Slowed orienting of covert visual-spatial attention in autism: Specific deficits associated with cerebellar and parietal abnormality

Abstract The most commonly reported finding from structural brain studies in autism 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 the majority of the more than 240 subjects with autism who were studied. We reported previously that patients with autism and those with acquired 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 patients who have additional or corollary parietal abnormality, like previously studied patients with acquired parietal damage, were also slow to detect and respond to information outside an attended location. Posner, Walker, Friedrich, and Rafal (1984) showed that patients with parietal lesions were slow to respond to contralesional information if they were attending an ipsilesional location. This study has replicated that finding in patients with autism who have developmental bilateral parietal abnormality, and found a strong correlation between the attentional deficits and the amount of neuroanatomic parietal abnormality in these patients. This is the first time in the study of autism that there 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 functional 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 attentional resources can be activated, while the parietal cortex affects the ability to use those resources for efficient information processing at locations outside an attended focus. Deficits in the speed and efficiency with which neural activity can be modulated to facilitate processing can clearly influence cognitive function. Such deficits may contribute to the behavioral disabilities that characterize autism.