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Prompted by oculomotor theories of attention, the present experiments explore the role of saccade activation in the generation of two cueing effects: exogenous capture (Experiment 1) and inhibition of return (IOR; Experiment 2). Exogenous capture is shortlived and marked by faster responding toward recently stimulated locations, whereas the longer-lasting IOR manifests as slower responding toward those locations. Within each experiment, Group A performed in a dual-task in which on most trials a peripheral target had to be identified but infrequently a central arrow probe called for an eye movement instead, while for Group B the tasks were the same except saccade trials were frequent and target identification trials were infrequent. In Experiment 1, for group A uninformative cues captured attention as measured by faster digit identification at the cued location, an effect not accompanied by saccade activation. For group B, cues generated saccade activation without capturing attention. Thus saccade activation need not accompany exogenous covert capture, and covert capture need not accompany saccade activation. In Experiment 2, group A exhibited IOR which slowed digit identification, but did not affect saccadic responding, while Group B exhibited no IOR in either digit identification or eye movement trials. This finding provides converging evidence that IOR can be dichotomized into two forms; one which delays motor production itself (Evidenced amply elsewhere, e.g., Taylor & Klein, 2000) and another which delays responding by applying inhibition at a perceptual-motor interface which can operate in independence from its motoric cousin.

Our behaviour is guided by the ability to predict future events. The predictive saccade paradigm has been shown to be a valuable tool that uses eye movements to measure the control of predictive behaviour. In this task, subjects follow a visual target that alternates or “steps” between two fixed locations at either predictable or unpredictable inter-stimulus time intervals (ISIs). Response times can be measured by subtracting the time of saccade initiation from the time of target appearance. When the ISI is predictable, saccadic reaction times (SRTs) become predictive (SRT <100ms) within 3-4 target steps, but when the ISI is unpredictable, the SRTs remain reactive to target appearance (SRT >100ms). The goal of our study was to investigate neural mechanisms controlling prediction by contrasting areas in the brain that were more active for predictive (PRED) versus reactive (REACT) saccades in young healthy adults using functional magnetic resonance imaging (fMRI). fMRI analysis revealed two distinct neural networks more recruited for REACT and PRED tasks. We observed greater activation for the REACT task compared to the PRED task in oculomotor network areas including the frontal, supplementary, parietal eye fields, dorsolateral prefrontal cortex, thalamus, and putamen. These structures are all involved with the control of saccades. We also observed greater activation for the PRED task compared to the REACT task in default network areas, including the medial prefrontal cortex, posterior cingulate cortex, inferior parietal lobule, and hippocampus. These structures are known to be involved with passive thinking when subjects are not focused on their external environments. We also observed greater activation for the PRED task in the cerebellum (crus I), which may serve as the internal clock that drives the regular rhythmic behaviour observed for predictive saccades. In summary, our findings suggest brain activation in the PRED task reflects automated and motor-timed responses, while that for the REACT task reflects externally-driven responses. Therefore, the predictive saccade task is an excellent tool for measuring prediction involving fast internally-guided responses. / Thesis (Master, Neuroscience Studies) -- Queen's University, 2011-08-12 10:21:37.744

Parkinson’s disease (PD) is associated with perceptual as well as motor disturbances. Unlike those with right-side onset (RPD), individuals whose motor symptoms begin on the left side of the body (LPD) may experience mild neglect of left hemispace. The functional cause of these perceptual abnormalities in LPD is unknown; possibilities include altered eye movements, changes in perceptual representation of left versus right hemispace, and attentional abnormalities. Three studies explored these possibilities in non-demented individuals with mild-moderate idiopathic PD (24-36 per experiment) and matched normal control adults (NC; 14-24 per experiment). Study 1 consisted of two psychophysical line-bisection experiments that used brief stimulus presentations to preclude exploratory eye movements. In both, participants judged whether a systematically adjusted hatchmark was left or rightward of a horizontal line’s midpoint. In the second, eye tracking was used to ensure that participants fixated during stimulus onset. The first experiment revealed neglect-like performance in LPD, but the second did not, suggesting that neglect may arise from biased eye gaze but not from abnormal saccades. Study 2 evaluated two hypotheses to explain spatial bias in LPD; one an active hypothesis in the literature that the representation of left hemispace is compressed, and the other a novel hypothesis that left hemispace is less salient than the right in LPD. Both hypotheses were assessed psychophysically, using spatial frequency and contrast discrimination paradigms, and neither was supported. Study 3 investigated whether endogenous visuospatial attentional abnormalities exist in PD, and particularly whether LPD show weaker attentional abilities in the left hemifield. A multiple-object tracking paradigm was used along with eye tracking to ensure that participants used only endogenous (not exogenous) attention. PD showed dilated temporal resolution of attention, and were less accurate in tracking multiple objects at once. LPD did not differ from RPD for either of these metrics. Overall the results suggest that there is no intrinsic difference in the representation of space in LPD relative to RPD or NC, but that visuospatial attention is altered in PD generally. The latter finding is particularly important for considering spatial navigation in individuals with PD even in early stages of the disease.

