scholarly journals Effect of Vergence on Human Ocular Following Response (OFR)

2009 ◽  
Vol 102 (1) ◽  
pp. 513-522 ◽  
Author(s):  
Anand C. Joshi ◽  
Matthew J. Thurtell ◽  
Mark F. Walker ◽  
Alessandro Serra ◽  
R. John Leigh

The human ocular following response (OFR) is a preattentive, short-latency visual-field–holding mechanism, which is enhanced if the moving stimulus is applied in the wake of a saccade. Since most natural gaze shifts incorporate both saccadic and vergence components, we asked whether the OFR was also enhanced during vergence. Ten subjects viewed vertically moving sine-wave gratings on a video monitor at 45 cm that had a temporal frequency of 16.7 Hz, contrast of 32%, and spatial frequency of 0.17, 0.27, or 0.44 cycle/deg. In Fixation/OFR experiments, subjects fixed on a white central dot on the video monitor, which disappeared at the beginning of each trial, just as the sinusoidal grating started moving up or down. We measured the change in eye position in the 70- to 150-ms open-loop interval following stimulus onset. Group mean downward responses were larger (0.14°) and made at shorter latency (85 ms) than upward responses (0.10° and 96 ms). The direction of eye drifts during control trials, when gratings remained stationary, was unrelated to the prior response. During vergence/OFR experiments, subjects switched their fixation point between the white dot at 45 cm and a red spot at 15 cm, cued by the disappearance of one target and appearance of the other. When horizontal vergence velocity exceeded 15°/s, motion of sinusoidal gratings commenced and elicited the vertical OFR. Subjects showed significantly ( P < 0.001) larger OFR when the moving stimulus was presented during convergence (group mean increase of 46%) or divergence (group mean increase of 36%) compared with following fixation. Since gaze shifts between near and far are common during natural activities, we postulate that the increase of OFR during vergence movements reflects enhancement of early cortical motion processing, which serves to stabilize the visual field as the eyes approach their new fixation point.

2008 ◽  
Vol 100 (4) ◽  
pp. 1848-1867 ◽  
Author(s):  
Sigrid M. C. I. van Wetter ◽  
A. John van Opstal

Such perisaccadic mislocalization is maximal in the direction of the saccade and varies systematically with the target-saccade onset delay. We have recently shown that under head-fixed conditions perisaccadic errors do not follow the quantitative predictions of current visuomotor models that explain these mislocalizations in terms of spatial updating. These models all assume sluggish eye-movement feedback and therefore predict that errors should vary systematically with the amplitude and kinematics of the intervening saccade. Instead, we reported that errors depend only weakly on the saccade amplitude. An alternative explanation for the data is that around the saccade the perceived target location undergoes a uniform transient shift in the saccade direction, but that the oculomotor feedback is, on average, accurate. This “ visual shift” hypothesis predicts that errors will also remain insensitive to kinematic variability within much larger head-free gaze shifts. Here we test this prediction by presenting a brief visual probe near the onset of gaze saccades between 40 and 70° amplitude. According to models with inaccurate gaze-motor feedback, the expected perisaccadic errors for such gaze shifts should be as large as 30° and depend heavily on the kinematics of the gaze shift. In contrast, we found that the actual peak errors were similar to those reported for much smaller saccadic eye movements, i.e., on average about 10°, and that neither gaze-shift amplitude nor kinematics plays a systematic role. Our data further corroborate the visual origin of perisaccadic mislocalization under open-loop conditions and strengthen the idea that efferent feedback signals in the gaze-control system are fast and accurate.


Perception ◽  
1986 ◽  
Vol 15 (5) ◽  
pp. 603-612 ◽  
Author(s):  
Michael J Wright

Adapting to a drifting grating (temporal frequency 4 Hz, contrast 0.4) in the periphery gave rise to a motion aftereffect (MAE) when the grating was stopped. A standard unadapted foveal grating was matched to the apparent velocity of the MAE, and the matching velocity was approximately constant regardless of the visual field position and spatial frequency of the adapting grating. On the other hand, when the MAE was measured by nulling with real motion of the test grating, nulling velocity was found to increase with eccentricity. The nulling velocity was constant when scaled to compensate for changes in the spatial ‘grain’ of the visual field. Thus apparent velocity of MAE is constant across the visual field, but requires a greater velocity of real motion to cancel it in the periphery. This confirms that the mechanism underlying MAE is spatially-scaled with eccentricity, but temporally homogeneous. A further indication of temporal homogeneity is that when MAE is tracked, by matching or by nulling, the time course of temporal decay of the aftereffect is similar for central and for peripheral stimuli.


