Vision, illusions, and reality.
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Biomedical subjects
Publications and source records attributed to Christopher Kennard.
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Visual stimuli can both inhibit and activate motor mechanisms. In one well-known example, the latency of saccadic eye movements is prolonged in the presence of a fixation stimulus, relative to the case in which the fixation stimulus disappears before the target appears. This automatic sensory-motor effect, known as the gap effect or fixation-offset effect, has been associated with inhibitory connections within the superior colliculus (SC). Visual information is provided to the SC and other oculomotor areas, such as the frontal eye fields (FEF), mainly by the magnocellular geniculostriate pathway, and also by the retinotectal pathway. We tested whether signals in these pathways are necessary to create fixation-related inhibition, by using stimuli invisible to them. We found that such stimuli, visible only to short-wave-sensitive cones (S cones), do produce fixation-related inhibition (including when warning effects were equated). We also demonstrate that this fixation-related inhibition cannot be explained by residual activation of luminance pathways and must be caused by a route separate from that of luminance fixation signals. Thus there are at least two routes that cause fixation-related inhibition, and direct sensory input to the SC or FEF by the magnocellular or retinotectal pathways is not required. We discuss the implications that there may be both cortical and collicular mechanisms.
A cellular model of the primate retina has been developed. Unlike existing models, it incorporates spatial non-uniformities, such as the random arrangement of L and M cones, and the radial dilation with eccentricity. Based on a population of ganglion cell activities, colour-image representation is modelled with the luminance and the R-G opponent channels. The developed model reproduces experimentally known properties in temporal and spatial vision. Furthermore, spatio-temporally coupled properties such as transition from positive to negative phases in an afterimage, are recapped. In colour vision, the model can explain the insensitivity in our colour perception to the L/M cone ratio.
The functional-neuroanatomic relationship that describes the involvement of the parietal cortex in visual search was investigated using repetitive transcranial magnetic stimulation (rTMS; 10 Hz, 500 ms in duration). Twelve adult participants performed feature-based visual search for a unique letter-without eye movements-under conditions that involved manipulations of search efficiency (efficient versus inefficient) and target-selection demands (set-size: 4 versus 10). rTMS was applied over the right posterior parietal cortex at the onset of the search array for all factorial conditions (0-500 ms); stimulation was additionally administered at 500 ms post-array onset (500-1000 ms) during inefficient search (set-size 10). Stimulation over the primary sensorimotor cortex served as a within-subjects control condition, and eye movements were monitored continuously. Significant increases in reaction time were restricted to parietal stimulation during inefficient search (set-size 10), with interference observed when rTMS was administered at the onset of the search array and at 500 ms post-array onset. The early effect was confined to target-present trials and the late effect was confined to target-absent trials, which may indicate temporally dissociable parietal involvement in target detection and response-based selection and/or search termination, respectively. Error rates did not vary significantly as a function of any of the independent variables. Taken together, these results are consistent with evidence from functional magnetic resonance studies indicating that inefficient feature-based visual search requires an intact parietal cortex, and also indicate that the parietal cortex is involved in inefficient search later than has been previously reported.
Controversy surrounds the role of human medial frontal cortex in controlling actions. Although damage to this area leads to severe difficulties in spontaneously initiating actions, the precise mechanisms underlying such "volitional" deficits remain to be established. Previous studies have implicated the medial frontal cortex in conflict monitoring and the control of voluntary action, suggesting that these key processes are functionally related or share neural substrates. Here, we combine a novel behavioral paradigm with functional imaging of the oculomotor system to reveal, for the first time, a functional subdivision of the pre-supplementary motor area (pre-SMA) into anatomically distinct areas that respond exclusively to either volition or conflict. We also demonstrate that activity in the supplementary eye field (SEF) distinguishes between success and failure in changing voluntary action plans during conflict, suggesting a role for the SEF in implementing the resolution of conflicting actions. We propose a functional architecture of human medial frontal cortex that incorporates the generation of action plans and the resolution of conflict.
