MR images accurately depict normal patterns of age-related change in intracranial space, whole brain, GM, WM, and CSF. These quantitative MR imaging data can be used in research studies and clinical settings for the detection of abnormalities in fundamental neuroanatomic parameters.

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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.

This morphometric study examined two aspects of corpus callosum development: pediatric cortico-callosal topography and developmental neuroplasticity subsequent to perinatal brain injury. In vivo magnetic resonance imaging was used to quantify the total midsagittal cross-sectional area and five anterioposterior subregions of the callosum in 10 children with focal lesions and 86 healthy volunteer control subjects. Nine of the ten children with early injury showed a reduction in the total area of the callosum relative to matched controls. The area of the total callosum cross-section was inversely proportional to the size of lesion. All patients displayed region-specific size reduction. This regional thinning bore a topographical relationship to the lesion sites. Reduction in anterior subregions 1, 2 and 3 was respectively associated with lesions in the anterior inferior frontal area, the middle and superior frontal region, and the precentral area. Attenuation of subregion 4 corresponded to anterior parietal lesions, and thinning of subregion 5 occurred with posterior parietal injury. This cortical-callosal pattern coincides with adult and nonhuman primate mappings. Callosal thinning despite the early onset of the lesions suggests limits to developmental neuroplasticity.

Using MRI methods previously shown to optimize visualization of cytoarchitectonic details in the body of the hippocampal formation caudal to the pes hippocampi, we imaged and quantified the hippocampus proper including the subiculum and the dentate gyrus in 33 autistic patients between the ages of 6 and 42 years and in 23 age-matched normal healthy volunteers. Measures of these structures in autistic patients and normal healthy volunteers differed nonsignificantly, by less than 1.4%, regardless of whether or not the autistic patients were retarded or had a history of seizure episodes. By contrast, measures of vermian lobules VI and VII and the posterior portion of the corpus callosum in these same autistic and normal volunteers differed significantly, by more than 9.9%. The lack of a significant difference in the cross-sectional size of the posterior hippocampal formation between autistic and normal 6- to 42-year-olds is discrepant with predictions based on some, but not all, autopsy studies. This suggests that there is a need for additional quantitative autopsy study of the hippocampal formation and quantitative MRI study of rostral hippocampal regions that we did not explore in the present report. Also, quantitative autopsy and MRI studies have yet to examine hippocampal development in autistic patients younger than 6 years of age; whether early stages of growth are normal or not is unknown.