SLOWED ORIENTING OF COVERT VISUAL-SPATIAL ATTENTION IN AUTISM - SPECIFIC DEFICITS ASSOCIATED WITH CEREBELLAR AND PARIETAL ABNORMALITY

The most commonly reported finding from structural brain studies in au tism is abnormality of the cerebellum. Autopsy and magnetic resonance imaging (MR) studies from nine independent research groups have found developmental abnormality of the cerebellar vermis or hemispheres in t he majority of the more than 240 subjects with autism who were studied . We reported previously that patients with autism and those with acqu ired damage to the cerebellum were slow to shift attention between and within sensory modalities. In this study, we found that patients with autism who come from a group with significant cerebellar abnormality were also slow to orient attention in space. A subgroup of these patie nts who have additional or corollary parietal abnormality, like previo usly studied patients with acquired parietal damage, were also slow to detect and respond to information outside an attended location. Posne r, Walker, Friedrich, and Rafal (1984) showed that patients with parie tal lesions were slow to respond to contralesional information if they were attending an ipsilesional location. This study has replicated th at finding in patients with autism who have developmental bilateral pa rietal abnormality, and found a strong correlation between the attenti onal deficits and the amount of neuroanatomic parietal abnormality in these patients. This is the first time in the study of autism that the re is evidence for a statistically significant association of the size of a specific brain structural abnormality with a specific behavioral deficit. These findings illustrate that in autism different patterns of underlying brain pathology may result in different patterns of func tional deficits. In conjunction with previous studies of patients with acquired lesions, these data have implications for the brain bases of normal attention. The cerebellum may affect the speed with which atte ntional resources can be activated, while the parietal cortex affects the ability to use those resources for efficient information processin g at locations outside an attended focus. Deficits in the speed and ef ficiency with which neural activity can be modulated to facilitate pro cessing can clearly influence cognitive function. Such deficits may co ntribute to the behavioral disabilities that characterize autism.