Mark Nawrot

Vision and cognition in Alzheimer's disease.

Alzheimers disease (AD) is known to affect visual pathways, but potential concomitant effects on vision and cognitive performance are not well understood. We studied 43 individuals with AD of mild severity and 22 individuals without dementia on a battery of tests designed to measure multiple aspects of basic and higher-order visual perception and cognition. All subjects performed on the same visual and cognitive test batteries. The results showed no differences between groups on tests of static visual acuity, stereoacuity, dynamic visual acuity or motion direction discrimination. However, individuals with AD performed significantly worse on tests of static spatial contrast sensitivity, visual attention, shape-from-motion, color, visuospatial construction and visual memory. Correlation analyses showed strong relationships between visual and cognitive scores. The findings show that AD affects several aspects of vision and are compatible with the hypothesis that visual dysfunction in AD may contribute to performance decrements in other cognitive domains. The pattern of involvement indicates that AD affects multiple visual neural pathways and regions. It is possible that better understanding of vision-related dysfunction could aid diagnosis and interventions to improve functional capacity in patients with dementia.

Assimilation and contrast in motion perception: explorations in cooperativity.

Motions within one region of the field influence motion seen elsewhere. To explore this phenomenon we used cinematograms comprised of alternating strips within which dots (i) tended to move in one direction, or (ii) moved in random directions (dynamic noise). When alternating strips were narrow, motion in one direction induced a similar direction of illusory motion in the adjoining dynamic noise (assimilation); when alternating strips were wide, motion tended to induce an illusory opposed motion in the dynamic noise (contrast). Since this illusory motion exhibits hysteresis, it probably results from spatially distributed, cooperative processes. The shift from assimilation to contrast, as the cinematograms strips increase in size, suggests that facilitatory and inhibitory influences of the network extend over different distances.

The interplay between stereopsis and structure from motion

In a series of psychophysical experiments, an adaptation paradigm was employed to study the influence of stereopsis on perception of rotation in an ambiguous kinetic depth (KD) display. Without prior adaptation or stereopsis, a rotating globe undergoes spontaneous reversals in perceived direction of rotation, with successive durations of perceived rotation being random variables. Following 90 sec of viewing a stereoscopic globe undergoing unambiguous rotation, the KD globe appeared to rotate in a direction opposite that experienced during the stereoscopic adaptation period. This adaptation aftereffect was short-lived, and it occurred only when the adaptation and test figures stimulated the same retinal areas, and only when the adaptation and test figures rotated about the same axis. The aftereffect was just as strong when the test and adaptation figures had different shapes, as long as the adaptation figure contained multiple directions of motion imaged at different retinal disparities. Nonstereoscopic adaptation figures had no effect on the perceived direction of rotation of the ambiguous KD figure. These results imply that stereopsis and motion strongly interact in the specification of structure from motion, a result that complements earlier work on this problem.

Motion perception deficits from midline cerebellar lesions in human

Although visual motion processing is commonly thought to be mediated solely by visual cortical areas, this human lesion study suggests that the cerebellum also has a role. We found motion direction discrimination deficits in a group of patients with acute midline cerebellar lesions. Unlike normals and patients with hemispheric cerebellar lesions, these patients with midline lesions were unable to discern a global motion vector in a local stochastic motion display. This resembles the perceptual defect reported following cortical area MT lesions in primates. This motion perception deficit may result from damage to a cerebellar mechanism involved in perceptual stabilization. Disruption of this comparator mechanism is sufficient to produce a severe motion perception deficit even though cortical visual processing mechanisms are still intact.

A neural network model of kinetic depth

We propose a network model that accounts for the kinetic depth in structure from motion phenomena. Using plausible neural mechanisms, the model accounts for (1) fluctuations in perception when viewing a simple kinetic depth stimulus, (2) disambiguation of this stimulus with stereoscopic information, and (3) subsequent bias of the percept of this stimulus following stereoscopic adaptation. The model comprises two levels: a layer of monocular directionally selective motion detectors that provide input to a second layer of disparity-selective and direction-selective binocular mechanisms. The network of facilitatory and inhibitory connections between binocular mechanisms gives rise to fluctuations in network activity that mimic the fluctuations in perception of kinetic depth in the absence of disparity information. The results of a psychophysical experiment are consistent with the nature of the proposed interactions.

