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The age-by-complexity effect is the dominant empirical pattern in cognitive aging. The current report investigates whether a specific high-level mechanism---an age-related decrease in the reliability of episodic accumulators---can account for the age-by-complexity-effect, which is commonly assumed to be caused by an unspecific, low-level deficit. Groups of younger and older adults are compared in six reaction time experiments, using orthogonal manipulations of early cognitive difficulty (e.g., Stroop condition) and episodic demands (e.g., stimulus-response mapping). The predicted three-way interaction of age and the two factors was observed fairly consistently across experiments. A modified Brinley analysis shows that different regression slopes in old-young-space are required for conditions with low and high episodic difficulty. As a methodological contribution, a Brinley regression model following from certain simple processing assumptions is developed. It is shown that in contrast to a standard Brinley meta-analysis, the regression slopes in this model are not influenced by theoretically un-interesting between-experiment variance.
We compared effects of covert spatial-attention shifts induced with exogenous or endogenous cues on microsaccade rate and direction. Separate and dissociated effects were obtained in rate and direction measures. Display changes caused microsaccade rate inhibition, followed by sustained rate enhancement. Effects on microsaccade direction were differentially tied to cue class (exogenous vs. endogenous) and type (neutral vs. directional). For endogenous cues, direction effects were weak and occurred late. Exogenous cues caused a fast direction bias towards the cue (i.e., early automatic triggering of saccade programs), followed by a shift in the opposite direction (i.e, controlled inhibition of cue-directed saccades, leading to a 'leakage' of microsaccades in the opposite direction). (C) 2004 Elsevier Ltd. All rights reserved
When the eyes fixate at a point in a visual scene, small saccades rapidly shift the image on the retina. The effect of these microsaccades on the latency of subsequent large-scale saccades may be twofold. First, microsaccades are associated with an enhancement of visual perception. Their occurrence during saccade target perception should, thus, decrease saccade latencies. On the other hand, microsaccades likely indicate activity in fixation-related oculomotor neurons. These represent competitors to saccade-related cells in the interplay of gaze holding and shifting. Consequently, an increase in saccade latencies after microsaccades would be expected. Here, we present evidence for both aspects of microsaccadic impact on saccade latency. In a delayed response task, participants made saccades to visible or memorized targets. First, microsaccade occurrence up to 50 ms before target disappearance correlated with 18 ms (or 8%) faster saccades to memorized targets. Second, if microsaccades occurred shortly (i.e., < 150 ms) before a saccade was required, saccadic reaction times in visual and memory trials were increased by about 40 ms (or 16%). Hence, microsaccades can have opposite consequences for saccade latencies, pointing at a differential role of these fixational eye movements in preparation of motor programs.
When the eyes fixate at a point in a visual scene, small saccades rapidly shift the image on the retina. The effect of these microsaccades on the latency of subsequent large-scale saccades may be twofold. First, microsaccades are associated with an enhancement of visual perception. Their occurrence during saccade target perception could, thus, decrease saccade latencies. Second, microsaccades are likely to indicate activity in fixation-related oculomotor neurons. These represent competitors to saccade-related cells in the interplay of gaze holding and shifting. Consequently, an increase in saccade latencies would be expected after microsaccades. Here, we present evidence for both aspects of microsaccadic impact on saccade latency. In a delayed response task, participants made saccades to visible or memorized targets. First, microsaccade occurrence up to 50 ms before target disappearance correlated with 18 ms (or 8%) faster saccades to memorized targets. Second, if microsaccades occurred shortly (i.e., < 150 ms) before a saccade was required, mean saccadic reaction time in visual and memory trials was increased by about 40 ms (or 16%). Hence, microsaccades can have opposite consequences for saccade latencies, pointing at a differential role of these fixational eye movements in the preparation of saccade motor programs
Using the gaze-contingent boundary paradigm with the boundary placed after word n, we manipulated preview of word n+2 for fixations on word n. There was no preview benefit for first-pass reading on word n+2, replicating the results of Rayner, Juhasz, and Brown (2007), but there was a preview benefit on the three-letter word n+1, that is, after the boundary, but before word n+2. Additionally, both word n+1 and word n+2 exhibited parafoveal-on-foveal effects on word n. Thus, during a fixation on word n and given a short word n+1, some information is extracted from word n+2, supporting the hypothesis of distributed processing in the perceptual span.
Using the gaze-contingent boundary paradigm with the boundary placed after word n, the experiment manipulated preview of word n + 2 for fixations on word n. There was no preview benefit for 1st-pass reading on word n + 2, replicating the results of K. Rayner, B. J. Juhasz, and S. J. Brown (2007), but there was a preview benefit on the 3- letter word n + 1, that is, after the boundary but before word n + 2. Additionally, both word n + 1 and word n + 2 exhibited parafoveal-on-foveal effects on word n. Thus, during a fixation on word n and given a short word n + 1, some information is extracted from word n + 2, supporting the hypothesis of distributed processing in the perceptual span.