Akinetopsia Research Articles

Akinetopsia in the Management of Loss

Akinetopsia in the Management of Loss

Motion perception as inconsistent

This paper offers an inconsistent model of motion perception. It was prompted by work on inconsistent motion due to Hegel and, following him, Priest. But the paper skirts Hegel's full scale idealism, by proposing that the inconsistency is with the cognitive contents of motion perception. The paper draws on work in the psychology of perception, and in the theory of inconsistency. I begin by noting the prima facie argument that temporal change threatens inconsistency, and canvassing ways in which this might be avoided. The orthodox reply to the prima facie argument is that one and the same thing can have different incompatible properties at different times. This is plausible when applied to motion in the physical world. However, applied to cognition, it can be seen that the phenomenon of phi or beta, combined with the mechanism of a Reichardt detector, lends support to one key step in the prima facie argument, namely re-identification over time. The inconsistency of the model is then seen to follow from application of the Fade Principle. Advantages of the model are stressed: including a simple explanation of the debilitating condition of akinetopsia, that is, motion blindness; and a suggestion as to how to account for the “moving now.”

Electrical Stimulation of the Human Homolog of the Medial Superior Temporal Area Induces Visual Motion Blindness

Despite tremendous advances in neuroscience research, it is still unclear how neuronal representations of sensory information give rise to the contents of our perception. One of the first and also the most compelling pieces of evidence for direct involvement of cortical signals in perception comes from electrical stimulation experiments addressing the middle temporal (MT) area and the medial superior temporal (MST) area: two neighboring extrastriate cortical areas of the monkey brain housing direction-sensitive neurons. Here we have combined fMRI with electrical stimulation in a patient undergoing awake brain surgery, to separately probe the functional significance of the human homologs, i.e., area hMT and hMST, on motion perception. Both the stimulation of hMT and hMST made it impossible for the patient to perceive the global visual motion of moving random dot patterns. Although visual motion blindness was predominantly observed in the contralateral visual field, stimulation of hMST also affected the ipsilateral hemifield. These results suggest that early visual cortex up to the stage of MT is not sufficient for the perception of global visual motion. Rather, visual motion information must be mediated to higher-tier cortical areas, including hMST, to gain access to conscious perception.

Distractor-induced blindness for orientation changes and coherent motion

The conscious perception of simple visual stimuli can be modulated by the presence of distractors. In the motion blindness paradigm, the detection of coherent motion is impaired when task-irrelevant motion distractors are presented prior to the target. Aim of this study was to examine the feature specificity of the distractor effect. For this reason, targets were either defined by motion coherence (“motion blindness”) or orientation changes (“orientation blindness”). In a series of three experiments we show that distractors have to share the feature characteristics of the target in order to reduce its detectability. However, independent inhibition sets for visual features can be activated if the targets’ characteristics are ambiguous.

What could homing pigeons tell us about navigational impairments in Alzheimer’s patients? Activational effects of odors

Navigation by path integration has been demonstrated in species as diverse as ants, homing pigeons, and humans. In a recent study of olfactory effects on path integration in young homing pigeons, we showed that birds deprived of odors during displacement to nearby release sites were disoriented, while those exposed to natural odors, or to artificial/novel odors, were homeward oriented. These findings show that olfactory input activates non-olfactory path integration systems and, in the absence of olfactory stimulation, cues normally used by young pigeons for path integration, failed to produce homeward orientation. Interestingly, in humans, olfactory dysfunction is frequently observed in patients in the early stages of Alzheimer’s disease. A large portion of those patients also exhibit a specific failure of path integration ability, including a deficit in perception of radial optic flow cues necessary for accurate heading determination (“motion blindness”). Here we suggest that loss of olfactory activation of path integrations systems could explain the navigational impairment in the early stages of Alzheimer's disease patients. Moreover, we propose that odor exposures, similar to experiments carried out with pigeons, provide a powerful non-invasive technique to determine whether deficits on olfactory activation play a significant role in this debilitating disease.