Right-hemisphere patients with left neglect often demonstrate abnormal visual search, re-examining stimuli to the right while ignoring those to the left. But re-fixations alone do not reveal if patients misjudge whether they have searched a location before. Here, we not only tracked the eye movements of 16 neglect patients during search, but also asked them to click a response button only when they judged they were fixating a target for the very first time. ''Re-clicking'' on previously found targets would indicate that patients erroneously respond to these as new discoveries. Lesions were mapped with high-resolution MRI. Neglect patients with damage involving the right intraparietal sulcus or right inferior frontal lobe ''re-clicked'' on previously found targets on the right at a pathological rate, whereas those with medial occipito-temporal lesions did not. For the intraparietal sulcus patients, the probability of erroneous re-clicks on an old target increased with time since first discovering it; whereas for frontal patients it was independent of search time, suggesting different underlying mechanisms in these two types of patient. Re-click deficits correlated with degree of leftward neglect, mainly due to both being severe in intraparietal cases. These results demonstrate that misjudging previously searched locations for new ones can contribute to pathological search in neglect, with potentially different mechanisms being involved in intraparietal versus inferior frontal patients. When combined with a spatial bias to the right, such deficits might explain why many neglect patients often re-examine rightward locations, at the expense of items to their left.
Homonymous visual field defects (HVFDs) are among the most common disorders that occur in brain damage, particularly after stroke. They lead to considerable disabilities, particularly with reading and visual exploration. A variety of different approaches, including optical aids and visual training techniques, have been examined for the rehabilitation of these HVFDs. Despite the considerable ingenuity that has been applied and anecdotal evidence that has accumulated, rigorously controlled trials that clearly establish efficacy of any method are lacking.
Visual orienting of attention and gaze are widely considered to be mediated by shared neural pathways, with automatic phenomena such as inhibition of return (IOR)--the bias against returning to recently visited locations--being generated via the direct pathway from retina to superior colliculus (SC). Here, we show that IOR occurs without direct access to the SC, by using a technique that employs stimuli visible only to short-wave-sensitive (S) cones. We found that these stimuli, to which the SC is blind , were quite capable of eliciting IOR, measured by traditional manual responses. Critically, however, we found that S cone stimuli did not cause IOR when saccadic eye movement responses were required. This demonstrates that saccadic IOR is not the same as traditional IOR, providing support for two separate cortical and collicular mechanisms of IOR. These findings represent a clear dissociation between visual orienting of attention and gaze.
BACKGROUND: Both oculomotor and neuropsychologic deficits have been used to support the hypothesis that schizophrenia is associated with prefrontal cortex dysfunction, but studies that have specifically investigated the relationships between these deficits have produced inconsistent findings. METHODS: We measured both smooth pursuit and antisaccade performance in a large group (n = 109) of patients with first-episode schizophrenia and a group of matched control subjects (n = 59) and investigated the relationship between performance on these tasks and performance on a range of executive tasks. We additionally explored the relationship between these variables and measures of psychopathology at presentation and duration of untreated psychosis. RESULTS: Antisaccade errors were significantly correlated with spatial working memory performance. Smooth pursuit gain did not correlate with any neuropsychologic measure. There were no reliable correlations between either oculomotor variables and measures of psychopathology and duration of untreated psychosis. CONCLUSIONS: These findings suggest that in schizophrenia working memory and antisaccade performance reflect the same abnormal prefrontal substrates and that smooth pursuit is mediated by a separate neural abnormality.
