-phase and overall net compensation in 9 subjects tested before and after 30% adaptive attenuation of VOR slow-phase gain. In each test series, subjects attempted to stabilize their gaze on a previously seen target during each of 40 brief (approximately 0.5 s) whole body rotations (40 degrees/s, 20 degrees amp) conducted in complete darkness. The adaptive experience comprised 2 h of full-field visual suppression of the VOR during sinusoidal rotation of subject and surround at 1/6 Hz and 40 degrees/s velocity amplitude. Before adaptation, the cumulative slow-phase and cumulative saccadic components produced on average 78% and 14% respectively of the ideal (100%) compensation, thus yielding an overall net compensation which was 92% of the desired value. After adaptation, the corresponding values in the same population were 53%, 18% and 71% respectively. Thus after adaptation, the combined saccadic-slow-phase response brought the final gaze position to a point in space that was systematically shifted in the direction of head rotation (i.e. undercompensation). Subjects re-exposed to 30 min of normal visual-vestibular interaction displayed a variety of recovery patterns using different combinations of slow and saccadic eye movements. However, there was a consistent "synergistic" tendency for saccadic eye movements to improve slow-phase performance, regardless of the subject's adaptive state. In one subject, compensatory saccadic eye movements corrected a consistent directional asymmetry in the slow-phase response. It is suggested that a conscious vestibular percept of self-rotation might underlie the combined saccadic-slow-phase response, and that the net under performance after adaptation might reflect attenuation of this percept relative to the actual rotational stimulus.

Effects of intracellular alkalinization on resting and agonist-induced vascular tone

To evaluate the influence of intracellular alkalinization on basal and agonist-induced vascular tone, we studied the effect of NH4Cl on rat aorta. NH4Cl induced a gradually developing contraction in a dose-dependent manner. Although the contractile response to 20 mM NH4Cl was associated with a latent period (LP) of 23.4 +/- 2.8 min, intracellular pH (pHi) measurements in cultured rat aortic smooth muscle cells showed that NH4Cl-induced intracellular alkalinization was immediate and transient, returning to basal pHi levels in about 30-35 min. Agents that elevate Ca2+, such as A23187 and high KCl, significantly reduced the LP associated with 20 mM NH4Cl-induced contraction. NH4Cl-induced contractions were sensitive to extracellular Ca2+ removal and to the addition of forskolin (1 microM); however, NH4Cl by itself did not cause Ca2+-influx as shown by 45Ca-uptake studies. Addition of 20 mM NH4Cl to precontracted tissues resulted in a transient relaxation, which was complete in approximately 10 min, followed by a contraction above the original level of tone. NH4Cl pretreatment caused time-dependent alterations in both the rapid and slow phases of phenylephrine and angiotensin II contractions. Rapid-phase of phenylephrine and angiotensin II contractions. Rapid-phase responses were diminished at shorter NH4Cl incubation times (10 min), whereas slow-phase response was augmented after a longer incubation (20 min). Overall, the vasorelaxant and vasoconstrictor effects induced by NH4Cl suggest a complex relationship between intracellular alkalinization and arterial contractility.

Asymmetries of optokinetic nystagmus in amblyopia: The effect of selected retinal stimulation

Open loop optokinetic eye movements were measured in response to monocular nasalward and temporalward visual field movement presented at four selected retinal sites in 6 strabismic amblyopes and 4 normal observers. Stimulus sites included the central retina (10 × 10 deg), a large field (40 × 32 deg), a large peripheral field with the center (10 × 10 deg) blocked out and a hemiretinal field (15 × 32 deg) excluding the fovea. We found directional preferences of OKN in amblyopia to nasalward stimulus movement for the foveal and concentric peripheral stimuli. The results of peripheral hemiretinal optokinetic stimulation of amblyopic subjects revealed a deficient OKN slow phase response from the temporal hemiretina, particularly for temporalward stimulus movement. There was no marked asymmetry of OKN in the normal group for the concentric stimuli. A normal preference was found for nasalward and temporalward stimulus field movement imaged on the nasal and temporal hemiretinae respectively. These results are interpreted in terms of a model of cortical and subcortical pathways for OKN derived from comparative studies of cat and monkey.

The cat's vestibulo-ocular reflex.

1. The conscious cat's vestibulo-ocular reflex (v.o.r.) has been studied using the electro-oculogram to measure eye movements. A servomotor was used to rotate the head horizontally while the body remained stationary. 2. The frequency content of natural head movements in the cat has been determined by Fourier analysis. The fastest and most kinked head movement profiles contain frequency components of significant power extending up to 7-10 Hz. 3. The transfer function of the v.o.r. slow-phase response was measured in the frequency range 0.2-7 Hz. At 1 Hz the average gain is 0.94 with a phase lead of 3 deg. At 7 Hz the gain has only fallen to 0.81 and the phase lag is 10 deg. This indicates that the v.o.r. can compensate to a considerable degree for the high-frequency components of natural head movements. 4. Rotation of the body around a stationary head in the absence of vision does not produce a measurable neck-ocular reflex. 5. The presence or absence of fast phases has no effect on the phase lead of the v.o.r. slow-phase response at 0.2 Hz. 6. V.o.r. fast phases never occur more frequently than 4/sec. 7. Fast phases do not function merely to recentre the eyes once a slow phase has driven them to extreme orbital eccentricities. Instead, fast phases occur early on and serve to offset gaze in the same direction as the head movement.

The contrast sensitivity, spatial resolution and velocity tuning of the cat's optokinetic reflex.

1. Optokinetic nystagmus has been evoked from two cats using horizontally moving vertical grating patterns with sinusoidally modulated wave forms (mean luminance 8.5 cd/m2). Eye movements were recorded by DC electro-oculography. 2. The velocity 'tuning' of the slow phase response was measured for high-contrast (0.8) gratings with spatial frequencies ranging from 0.18 to 2.8 cycles/deg. Irrespective of spatial frequency, the gain of slow phase tracking always declined as the stimulus velocity exceeded 5-8 deg/sec. 3. The effect of variations in grating contrast on the gain of slow phase tracking was investigated for spatial frequencies ranging from 0.04 to 2.8 cycles/deg. These gratings always moved at a velocity of 3 deg/sec. Reductions in grating contrast produced a fall in the gain of slow phase tracking. At any given contrast, the extent of the fall in gain depended on spatial frequency. At no value of spatial frequency was an optokinetic response demonstrable when the contrast fell below 0.02. 4. The above results have been used to derive the threshold contrast for evoking an optokinetic response at each spatial frequency tested. A contrast sensitivity function is plotted from these threshold contrasts, and this is compared with previous estimates of the cat's contrast sensitivity function derived from measurements of visual discrimination and cortical evoked potentials.

Analysis of the biphasic optokinetic response in the crab Carcinus meanas

Steplike displacements of a striped pattern elicit biphasic optokinetic responses in the crab Carcinus maenas. Both the first fast phase and the second slow phase response are caused by interactions between adjacent ommatidia. The analysis of the influence of the pattern contrast revealed that both phases can only be identified by means of their time courses. On the basis of the correlation model for movement perception experiments are deviced to elicit both phases separately. For this purpose the presentation time of the pattern prior to and the duration of the interruption of the presentation during steplike displacement had to be varied, respectively, without changing the background illumination. The experimental results verified the assumption that two independent processes underlie the two phases of the response. The contribution of both subsystems to the response can be calculated according to the correlation model. Computer simulations of the step responses under closed loop conditions describe the experimental data well. The relation between step responses and responses to uniform motion of a striped pattern are discussed.