Inhibition related impairments of coherent motion perception in the attention-induced motion blindness paradigm

A striking effect of selective attention on perception of first- and second-order motion has been termed 'attention-induced motion blindness' or AMB (Sahraie et al., 2001). The AMB paradigm is based on a rapid serial visual presentation (RSVP) task and causes a severe transient impairment of the detection of coherent motion in a random dot kinematogram (RDK). The effect crucially depends on irrelevant motion intervals (distractors) prior to the motion target. To account for this phenomenon, both psychophysical and electrophysiological studies point to the existence of a post-perceptual gate operated by attentional mechanisms that limits access to the encoded motion signals by higher cortical areas. Here, we report in a first experiment that the presentation of motion distractors reduces motion sensitivity (operationalised as motion coherence threshold) which is in line with the assumption of a temporal carry-over effect of distractor inhibition. In a second experiment, we show that the rate of recovery of AMB is independent of target salience. The results of the third experiment provide evidence against the assumption that AMB is due to a shift or expansion of the 'attentional spotlight'.

The effect of perceptual load on attention-induced motion blindness: The efficiency of selective inhibition.

Recent visual marking studies have shown that the carry-over of distractor inhibition can impair the ability of singletons to capture attention if the singleton and distractors share features. The current study extends this finding to first-order motion targets and distractors, clearly separated in time by a visual cue (the letter X). Target motion discrimination was significantly impaired, a result attributed to the carry-over of distractor inhibition. Increasing the difficulty of cue detection increased the motion target impairment, as distractor inhibition is thought to increase under demanding (high load) conditions in order to maximize selection efficiency. The apparent conflict with studies reporting reduced distractor inhibition under high load conditions was resolved by distinguishing between the effects of "cognitive" and "perceptual" load.

Specifying the distractor inhibition account of attention-induced motion blindness

There is growing evidence that motion perception is modulated by visual selective attention. In the ‘attention-induced motion blindness’ paradigm the detection of coherent motion in a random dot kinematogram (RDK) is impaired in a rapid serial presentation task [Sahraie, A., Milders, M., & Niedeggen, M. (2001). Attention induced motion blindness. Vision Research, 41, 1613–1617]. The effect depends on irrelevant motion episodes (distractors) prior to the target. In this study, we show that both the number and timing of distractors affect detection performance, allowing for implications on the build-up and release of inhibition. Furthermore, we rule out the possibility that subjects falsely classify targets as distractors due to uncertainty of temporal order.

Symptoms of Akinetopsia Associated with Traumatic Brain Injury and Alzheimer's Disease

Objective: To describe two patients with symptoms of cerebral akinetopsia (or loss of motion vision) associated with traumatic brain injury (TBI) and Alzheimer's disease. Background: Symptomatic cerebral akinetopsia is defined as the conscious loss of visual motion perception due to extrastriate cortical lesions. There are only two previous clinical reports of symptomatic cerebral akinetopsia. Methods: Clinical evaluations and magnetic resonance imaging (MRI) were conducted on two patients who presented for neuro-ophthalmic consultation with complaints of loss of motion vision in the setting TBI and Alzheimer's disease. Results: Both patients reported an inability to perceive visual motion, with otherwise normal afferent visual function. Each had evidence for bilateral posterior cortical injury, with sparing of the striate cortex. Conclusions: These cases provide additional clinical evidence that damage to bilateral, extrastriate visual cortex can produce symptoms of motion blindness, and they provide the first descriptions of symptoms of cerebral akinetopsia associated with TBI and Alzheimer's disease. Furthermore, they demonstrate that bilateral dysfunction may be necessary for symptoms of motion blindness.