Active vision is a dynamic process involving the flexible coordination of different gaze strategies to achieve behavioral goals. Although many complex behaviors rely on an ability to efficiently switch between gaze-control strategies, few studies to date have examined mechanisms of task level oculomotor control in detail. Here, we report five experiments in which subjects alternated between conflicting stimulus-saccade mappings within a block of trials. The first experiment showed that there is no performance cost associated with switching between pro and anti saccades. However, follow-up experiments demonstrate that whenever subjects alternate between arbitrary stimulus-saccade mappings, latency costs are apparent on the first trial after a task change. More detailed analysis of switch costs showed that latencies were particularly elevated for saccades directed toward the same location that had been the target for a saccade on the preceeding trial. This saccade "inhibition of return" effect was most marked when unexpected error feedbacks cued task switches, suggesting that saccade selection processes are modulated by reward. We conclude that there are two systems for saccade control that differ in their characteristics following a task switch. The "reflexive" control system can be enabled/disabled in advance of saccade execution without incurring any performance cost. Switch costs are only observed when two or more arbitrary stimulus-saccade mappings have to be coordinated by a "symbolic" control system.
Saccades are rapid eye movements that move the line of sight between successive points of fixation; they are among the best understood of movements, possessing dynamic properties that are easily measured. Saccades have become a popular means to study motor control, cognition and memory, and are often used in conjunction with techniques such as functional imaging and transcranial magnetic stimulation. It has been possible to identify several, distinct populations of neurons, from brainstem to cerebral cortex, that contribute to behaviours ranging from reflexive glances to memorized sequences of saccades during learned tasks. This progress has led to the development of schemes for the neurobiology of saccades that imply an equivalence of a region of the brain with specific behaviours (e.g. prefrontal cortex with memory-guided saccades). In fact, multiple neuronal populations contribute to each type of saccadic behaviour, be it 'reflexive' or 'complex'. Furthermore, an important difference exists between cortical areas that encode visual stimuli or desired saccades over a population of neurons as 'place maps', and motoneurons in oculomotor, trochlear and abducens nuclei that dictate eye rotations in terms of their discharge rates. This dichotomy implies that a 'spatial-temporal transformation' of saccadic signals must occur between cerebral cortex and ocular motoneurons, to which the superior colliculus and cerebellum contribute. Consideration of such factors may broaden the value of saccades, which can be used to test a range of hypotheses, and provide a simple scheme for understanding clinical disorders of saccades; some illustrative video clips are available as supplementary material at Brain Online.
Albino mammals lacking melanin in the embryonic retinal pigment epithelium (RPE) have abnormal retinal decussation patterns at the optic chiasm: their uncrossed projections are smaller and arise from fewer, more peripheral temporal retinal ganglion cells than in con-specific wild-types. To determine whether these abnormalities generalize to nonmammalian mutants, we used anterograde and retrograde labeling methods to compare the distribution of retinal projections to the thalamus in adult normal and albino Xenopus frogs. In both pigmentation phenotypes, crossed retinal terminations covered approximately 80% of the neuropil of Bellonci (nB) and corpus geniculatum thalamicum (cgt) and uncrossed inputs occupied, respectively, approximately 75% and 25% of these two main visual centers. In the wild-type frogs and in the albinos, ganglion cells giving rise to the crossed projections were distributed throughout the retina, whereas ipsilaterally projecting cells were confined to a specific ventrotemporal retinal division. This region comprised approximately 40% of the total retinal area, was bordered by a well-defined line of decussation, and contained an average of approximately 3,000 ipsilaterally projecting ganglion cells of equivalent soma sizes in the two pigmentation phenotypes. In summary, we found no evidence of chiasmatic misrouting in the uncrossed retinothalamic projections of albino Xenopus, even though these pathways are substantial in normal frogs and share features in common with mammalian retinogeniculate projections. Our findings suggest that congenital RPE melanin deficiency results in major defects in the development of the retina and its central projections only in mammals.
