Figure 1.
Schematic representations of the saccade adaptation test.
A.) Participants were instructed to shift their gaze to peripheral targets when they appeared. After subjects initiated their saccade, the target stepped inward from the ±12 deg location to ±9 deg in the same visual hemifield. B) Schematic representations of double-step target displacement and traces of non-adapted and adapted saccades.
Table 1.
Demographic characteristics of individuals with autism spectrum disorders (ASD) and healthy control subjects.
Figure 2.
Saccade amplitudes for subjects with autism spectrum disorders (ASD) and healthy controls during adaptation and recovery.
The natural logarithmic model fit is presented for adaptation, and each data point represents the group mean for an individual trial. Subjects with ASD showed reduced rates of learning (p<.01). The linear fit is presented for recovery data. There was no difference in the rate at which subjects with ASD and healthy controls increased their amplitudes during the recovery phase (p = .66).
Table 2.
Saccade amplitude and amplitude variability on 12 deg trials for individuals with autism spectrum disorders (ASD) and healthy controls during baseline testing, adaptation, and post-adaptation recovery.
Figure 3.
Cumulative frequency of adaptation rates (i.e., rate of amplitude reduction) for subjects with autism spectrum disorders (ASD) and healthy controls.
Positive values represent faster learning rates. Triangles are used to represent non-adapters for both diagnostic groups. Asterisks (*) are used to identify two control subjects whose rates of adaptation were statistically significant (p<.05) but also less than those of two non-adapting subjects with ASD. These two controls made more saccades that could be scored during adaptation (151 and 170 out of 180 respectively) than the two non-adapting subjects with ASD whose learning rate was faster but non-significant (133 and 135 out of 180 respectively). If these two subjects with ASD are re-classified as adapters, there is still a higher proportion of non-adapting ASD subjects compared to healthy controls (ASD: 27% (15/56); controls: 6% (3/53); X21 = 8.81, p<.01).
Figure 4.
Standard deviation of the amplitude of primary saccades, a measure of trial-wise variability in saccade accuracy, during baseline testing, adaptation and recovery.
Data are presented in blocks of 10 trials. Subjects with autism spectrum disorders (ASD) showed greater trial-wise variability in saccade accuracy during each phase of testing (p<.01), but the rates at which variability changed during each of the phases were not different between subjects with ASD and healthy controls (p>.10).
Figure 5.
Relationships between saccade adaptation and manual motor performance.
The number of errors during the manual motor test were averaged across hands and are presented for subjects with ASD in relation to A) the rate at which they adapted and B) their trial-to-trial amplitude variability across baseline testing and the adaptation and recovery phases.
Figure 6.
Figure 6. Schematic representation of a sagittal view of the cerebellar “oculomotor” vermis - brainstem circuitry involved in the adaptation of saccadic eye movements.
Retinal error information reaches the inferior olive (IO), which in turn projects ascending climbing fibers that create complex spike action potentials at synapses on the Purkinje cell (PC) body and proximal dendrites. PCs also receive input via mossy fibers projecting from the nucleus reticularis tegmenti pontis (NRTP), which receives a saccade command from the superior colliculus (SC). Rapid, simple spike discharges occur at the synapses of mossy fiber-parallel fiber inputs to PCs. The complex spike firing of the climbing fiber-PC synapses induces a long-term depression (LTD) of simple spikes that is thought to be the mechanism guiding saccade adaptation. Changes in PC simple spike bursts modify saccade trajectories by altering the level of inhibitory output to fastigial nuclei (FN), which in turn modulate inhibitory (IBN) and excitatory burst neuron activity (EBN) in the brainstem burst generator (BBG). The BBG innervates abducens motoneurons (MN) that control horizontal eye movements via lateral and medial extraocular muscles.