Abstract

We analysed location priming effects, and thus the ability to integrate visual information across subsequent trials in the three studies presented in the following chapters. Based on previous findings in healthy subjects priming effects occur under conditions that require no attentional shifts in-between subsequent trials, i.e. with the subject’s fixation maintained and the search displays presented at retinotopically equal locations with respect to the fixation cross (Maljkovic & Nakayama, 1996; Geyer, Krummenacher, & Müller, 2007). In study 1 we tested whether location-based priming effects would outlive spatial shifts of attention in healthy subjects. The basic assumption, derived from Pisella and Mattingley´s (2004) account was they would, and that the outliving would be based on intact spatial remapping mechanisms operating in healthy subjects along with attention shifts. The aim of study 1 in view of further investigations in patients, i.e. in studies 2 and 3 was to test the suitability of the priming paradigm to serve our purpose to investigate spatial remapping abilities, and furthermore, in patients, purported deficits. To test whether priming effects would outlive saccadic shifts of overt attention, subjects had to re-fixate the fixation cross in turns on the left and on the right side of the monitor between subsequent trials. In two separate experiments priming effects were measured at post-saccadically retinotopic and spatiotopic locations, respectively, and compared to effects in a control experiment requiring no attention shifts. The experiments were also applied in study 2. To test whether priming effects would outlive covert shifts of attention subjects´ attention was distracted between subsequent trials while their fixation was maintained. In two separate experiments priming effects were measured after exogenous and endogenous distraction, respectively, and compared to a control experiment without distraction. The experiments were also applied in study 3. The presence of priming effects despite interfering attention shifts could be taken as evidence that processes that integrate visual information along with attention shifts, i.e. spatial remapping mechanisms, operate flawlessly in healthy subjects. The aim of study 2 was to test whether the parietal cortex provides the neural correlate of spatial remapping as assumed by Pisella and Mattingley (2004). To that end, we tested whether spatial remapping deficits would occur after saccadic shifts of overt attention in patients with right parietal lesions. Deficits were expected to be indicated by altered or disturbed priming effects in those patients as compared to priming effects in healthy control subjects and furthermore, in patients with right-hemispheric lesions not involving the parietal lobe. Latter patients (without parietal lesions) were tested, to control for and differentiate between deficits occurring more generally after right-hemispheric damages and specific deficits occurring after right parietal damages. Moreover, given the crucial role of priming for visual search (Chun & Nakayama, 2000) disturbed priming as an indicator of deficient spatial remapping would provide support for the assumption made by Pisella and Mattingley (2004) that spatial remapping deficits contribute to visual search impairments as they are often observed in patients with right parietal lesions. The aim of study 3 was to test the model’s assumption that spatial remapping is required after spatial shifts of covert attention. Again, we compared priming effects of patients with right parietal lesions to those of patients with right-hemispheric lesions without parietal involvement, and healthy subjects. We expected priming effects to be disturbed in patients with right parietal lesions provided that covert attention shifts induce spatial remapping requirements, and that the anatomical site of spatial remapping mechanisms operating to integrate visual information across spatial shifts of covert attention is located in the parietal lobe.