Eye movements provide the extra-retinal signal required for the perception of depth from motion parallax

It has been unclear whether the perception of depth from motion parallax is an entirely visual process or whether it requires extra-retinal information such as head movements, vestibular activation, or eye movements. Using a motion aftereffect and static test stimulus technique to eliminate visual cues to depth, this psychophysical study demonstrates that the visual system employs a slow eye movement signal, optokinetic response (OKR) in particular, for the unambiguous perception of depth from motion parallax. A vestibular signal, or vestibularly driven eye movement signal is insufficient for unambiguous depth from motion parallax. Removal of the OKR eye movement signal gives rise to ambiguous perceived depth in motion parallax conditions. Neurophysiological studies suggest a possible neural mechanism in medial temporal and medial superior temporal cortical neurons that are selective to depth, motion, and direction of eye movement.

MT Neurons Combine Visual Motion with a Smooth Eye Movement Signal to Code Depth-Sign from Motion Parallax

The capacity to perceive depth is critical for an observer to interact with his or her surroundings. During observer movement, information about depth can be extracted from the resulting patterns of image motion on the retina (motion parallax). Without extraretinal signals related to observer movement, however, depth-sign (near versus far) from motion parallax can be ambiguous. We previously demonstrated that MT neurons combine visual motion with extraretinal signals to code depth-sign from motion parallax in the absence of other depth cues. In that study, head translations were always accompanied by compensatory tracking eye movements, allowing at least two potential sources of extraretinal input. We now show that smooth eye movement signals provide the critical extraretinal input to MT neurons for computing depth-sign from motion parallax. Our findings demonstrate a powerful modulation of MT activity by eye movements, as predicted by human studies of depth perception from motion parallax.

The pursuit theory of motion parallax

Although motion parallax is closely associated with observer head movement, the underlying neural mechanism appears to rely on a pursuit-like eye movement signal to disambiguate perceived depth sign from the ambiguous retinal motion information [Naji, J. J., & Freeman, T. C. A. (2004). Perceiving depth order during pursuit eye movement. Vision Research, 44, 3025-3034; Nawrot, M. (2003). Eye movements provide the extra-retinal signal required for the perception of depth from motion parallax. Vision Research, 43, 1553-1562]. Here, we outline the evidence for a pursuit signal in motion parallax and propose a simple neural network model for how the pursuit theory of motion parallax might function within the visual system. The first experiment demonstrates the crucial role that an extra-retinal pursuit signal plays in the unambiguous perception of depth from motion parallax. The second experiment demonstrates that identical head movements can generate opposite depth percepts, and even ambiguous percepts, when the pursuit signal is altered. The pursuit theory of motion parallax provides a parsimonious explanation for all of these observations.

On the perceptual identity of dynamic stereopsis and kinetic depth.

This paper presents a set of experiments demonstrating novel interactions between kinetic depth (depth-from-motion) and dynamic stereopsis (depth-from-disparity). Previous research has shown that adaptation to a moving stereoscopic figure influences the subjective percept of a subsequently viewed kinetic depth figure. In this paper the interactions between kinetic depth and dynamic stereopsis are shown to be very robust and to occur in situations involving perceptual priming. It is also found that kinetic depth and dynamic stereo stimuli are indistinguishable when the stereoscopic stimulus has small, but perceptually salient, disparity. These results are consistent with the hypothesis that stimuli for kinetic depth and for dynamic stereopsis engage a common neural network.

A human visual disorder resembling area V4 dysfunction in the monkey

We surveyed a broad range of visual functions in a man who complained of abnormal color experience and inability to recognize faces following bilateral damage in the visual cortex. A lesion in his right visual cortex caused complete left visual field loss. A lesion in his left visual cortex, located entirely below the calcarine fissure, affected the vision in his remaining hemifield, the right one. Psychophysical testing showed severely defective color vision and pattern processing, but relatively normal luminance contrast detection thresholds. The finding of normal spatial contrast sensitivity and static stereopsis did not resemble a parvocellular defect of the type described in the monkey. The abilities to detect global coherent motion among noise, structure from motion and dynamic stereopsis, and to pursue moving targets showed normal motion processing at several levels. Together with normal flicker perception, these results excluded magnocellular or MT-like defects. Altogether, the findings mimic area V4 dysfunction.