Autism spectrum disorders (ASD) are lifelong neurodevelopmental syndromes that affect social, cognitive, and sensorimotor development 
. While once considered rare, ASD now are known to affect ~1 in 88 children, and 1 in 54 males 
. The etiology(ies) of ASD remains poorly understood. Studies of their neural bases indicate diverse and variably affected brain systems. The cerebellum is one of few brain structures consistently implicated in ASD and in known single-gene disorders associated with ASD [e.g., Fragile X syndrome, Joubert syndrome; 
]. Reduced Purkinje cell density has been repeatedly documented 
, and cells in the deep nuclei to which Purkinje cells project are abnormal in size and number 
. Several studies have indicated that the volume of the cerebellar vermis is smaller in ASD 
, while cerebellar hemisphere volumes appear to be enlarged 
(although see 
for negative findings).
The cerebellum plays a fundamental role in controlling the precision of movements 
. Motor abnormalities have been noted in ASD since these disorders were originally described 
. More recent quantitative studies have documented impaired control of limb movements, including gait alterations, dysmetric manual movements and dyspraxia 
. The severity of these abnormalities are predictive of functional outcomes 
and may be the earliest identifiable features of the disorder 
. There is some evidence that the profile of motor control and praxis deficits associated with ASD may be unique to the disorder, but more detailed characterization of motor impairments in ASD is needed 
Eye movement studies have shown atypical gaze fixation, increased trial-to-trial amplitude variability of saccadic eye movements, and reduced accuracy of smooth pursuit eye movements in individuals with ASD and their unaffected first-degree relatives 
. While initial reports suggested that saccade accuracy is intact in ASD 
, several studies using higher-resolution eye movement monitors have found modest hypometria (i.e., undershooting of targets) 
that may recover at least partially over the course of development 
. Functional MRI studies have identified atypical activation in cerebellum, motor cortex, and basal ganglia during tasks of eye and hand movements 
The cerebellum’s role in controlling movement accuracy may be more directly assessed by systematically inducing movement error so that the motor system is forced to adapt 
. Adaptation of arm movements involves cerebellum, primary motor cortex and parietal area 5 
. Despite the cerebellum’s known role in adapting limb movements, adaptation of limb movements has been shown to be intact in patients with cerebellar ataxia 
. This suggests that neocortical reorganization may compensate for altered cerebellar adaptation mechanisms. Adaptation of limb movements appears to be unaffected in ASD 
Adaptation of saccadic eye movements appears to be primarily dependent on the posterior cerebellum, including lobules VI and VII of the vermis 
. Selective lesions of the cerebellar vermis lead to long-term disruptions in saccadic eye movement adaptation and the inability to consistently regulate eye movement amplitudes 
. In non-human primates, hypometria of visually guided saccades also is seen immediately after ablation of the vermis, but appears largely to resolve after only a few weeks 
. Saccade adaptation is also altered in patients with cerebellar infarcts, but only if the vermis is affected 
. It remains to be determined whether saccade adaptation is impaired in ASD.
Saccade adaptation has been well studied using laboratory paradigms in which intrasaccadic shifts in target location are generated immediately after saccade initiation, inducing a relatively constant error in the landing position 
. Subjects gradually adjust their saccade amplitudes to reduce movement error with practice, although detection of the target displacement is often not consciously recognized because of the visual blanking during saccades.
In the present study, we utilized a conventional intrasaccadic target step paradigm to study saccade adaptation and the integrity of the cerebellar vermis in individuals with ASD (). We reasoned that if individuals with ASD have a deficit involving the cerebellar vermis, then they will adapt at a slower rate than healthy controls, and they will show greater trial-to-trial variability in the amplitude of their saccades. We also predicted that cerebellar-dependent motor deficits evident in the oculomotor system would be associated with motor control impairments in the manual system. Therefore, we examined saccade adaptation rates and amplitude variability in relation to performance on a traditional neuropsychological test of manual motor control.
Schematic representations of the saccade adaptation test.