Visual search and visual working memory in patients with chronic focal cortical lesions.

Visually guided behavior is known to involve temporo-parietal, inferotemporal, and prefrontal cortex and each of these areas appears to contribute to visual working memory. We explored the extent to which chronic lesions in one of these cortical areas affect visually guided oculomotor performance. We also explore whether possible impairments become more pronounced with increasing memory load. With this aim we recorded saccadic eye movements in 19 patients with a chronic focal postsurgical lesion in either temporo-parietal, inferior temporal or prefrontal cortex. Their results are compared to those of 19 age-matched volunteers. The subjects performed three different visual search tasks with increasing memory load: Instructed search, cue-guided search and memory-guided search. In addition, the latter task was performed with a short (1 s) and a long (6 s) delay. All tasks required the subjects to make a saccade to a single target presented together with one or three distractors. The results indicate that patients with inferotemporal lesions make the most task-related errors. Saccadic reaction times (SRTs) were significantly prolonged in patients with temporo-parietal and prefrontal lesions, but were unaffected in the patients with lesions in the inferotemporal cortex. The spatial accuracy of saccades was lowest in patients with temporo-parietal lesions. An increase in memory load led to more errors, to longer reaction times and to lower saccadic precision. However, the effect was similar across the three patient groups and the controls. An error analysis indicated that both patients and controls tended to weight global (luminance contrast and form) features higher than local features (line-segment orientation) when making difficult perceptual decisions.

Poor saccadic control correlates with dyslexia.

A large group of subjects, either average readers or reading/spelling disabled subjects (n = 185; age between 8-25 years; M = 13 +/- 4 years), were tested in various standardized cognitive tasks including reading/spelling assessment and in non-cognitive saccadic eye movement tasks. Dyslexics were separated into a subgroup (D1) with deficits in the serial auditory short-term memory and a subgroup (D2) with an isolated low achievement in reading/writing. Control subjects had no relevant cognitive deficit of any type. Saccadic eye movements were measured in a single target and in a sequential-target task. A significant correlation was found between abnormal saccadic control and reading disability. The two dyslexic groups showed only slight differences. As compared to the control group, the mean values of the standard deviations of the saccadic reaction times (SRT) and the amount of late saccades (SRT > 700) were significantly increased in both dyslexic groups and especially in group D1 who also showed an increased amount of anticipatory saccades. The number of express saccades (SRT = 80-134 ms) was increased, but not significantly, in D2 dyslexics. Both dyslexic groups produced significantly more regressive saccades in the sequential-target task. The correlation between saccadic variables and "reading factor" was 0.4. Significant deviations from normal performance of the saccadic variables were found in an estimated 50% of the dyslexics as compared to 20% of the control subjects. In spite of their worse level in saccadic control, dyslexics also developed with age in the eye movement performance as the control subjects did. Yet, the development was slower in group D1. It is suggested that reading process and saccade system are both controlled by visuo spatial attention and fixation systems that maybe impaired or develop slowly in many dyslexic subjects.

Human express saccade makers are impaired at suppressing visually evoked saccades.

1. We report the oculomotor behavior of human subjects who produce unusually high numbers (> 30%) of express saccades (latency range 85-135 ms) in the overlap saccade task, where express saccades are usually absent or small in number (< 15%). We refer to these subjects as "express saccade makers" (ES makers). 2. We tested the hypothesis that ES makers have difficulties in maintaining fixation and in suppressing unwanted saccades to a suddenly appearing peripheral target by comparing the performances of 10 ES makers and 10 control subjects in gap and overlap antisaccade tasks and in a memory-guided saccade task. 3. The ES makers produced between 35% and 95% incorrect saccades toward the stimulus (prosaccades) in the antisaccade tasks, compared with control subjects, who produced < 20%. Their correct antisaccades appeared to be normal. 4. We further tested the ability of ES makers to maintain fixation and to avoid reflexive saccades to the onset of a target in the memory-guided saccade task. ES makers tended to glance to the briefly presented cue in many trials (4 of them in 50-80% of the trials) instead of delaying the saccade until fixation point offset. Most of the inappropriate saccades had latencies in the range of express saccades. 5. These results can be associated with the finding of fixation related neurons in different cortical and subcortical brain regions (e.g., inferior-parietal and frontal cortex, basal ganglia, superior colliculus). The unusual number of express saccades made by the ES makers in the standard overlap and gap tasks, and their unwanted short-latency reflexive saccades to the target in the memory-guided saccade task, are reminiscent of the performance in these tasks of monkeys whose collicular fixation neurons were chemically deactivated. The collicular fixation neurons are probably the final common pathway in the control of active fixation, and are in mutual inhibitory relationship with the saccade cells. 6. The decreased saccadic control observed in the ES makers suggests that saccade execution in humans is also gated by a fixation system. These ES makers may have reduced voluntarily control over saccade generation as a result of a defect or poor development of their fixation system.

Separate populations of visually guided saccades in humans: reaction times and amplitudes.

The saccadic eye movements of 20 naive adults, 7 naive teenagers, 12 naive children, and 4 trained adult subjects were measured using two single target saccade tasks; the gap and the overlap task. In the gap task, the fixation point was switched off before the target occurred; in the overlap task it remained on until the end of each trial. The target position was randomly selected 4 degrees to the left or 4 degrees to the right of the fixation point. The subjects were instructed to look at the target when it appeared, not to react as fast as possible. They were not given any feedback about their performance. The results suggest that, in the gap task, most of the naive subjects exhibit at least two (the teenagers certainly three) clearly separated peaks in the distribution of the saccadic reaction times. The first peak occurs between 100 and 135 ms (express saccades), the second one between 140 and 180 ms (fast regular), and a third peak may follow at about 200 ms (slow regular). Other subjects did not show clear signs of two modes in the range of 100 to 180 ms, and still others did not produce any reaction times below 135 ms. In the overlap task as well three or even more peaks were obtained at about the same positions along the reaction time scale of many, but not all subjects. Group data as well as those of individual subjects were fitted by the superposition of three gaussian functions. Segregating the reaction time data into saccades that over- or undershoot the target indicated that express saccades almost never overshoot. The results are discussed in relation to the different neural processes preceding the initiation of visually-guided saccades.