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A critical question in neurology is how the brain reorganizes its structure and function following injury. Here, we consider oculomotor control following a massive brain lesion, a hemispherectomy. We used the oblique anti-saccade task which requires the suppression of a saccade towards a visual cue, flashed anywhere in a patient's seeing hemifield, and the generation, in the dark, of an anti-saccade to a task-dependent location in the opposite blind hemifield; inverting either the horizontal or both horizontal and vertical components. Anti-saccades require a visuo-motor vector inversion that normally involves bilateral interactions between frontal, parietal and subcortical structures across both hemispheres. Here, oblique anti-saccades presented a major challenge to the patient's single hemisphere, requiring one site in visual cortex to communicate with an instruction-dependent site in oculomotor cortex. Patients with discrete frontal lobe damage can be strongly impaired in anti-saccades. By contrast, hemispherectomy patients performed oblique anti-saccades normally, contrasting with their permanent contralesional hemianopia and severe hemiparesis., (Copyright © 2018 Elsevier Ltd. All rights reserved.)

During gaze shifts, the eyes and head collaborate to rapidly capture a target (saccade) and fixate it. Accordingly, models of gaze shift control should embed both saccadic and fixation modes and a mechanism for switching between them. We demonstrate a model in which the eye and head platforms are driven by a shared gaze error signal. To limit the number of free parameters, we implement a model reduction approach in which steady-state cerebellar effects at each of their projection sites are lumped with the parameter of that site. The model topology is consistent with anatomy and neurophysiology, and can replicate eye-head responses observed in multiple experimental contexts: 1) observed gaze characteristics across species and subjects can emerge from this structure with minor parametric changes; 2) gaze can move to a goal while in the fixation mode; 3) ocular compensation for head perturbations during saccades could rely on vestibular-only cells in the vestibular nuclei with postulated projections to burst neurons; 4) two nonlinearities suffice, i.e., the experimentally-determined mapping of tectoreticular cells onto brain stem targets and the increased recruitment of the head for larger target eccentricities; 5) the effects of initial conditions on eye/head trajectories are due to neural circuit dynamics, not planning; and 6) "compensatory" ocular slow phases exist even after semicircular canal plugging, because of interconnections linking eye-head circuits. Our model structure also simulates classical vestibulo-ocular reflex and pursuit nystagmus, and provides novel neural circuit and behavioral predictions, notably that both eye-head coordination and segmental limb coordination are possible without trajectory planning., (Copyright © 2016 the American Physiological Society.)

Recent studies in monkeys have identified a 'polysensory, defensive zone', in the ventral premotor cortex, stimulation of which results in coordinated multisegmental movements reminiscent of those normally produced by animals that react to head-directed threatening stimuli. Here, we describe gaze movements evoked in the head-fixed and head-unrestrained monkey by electrical stimulation of the polysensory zone. Centring eye movements were elicited at all sites and under both conditions. With the head free to move, ipsilateral head movements always accompanied evoked eye movements and carried gaze into a final steady-state position in ipsilateral body space. Our results support the hypothesis that stimulation of the polysensory zone generates avoidance behaviours in which gaze is moved away from a head-directed threatening stimulus.

Combined eye-head movements are routinely used to orient the visual axis (gaze) rapidly in space. The gaze control system can be modeled using a feedback system in which an internally created instantaneous gaze position error signal equivalent to the distance between the target and the current gaze position is used to drive brainstem eye and head motor circuits. The visual axis is driven until this gaze position error (GPE) is zero. The neural structure of the feedback system is discussed here. The midbrain's superior colliculus (SC) is implicated in gaze control but its 'location' in the feedback circuitry is debated. Our moving hill hypothesis proposed that the SC is within the feedback loop and that GPE is encoded topographically by a moving locus of activity on the motor map. In cat, fixation neurons of the superior colliculus encode GPE, which supports this model. Our preliminary evidence in both monkey and cat shows that neurons on the motor map respond to and encode, at very short latency, gaze shift perturbations. This further supports the hypothesis that the SC is within the gaze feedback loop.

