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Biomedical subjects

Adrian G Lasker

Publications and source records attributed to Adrian G Lasker.

4 recordsLinked to original sources

Sensory versus motor information in the control of predictive saccade timing.

Humans readily make predictive saccades to periodic alternating targets. This predictive behavior depends on internal monitoring of timing error of past saccades in order to determine the time of initiation of future saccades; our earlier studies have confirmed this by finding correlations between latencies of consecutive predictive saccades. It is natural to consider that timing error is determined by visual detection of the difference between the time the target appears and the time the eyes arrive at the target; this in turn implies that saccades must actually be produced in order for their timing errors to be determined and predictive saccade timing to be established. We tested this hypothesis by having subjects view alternating visual targets while fixating a central target in order to eliminate saccade production. After six alternating target presentations, subjects began tracking the alternating targets. Tracking performance was assessed with an error measure that compared saccade latency and inter-saccade interval with desired values (zero and inter-stimulus interval, respectively). Errors in this Prior Viewing paradigm were compared to those from a conventional De Novo paradigm in which saccades began as soon as the alternating targets were presented. Saccades under Prior Viewing reached a low-error steady predictive state more rapidly than under De Novo tracking. The initial saccade under Prior Viewing had a higher latency than the others, suggesting that this saccade was reactive even though the paradigm is predictable; other reasons for this higher latency include time to disengage from the fixation target and time required to pre-program the initial set of saccades. The results show that visual detection of timing error from an actual motor act (saccades) is not necessary to establish predictive saccadic pacing: sensory-only information from viewing the moving targets can help to establish this predictive state.

Brain↗

Ocular motor indicators of executive dysfunction in fragile X and Turner syndromes.

Fragile X and Turner syndromes are two X-chromosome-related disorders associated with executive function and visual spatial deficits. In the present study, we used ocular motor paradigms to examine evidence that disruption to different neurological pathways underlies these deficits. We tested 17 females with fragile X, 19 females with Turner syndrome, and 40 females with neither disorder who comprised the comparison group. Group differences emerged for both the fragile X and Turner syndrome groups, each relative to the comparison group: Females with fragile X had deficits in generating memory-guided saccades, predictive saccades, and saccades made in the overlap condition of a gap/overlap task. Females with Turner syndrome showed deficits in generating memory-guided saccades, but not during either the predictive saccade or gap/overlap task. Females with Turner syndrome, but not females with fragile X, showed deficits in visually guided saccades and anti-saccades. These findings indicate that different brain regions are affected in the two disorders, and suggest that different pathways lead to the similar cognitive phenotypes described for fragile X and Turner syndromes.

Adolescent↗

Ocular motor behavior of children with neurofibromatosis 1.

Patients with neurofibromatosis 1 show neurocognitive deficits including abnormal visuospatial performance, but oculomotor behavior has not been studied. We recorded saccades in neurofibromatosis 1 and normal children, ages 6 to 12 years. Patients showed increased latency and diminished amplitude to more eccentric targets for both visually guided and memory-guided saccades. Subtracting the latencies of visually guided saccades from memory-guided saccades produced no differences between groups. For predictive saccades (0.5 Hz), patients with neurofibromatosis 1 generated fewer anticipatory saccades than normal subjects, but patients with neurofibromatosis 1 made more direction errors in an antisaccade task. Patients with neurofibromatosis 1 show saccade abnormalities that are not easily ascribed to dysfunction within single cortical areas. Rather, the findings likely reflect (1) partial involvement of different components of a widely distributed cerebral network that controls saccades, (2) impaired visuomotor maturation in a brain abnormal early in development, and (3) excessive gamma-aminobutyric acid-mediated inhibition, which could influence basal ganglia pathways that modulate superior colliculus activity.

Basal Ganglia↗