Central inhibition ability modulates attention-induced motion blindness

Impaired motion perception can be induced in normal observers in a rapid serial visual presentation task. Essential for this effect is the presence of motion distractors prior to the motion target, and we proposed that this attention-induced motion blindness results from high-level inhibition produced by the distractors. To investigate this, we compared the extent of the attention-induced motion blindness effect with performance on central inhibition tasks: Stroop colour naming and negative priming. A negative correlation between Stroop interference and motion performance reflected that low Stroop scores, indicative of strong inhibition ability, was associated with more severe impairments in motion perception. This association could not be explained by individual differences in fluid intelligence, task switching or response speed. Negative priming was not specifically associated with attention-induced motion blindness. The results confirm that attention can modulate motion perception and suggest that the processes involved may be shared with high-level cognitive abilities.

Thirty years of a very special visual area, Area V5.

Thirty years of a very special visual area, Area V5.

Direction-selective motion blindness after unilateral posterior brain damage.

Motion blindness (MB) is defined as the selective disturbance of visual motion perception despite intact perception of other features of the visual scene. MB is characterized by a pandirectional deficit of motion direction discrimination and is assumed to result from damage to the visual motion pathway, especially area MT/V5. However, the most characteristic feature of primate MT/V5 neurons is not their motion selectivity but their preference for one direction of motion (direction selectivity), which changes incrementally at neighbouring columns. In addition to this microscopic directional organization, studies in nonhuman and human primates suggest that single directions of motion are also coded at a more macroscopic level. We thus hypothesized that if MB in humans results from damage to direction-selective neurons in the visual motion pathway, posterior brain damage might cause MB which is direction selective, not pandirectional. The present study investigated motion direction discrimination in patients with posterior unilateral brain damage and determined separate psychophysical thresholds for the four cardinal directions. In addition, we analysed whether the direction of erroneous motion perception (i.e. the perception of right motion for upward motion) was random or showed a directional bias. We report three principal findings. First, motion direction discrimination was severely impaired in one or two directions while it was normal in the other directions. This constituted direction-selective MB. Second, MB was characterized not only by a quantitative direction-selective increase in psychophysical thresholds but also by a qualitative impairment of perceiving motion direction systematically in wrong directions. Both findings suggest that the cortical modules specialized for the perception of a single direction of motion might be larger than previously thought. Third, lesion analysis showed that unilateral damage, not only the human homologue of MT/V5 but also to parieto-occipital cortex, leads to MB.

Dog phobia in a motion-blind patient

Introduction. A prominent neurophysiological model of phobia generation holds that specific phobia might result from the uncoupling of unaware subcortical fear responses from aware cortical fear responses. Former responses are thought to be automatic and fast, providing approximate information about the external stimulus, whereas the latter responses are more controlled and allow comparison with previous experience. Since only the cortical pathway carries information available to awareness, this model also accounts for the striking irrationality of specific phobia in humans. Methods. Here, we report neuropsychological and neuro-opthalmological findings in a 41-year-old patient who developed severe dog phobia following bilateral parietal lobe damage. Results. The examinations showed a severe deficit in visual motion perception (visual motion blindness or akinetopsia) as well as spatial vision. Importantly, the patient was largely unaware of his visual deficits. Conclusion. Based on the present observation it is argued that irrational fear, as found in specific phobia, might not only result from a general uncoupling of aware cortical from unaware subcortical fear responses, but also from a functionally similar dissociation at the cortical level.

Is experimental motion blindness due to sensory suppression? An ERP approach

Recent psychophysical studies have revealed attentional modulation of visual motion perception and interest now focuses on the locus of this interaction. Using event-related brain potentials (ERPs) we examined whether transient motion blindness evoked in a dual task [ Vision Res. 41 (2001) 1613–1617] is related to a selection process occurring at the stage of sensory processing or at a higher level. In our paradigm, a particular change of colour of the fixation point cued the subject to detect a brief episode of coherent random dot motion embedded in a succession of episodes of incoherent motion. Detection of the coherent motion was significantly impaired when it occurred simultaneously with the colour cue, and recovered over the subsequent 300 ms. This functional relationship was reflected in the amplitude of a sensory, motion-evoked component (N200), and in a late positive complex (P300). However, a direct comparison of ERPs produced by stimuli that were detected or missed revealed differences only in the P300 component. These results indicate that attenuation of sensory motion processing does not account for this transient, attention-induced deficit in visual motion perception.