La esclerosis múltiple es una en enfermedad neurodegenerativa, progresiva e inflamatoria del sistema nervioso central, en la cual interaccionan dos entidades clínicas: la inflamación y la neurodegeneración. Esto implica la alteración de capacidades motoras, sensoriales y de coordinación. El sistema visual, por su amplia implicación neurológica, es una de las capacidades más afectadas en el transcurso de la enfermedad. Cuadros clínicos característicos como la neuritis óptica o la oftalmoplejía internuclear han sido ampliamente estudiados por su alta prevalencia. Otras alteraciones como el adelgazamiento de las diferentes capas retinianas, la reducción de la sensibilidad al contraste o la aparición de nistagmo también han sido sobradamente informadas. En cambio, la función binocular no ha sido objeto de tan exhaustivo estudio, probablemente por la porque la sintomatología asociada a un problema binocular no se manifiesta de forma tan grave o incapacitante como en otras capacidades motoras, sensoriales y/o de coordinación. O porque, anomalías en la visión binocular son sutiles y podrían estar enmascaradas porque se evita la realización de tareas visuales como la lectura. Por este motivo, la presente tesis ha fijado como objetivo caracterizar la binocularidad y oculomotricidad mediante la valoración de la capacidad vergencial, las sacadas, la fijación, la sensibilidad macular y la estereopsis. Se han detectado alteraciones en algunas funciones oculomotoras como la fijación en pacientes con EM, describiendo una mayor inestabilidad con un patrón elipsoidal vertical. Pero este hallazgo no se traduce en una alteración de las sacadas verticales, de hecho, son las horizontales las que presentan mayor dificultad para estos pacientes. Además de esto, los pacientes con EM ven reducida la estereopsis y la capacidad de divergir. Y aunque presentan síntomas que podrían ser compatibles con alteraciones binoculares como la insuficiencia de convergencia, los signos clínicos no caracterizan tal afectación. Así pues, la afectación binocular y oculomotora en pacientes con EM es extensa y presenta una gran variabilidad intra-sujeto, al igual que ocurre en el transcurso mismo de la enfermedad a nivel sistémico.

Yes / When we track an object moving in depth, our eyes rotate in opposite directions. This type of “disjunctive” eye movement is called horizontal vergence. The sensory control signals for vergence arise from multiple visual cues, two of which, changing binocular disparity (CD) and inter-ocular velocity differences (IOVD), are specifically binocular. While it is well known that the CD cue triggers horizontal vergence eye movements, the role of the IOVD cue has only recently been explored. To better understand the relative contribution of CD and IOVD cues in driving horizontal vergence, we recorded vergence eye movements from ten observers in response to four types of stimuli that isolated or combined the two cues to motion-in-depth, using stimulus conditions and CD/IOVD stimuli typical of behavioural motion-in-depth experiments. An analysis of the slopes of the vergence traces and the consistency of the directions of vergence and stimulus movements showed that under our conditions IOVD cues provided very little input to vergence mechanisms. The eye movements that did occur coinciding with the presentation of IOVD stimuli were likely not a response to stimulus motion, but a phoria initiated by the absence of a disparity signal. / Supported by NIH EY018875 (AMN), BBSRC grants BB/M001660/1 (JH), BB/M002543/1 (AW), and BB/MM001210/1 (MB).