“…Many other aberrant connections have also been identified in ASD, including additional connections of classically considered nonmotor areas of the cerebellum to sensorimotor cerebral cortices: particularly, regions of the occipital lobe, premotor and primary motor cortices, and primary somatosensory cortex [ 63 ]. Atypical eye gaze [ 67 ], delayed orienting [ 68 ], impairments in smooth pursuit [ 69 ], altered movement perception, and deficits in facial perception [ 70 ] demonstrated by individuals with ASD (details reviewed by [ 71 , 72 ]) are likely mediated by these abnormal sensorimotor connections, other alterations in olivofloccular circuitry [ 73 ], and altered PC activity and number. In rodents, some PC projections bypass the DCN and synapse directly within the vestibular nuclei, suggesting that PC alterations in ASD could directly exacerbate vestibuloocular reflex abnormalities [ 74 , 75 ].…”