2006 ◽  
Vol 95 (6) ◽  
pp. 3712-3726 ◽  
Author(s):  
Frédéric V. Barthélemy ◽  
Ivo Vanzetta ◽  
Guillaume S. Masson

Visual neurons integrate information over a finite part of the visual field with high selectivity. This classical receptive field is modulated by peripheral inputs that play a role in both neuronal response normalization and contextual modulations. However, the consequences of these properties for visuomotor transformations are yet incompletely understood. To explore those, we recorded short-latency ocular following responses in humans to large center-only and center-surround stimuli. We found that eye movements are triggered by a mechanism that integrates motion over a restricted portion of the visual field, the size of which depends on stimulus contrast and increases as a function of time after response onset. We also found evidence for a strong nonisodirectional center-surround organization, responsible for normalizing the central, driving input so that motor responses are set to their most linear contrast dynamics. Such response normalization is delayed about 20 ms relative to tracking onset, gradually builds up over time, and is partly tuned for surround orientation/direction. These results outline the spatiotemporal organization of a behavioral receptive field, which might reflect a linear integration among subpopulations of cortical visual motion detectors.


1988 ◽  
Vol 60 (3) ◽  
pp. 940-965 ◽  
Author(s):  
M. R. Dursteler ◽  
R. H. Wurtz

1. Previous experiments have shown that punctate chemical lesions within the middle temporal area (MT) of the superior temporal sulcus (STS) produce deficits in the initiation and maintenance of pursuit eye movements (10, 34). The present experiments were designed to test the effect of such chemical lesions in an area within the STS to which MT projects, the medial superior temporal area (MST). 2. We injected ibotenic acid into localized regions of MST, and we observed two deficits in pursuit eye movements, a retinotopic deficit and a directional deficit. 3. The retinotopic deficit in pursuit initiation was characterized by the monkey's inability to match eye speed to target speed or to adjust the amplitude of the saccade made to acquire the target to compensate for target motion. This deficit was related to the initiation of pursuit to targets moving in any direction in the visual field contralateral to the side of the brain with the lesion. This deficit was similar to the deficit we found following damage to extrafoveal MT except that the affected area of the visual field frequently extended throughout the entire contralateral visual field tested. 4. The directional deficit in pursuit maintenance was characterized by a failure to match eye speed to target speed once the fovea had been brought near the moving target. This deficit occurred only when the target was moving toward the side of the lesion, regardless of whether the target began to move in the ipsilateral or contralateral visual field. There was no deficit in the amplitude of saccades made to acquire the target, or in the amplitude of the catch-up saccades made to compensate for the slowed pursuit. The directional deficit is similar to the one we described previously following chemical lesions of the foveal representation in the STS. 5. Retinotopic deficits resulted from any of our injections in MST. Directional deficits resulted from lesions limited to subregions within MST, particularly lesions that invaded the floor of the STS and the posterior bank of the STS just lateral to MT. Extensive damage to the densely myelinated area of the anterior bank or to the posterior parietal area on the dorsal lip of the anterior bank produced minimal directional deficits. 6. We conclude that damage to visual motion processing in MST underlies the retinotopic pursuit deficit just as it does in MT. MST appears to be a sequential step in visual motion processing that occurs before all of the visual motion information is transmitted to the brainstem areas related to pursuit.(ABSTRACT TRUNCATED AT 400 WORDS)


2003 ◽  
Vol 3 (11) ◽  
pp. 2 ◽  
Author(s):  
B. M. Sheliga ◽  
F. A. Miles
Keyword(s):  

2019 ◽  
Vol 6 (3) ◽  
pp. 190114
Author(s):  
William Curran ◽  
Lee Beattie ◽  
Delfina Bilello ◽  
Laura A. Coulter ◽  
Jade A. Currie ◽  
...  

Prior experience influences visual perception. For example, extended viewing of a moving stimulus results in the misperception of a subsequent stimulus's motion direction—the direction after-effect (DAE). There has been an ongoing debate regarding the locus of the neural mechanisms underlying the DAE. We know the mechanisms are cortical, but there is uncertainty about where in the visual cortex they are located—at relatively early local motion processing stages, or at later global motion stages. We used a unikinetic plaid as an adapting stimulus, then measured the DAE experienced with a drifting random dot test stimulus. A unikinetic plaid comprises a static grating superimposed on a drifting grating of a different orientation. Observers cannot see the true motion direction of the moving component; instead they see pattern motion running parallel to the static component. The pattern motion of unikinetic plaids is encoded at the global processing level—specifically, in cortical areas MT and MST—and the local motion component is encoded earlier. We measured the direction after-effect as a function of the plaid's local and pattern motion directions. The DAE was induced by the plaid's pattern motion, but not by its component motion. This points to the neural mechanisms underlying the DAE being located at the global motion processing level, and no earlier than area MT.


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