A growing body of evidence supports the link between eye movement anomalies and brain health. Indeed, the oculomotor system is composed of a diverse network of cortical and subcortical structures and circuits that are susceptible to a variety of degenerative processes. Here we show preliminary findings from the baseline measurements of an ongoing longitudinal cohort study in MS participants, designed to determine if disease and cognitive status can be estimated and tracked with high accuracy based on eye movement parameters alone. Using a novel gaze-tracking technology that can reliably and accurately track eye movements with good precision without the need for infrared cameras, using only an iPad Pro embedded camera, we show in this cross-sectional study that several eye movement parameters significantly correlated with clinical outcome measures of interest. Eye movement parameters were extracted from fixation, pro-saccade, anti-saccade, and smooth pursuit visual tasks, whereas the clinical outcome measures were the scores of several disease assessment tools and standard cognitive tests such as the Expanded Disability Status Scale (EDSS), Brief International Cognitive Assessment for MS (BICAMS), the Multiple Sclerosis Functional Composite (MSFC) and the Symbol Digit Modalities Test (SDMT). Furthermore, partial least squares regression analyses show that a small set of oculomotor parameters can explain up to 84% of the variance of the clinical outcome measures. Taken together, these findings not only replicate previously known associations between eye movement parameters and clinical scores, this time using a novel mobile-based technology, but also the notion that interrogating the oculomotor system with a novel eye-tracking technology can inform us of disease severity, as well as the cognitive status of MS participants. [ABSTRACT FROM AUTHOR]

The idea that eye movements can reflect certain aspects of brain function and inform on the presence of neurodegeneration is not a new one. Indeed, a growing body of research has shown that several neurodegenerative disorders, such as Alzheimer's and Parkinson's Disease, present characteristic eye movement anomalies and that specific gaze and eye movement parameters correlate with disease severity. The use of detailed eye movement recordings in research and clinical settings, however, has been limited due to the expensive nature and limited scalability of the required equipment. Here we test a novel technology that can track and measure eye movement parameters using the embedded camera of a mobile tablet. We show that using this technology can replicate several wellknown findings regarding oculomotor anomalies in Parkinson's disease (PD), and furthermore show that several parameters significantly correlate with disease severity as assessed with the MDS-UPDRS motor subscale. A logistic regression classifier was able to accurately distinguish PD patients from healthy controls on the basis of six eye movement parameters with a sensitivity of 0.93 and specificity of 0.86. This tablet-based tool has the potential to accelerate eye movement research via affordable and scalable eye-tracking and aid with the identification of disease status and monitoring of disease progression in clinical settings. [ABSTRACT FROM AUTHOR]

Most people easily learn to recognize new faces and places, and with more extensive practice they can become experts at visual tasks as complex as radiological diagnosis and action video games. Such perceptual plasticity has been thoroughly studied in the context of training paradigms that require constant fixation. In contrast, when observers learn under more natural conditions, they make frequent saccadic eye movements. Here we show that such eye movements can play an important role in visual learning. Observers performed a task in which they executed a saccade while discriminating the motion of a cued visual stimulus. Additional stimuli, presented simultaneously with the cued one, permitted an assessment of the perceptual integration of information across visual space. Consistent with previous results on perisaccadic remapping [M. Szinte, D. Jonikaitis,M. Rolfs, P. Cavanagh, H. Deubel, J. Neurophysiol. 116, 1592–1602 (2016)], most observers preferentially integrated information from locations representing the presaccadic and postsaccadic retinal positions of the cue. With extensive training on the saccade task, these observers gradually acquired the ability to perform similar motion integration without making eye movements. Importantly, the newly acquired pattern of spatial integration was determined by the metrics of the saccades made during training. These results suggest that oculomotor influences on visual processing, long thought to subserve the function of perceptual stability, also play a role in visual plasticity. [ABSTRACT FROM AUTHOR]