Attention induced motion blindness

Recent studies have shown evidence for modulation of cortical activity by attention in visual areas involved in motion processing. Behavioural effects of this modulation have only been reported for high-order, but not for luminance-based motion. We show that attentional load can even affect the perception of a first-order motion inducing a short-termed motion blindness. The detection of transient coherent motion embedded in a rapid serial visual presentation was severely impaired if colour features were to be processed simultaneously. The findings reported here show attentional requirements can affect motion perception. This effect can not be explained by motion adaptation or priming and may instead arise from the suppression of irrelevant stimuli.

Seeing Two as One: Linking Apparent Motion and Repetition Blindness

Object tokens are episodic visual representations that mediate the ability to track visual events as they move about and change over time. Multiple tokens also allow the viewer to individuate multiple instances of a single type of object. In the present study, we established a functional link for object tokens in two seemingly disparate visual phenomena: apparent motion and repetition blindness (RB). In RB, repeated items are more difficult to perceive than unrepeated items. Using displays in which two sets of alphanumeric characters streamed in opposite directions across a computer screen in apparent motion, we found increased RB for targets appearing within a single apparent motion stream, relative to targets in different apparent motion streams. The results are inconsistent with refractory period or memory retrieval accounts of RB and support the role of object tokens in both apparent motion and RB.

Evidence for a sound movement area in the human cerebral cortex.

Human listeners can localize sounds by the difference in both arrival time (phase) and loudness between the two ears. Movement of the sound source modulates these cues, and responses to moving sounds have been detected in animals in primary auditory cortex and in humans in other cortical areas. Here we show that detection of changes in the interaural phase or amplitude difference occurs through a mechanism distinct from that used to detect changes in one ear alone. Moreover, a patient with a right hemisphere stroke is unable to detect sound movement, regardless of whether it is defined by phase or by loudness cues. We propose that this deficit reflects damage to a distinct cortical area, outside the classical auditory areas, that is specialized for the detection of sound motion. The deficit is analagous to cerebral akinotopsia (motion blindness) in the visual system, and so the auditory system may, like the visual system, show localization of specialized functions to different cortical regions.

Cerebral visual motion blindness: transitory akinetopsia induced by transcranial magnetic stimulation of human area V5.

The perception of visual motion can be selectively and reversibly compromised by transcranial magnetic stimulation (TMS) of a small region of cortex, roughly 1 cm in diameter and corresponding in position to human area V5. The reversible inactivation of a small and specialized visual area which receives its predominant input from area V1 and sends a powerful return (re-entrant) input back to it allowed us to study for the first time the backward influence of area V5 on area V1. In contrast to the complete and temporary visual motion blindness which occurs during stimulation of V5, a less-prominent interference with the perception of visual motion occurs at 70-80 ms after the onset of the visual stimulus when TMS is applied to V1. Because V5 is critical for the perception of coherent motion, and because an intact re-entry of signals from V5 to V1 is essential for the conscious perception of visual motion, the results obtained with stimulation of V1 must be caused by a disruption of the re-entrant signals from V5 to V1.

CEREBRAL AKINETOPSIA (VISUAL MOTION BLINDNESS)

Cerebral akinetopsia is a syndrome in which a patient loses specifically the ability to perceive visual motion following cortical lesions outside the striate cortex. There has been only one good case of akinetopsia in the published literature. Yet that case was immediately accepted by the neurological world. In this, cerebral akinetopsia differs markedly from cerebral achromatopsia, the evidence for which was strongly contested for the better part of a century (Zeki, 1990). This article complements the one on cerebral achromatopsia, traces the history of akinetopsia and enquires into why it was so much more readily acceptable than achromatopsia.