Parkinson's disease patients are known to suffer loss of dopaminergic input to the rostral caudate nucleus. Recent functional magnetic resonance imaging (fMRI) studies have implicated this structure in the transformation of spatial information in memory to guide action, suggesting that memory to motor transformations may be selectively impaired in Parkinson's disease. In order to investigate this possibility we tested a group of Parkinson's disease patients (PDs) using a memory-guided pointing task. Of interest was whether patients showed reduced accuracy in the task as a function of memory load. Twelve PD patients and 13 elderly controls were asked to recall single or four step target sequences with 2 time delays (500 and 3,500 ms). In all memory-guided conditions PD patients showed increased variability in memory-guided movement end-points. This effect was not affected by delay, number of items, or the sequence familiarity. The results are consistent with increased variability in memory-motor transformations in early PD, due to dopamine depletion within the rostral caudate nucleus.
A saccade involves both a step in eye position and an obligatory shift in spatial attention. The traditional division of saccades into two types, the "reflexive" saccade made in response to an exogenous stimulus change in the visual periphery and the "voluntary" saccade based on an endogenous judgement to move gaze, is supported by lines of evidence which include the longer onset latency of the latter and the differential effects of lesions in humans and primates on each. It has been supposed that differences between the two types of saccade derive from differences in how the spatial attention shifts involved in each are processed. However, while functional imaging studies have affirmed the close link between saccades and attentional shifts by showing they activate overlapping cortical networks, attempts to contrast exogenous with endogenous ("covert") attentional shifts directly have not revealed separate patterns of cortical activation. We took the "overt" approach, contrasting whole reflexive and voluntary saccades using event-related fMRI. This demonstrated that, relative to reflexive saccades, voluntary saccades produced greater activation within the frontal eye fields and the saccade-related area of the intraparietal sulci. The reverse contrast showed reflexive saccades to be associated with relative activation of the angular gyrus of the inferior parietal lobule, strongest in the right hemisphere. The frequent involvement of the right inferior parietal lobule in lesions causing hemispatial neglect has long implicated this parietal region in an important, though as yet uncertain, role in the awareness and exploration of space. This is the first study to demonstrate preferential activation of an area in its posterior part, the right angular gyrus, during production of exogenously triggered rather than endogenously generated saccades, a finding which we propose is consistent with an important role for the angular gyrus in exogenous saccadic orienting.
PURPOSE OF REVIEW: A greater understanding of the underlying component mechanisms of normal visual search provides explanations for disturbances seen in certain neurological conditions. This review focuses on recent advances in this field which bear on the neurology of visual search in health and disease. RECENT FINDINGS: Foremost, visual search requires a normal apparatus for the application of attentional resources to the visual environment and, with that facility lost in hemispatial neglect, search becomes uselessly stuck within one portion of the field. New evidence suggests that loss of normal registration of where the eyes have been compounds the problem. Even if attention can be deployed flexibly, its parameters must be chosen strategically, in terms of saccade amplitude, size of attentional window at each fixation and search path taken. Evidence is growing that the prefrontal cortex plays a complex role in this strategic control. Rehabilitation strategies of the future may be tailored according to which component functions have been lost in different patient groups. SUMMARY: Visual search is a dominant human activity and provides not only a window into how brain function is deranged after structural damage, but also offers the prospect of an ideal modality through which to deliver future behavioural therapies. New techniques have advanced our understanding of the physiology of visual search enormously in the past few decades. The time is now ripe in which to begin to integrate these findings into our understanding of the pathophysiology and treatment prospects of neurological disorders like hemispatial neglect, hemianopia and other deficits after stroke.
We investigated the organisation of working memory processes by examining how a secondary memory task interferes with the accuracy of memory-guided saccades. A target was flashed at a random location, followed by a Kanji character. Subjects had to remember the location of the target and the Kanji character, and then they had to make a saccade towards the remembered target location. A second Kanji character was displayed and the subject had to decide if it was same or different. The performance of seven non-Kanji reader's were compared with six fluent Kanji readers in the task. Memorisation of Kanji characters was found to interfere with the accuracy of memory-guided saccades made by non-Kanji, but not by Kanji readers. These findings directly contradict accounts of working memory function which propose that spatial and visual object memory are functionally discrete.
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