Our ability to explore our surroundings requires a combination of high-resolution vision and frequent rotations of the visual axis toward objects of interest. Such gaze shifts are themselves a source of powerful retinal stimulation, and so the visual system appears to have evolved mechanisms to maintain perceptual stability during movements of the eyes in space. The mechanisms underlying this perceptual stability can be probed in the laboratory by briefly presenting a stimulus around the time of a saccadic eye movement and asking subjects to report its position. Under such conditions, there is a systematic misperception of the probes toward the saccade end point. This perisaccadic compression of visual space has been the subject of much research, but few studies have attempted to relate it to specific brain mechanisms. Here, we show that the magnitude of perceptual compression for a wide variety of probe stimuli and saccade amplitudes is quantitatively predicted by a simple heuristic model based on the geometry of retinotopic representations in the primate brain. Specifically, we propose that perisaccadic compression is determined by the distance between the probe and saccade end point on a map that has a logarithmic representation of visual space, similar to those found in numerous cortical and subcortical visual structures. Under this assumption, the psychophysical data on perisaccadic compression can be appreciated intuitively by imagining that, around the time of a saccade, the brain confounds nearby oculomotor and sensory signals while attempting to localize the position of objects in visual space. [ABSTRACT FROM AUTHOR]

In three patients who had one cortical hemisphere removed surgically (hemidecortication), we studied visually-triggered saccades directed contralateral to the intact cortical hemisphere (i.e., ipsilesional saccades). Both saccade reaction times (SRTs) and accuracy of these saccades have been reported as abnormal in hemidecorticate patients, but not monkeys. One explanation for this difference is that deficits in hemidecorticate patients may not have been directly caused by removal of cortical oculomotor structures themselves, but may have been a manifestation of compensatory strategies used to cope with contralesional hemianopia. We hypothesized that deficits in saccade performance to the ipsilesional (seeing) visual hemifield would be directly linked to how easily patients could localize targets in their blind hemifield with searching saccades. To test this hypothesis, we examined how deficits in our patients varied when targets were: (1) randomly presented to either the seeing or blind hemifield for long durations thereby permitting searching saccades in the blind hemifield; (2) presented as in Experiment 1, but briefly flashed thereby removing visual feedback prior to saccade onset thereby rendering searching saccades useless; (3) briefly flashed as in Experiment 2, but at random locations in only the seeing hemifield (blind hemifield irrelevant). Mean SRTs to the seeing hemifield were 165 ms longer than normal in Experiment 2, but only about 40 ms longer in Experiments 1 and 3. Saccade accuracy was characterized by task-dependent hypometria in all three experiments with a mean undershoot of about twice the amplitude variance. The largest undershoots were in Experiments 2 and 3. Our data suggest that deficits resulted from the direct effects of the lesions themselves coupled with context-dependent strategies used to cope with contralesional hemianopia. [ABSTRACT FROM AUTHOR]

Rapid coordinated eye- head movements, called saccadic gaze shifts, displace the line of sight from one location to another. A critical structure in the gaze control circuitry is the superior colliculus (SC) of the midbrain, which drives gaze saccades by relaying cortical commands to brainstem eye and head motor circuits. We proposed that the SC lies within a gaze feedback loop and generates an error signal specifying gaze position error (GPE), the distance between target and current gaze positions. We investigated this feedback hypothesis in cats by briefly stopping head motion during large (&asym;50°) gaze saccades made in the dark. This maneuver interrupted intended gaze saccades and briefly immobilized gaze (a plateau). After brake release, a corrective gaze saccade brought the gaze on goal. In the caudal SC, the firing frequency of a cell gradually increased to a maximum that just preceded the optimal gaze saccade encoded by the position of the cell and then declined back to zero near gaze saccade end. In brake trials, the activity level just preceding a brake-induced plateau continued steadily during the plateau and waned to zero only near the end of the corrective saccade. The duration of neural activity was stretched to reflect the increased time to target acquisition, and firing frequency during a plateau was proportional to the GPE of the plateau. In comparison, in the rostral SC, the duration of saccade-related pauses in fixation cell activity increased as plateau duration increased. The data show that the cat's SC lies in a gaze feedback loop and that it encodes GPE. [ABSTRACT FROM AUTHOR]