In this article, methods for measuring brain morphologic features on magnetic resonance images are described and normative data are provided for six morphologic variables. An estimated function relating age (ranging from 8 to 79 years) to average values is given for each measure. A linear decrease over the age range is observed in the volume of the cerebrum. Linear increases are observed in measures of ventricular and sulcal fluid. A curvilinear decrease in cortical volume is found and is demonstrable even in young adults. Highly nonlinear increases in the volume of signal hyperintensities are observed in cortical and subcortical regions. The methods described may be used to provide an age-adjusted index of morphologic abnormality for each subject on any of the measures. They are currently in use in ongoing neurobehavioral studies of patients with nonfocal brain abnormalities and primary disorders of affect and cognition.

The corpus callosum is the major axonal commissure of the brain, connecting the two cerebral hemispheres and providing communication between the cortical and subcortical neurons. With MR imaging in the sagittal plane, the corpus callosum can be depicted in great detail. We review the normal anatomy, development, and process of myelination of the corpus callosum. The MR features of various pathologic conditions involving the corpus callosum are described. Finally, we discuss the evolving role of MR imaging in neuropsychiatric diseases with respect to the corpus callosum.

Previous work demonstrated enlargement of the neocerebellar vermis in Williams' syndrome (WS), despite diminished volumes in the cerebral hemispheres. We present the first in vivo volumetric study of any structure within the cerebellar hemispheres. Using MRI, we identified and reliably measured the neocerebellar tonsils in WS subjects; Down's syndrome (DS) subjects matched for age, IQ, and cerebral volume; and age-matched normal controls. WS tonsils were equal in size to control tonsils and larger than DS tonsils. In proportion to the cerebrum, WS tonsils were larger than controls'. These results coincide with the remarkable neuropsychological preservation of language and affect in WS, despite general cognitive impairment. They contrast with the neocerebellar vermal hypoplasia seen in autism, with its communicative and affective deficits. Additionally, two WS subjects showed Chiari type I malformations, but the average tonsillar position in WS was not found to be different than in controls.

Neurobehavioral studies of Williams syndrome (WS) and Down syndrome (DS) have revealed distinct profiles of cognitive strengths and weaknesses. In a previous report, we described several gross brain morphologic distinctions on magnetic resonance images between these two disorders. While the observed cerebral hypoplasia was of equal degree in the two groups, cerebellar size was entirely normal in the subjects with WS but dramatically reduced in subjects with DS. In WS, paleocerebellar vermal lobules subtended a smaller area on midsagittal sections, but neocerebellar lobules were actually larger. These results suggested important distinctions between WS and DS in terms of the action and anatomic targets of factors that alter brain development in these syndromes. The present study extends the earlier findings by focusing in detail on the morphologic features of the cerebral hemispheres, particularly cerebral gray matter. The results suggest that some frontal and temporal limbic structures are relatively preserved in WS, while some basal ganglia and diencephalic structures are relatively preserved in DS.

In the present study using magnetic resonance imaging (MRI), age changes in the morphology of the cerebral cortex, greatest in the frontal and parietal convexities, were observed during adolescence. Results suggest that increases in cerebrospinal fluid (CSF) within the sulci of these cortical regions accompany grey matter decreases. Smaller reductions in volume are also observed in subcortical grey matter nuclei. These apparent grey matter volume reductions presumably reflect processes of late brain maturation. The changes may be related to decreasing neural plasticity.

Using magnetic resonance imaging 20 language- and learning-impaired children were compared with 12 normal control subjects. Gross brain structure was remarkably normal in the language- and learning-impaired group. Semiautomated morphometry was used to measure hemispheric volumes and cerebral asymmetries in six cerebral regions. The volume of the left posterior perisylvian region was significantly reduced in language- and learning-impaired children. Asymmetries in inferoanterior and superoposterior cerebral regions were also significantly different in this group. Results of descriptive group comparisons of estimated volumes of other cerebral gray-matter structures raise the possibility that some language- and learning-impaired children may have additional volume reductions in cortical and subcortical structures. The results suggest that hemispheric specialization of function may be anomalous in this population.

Autism is a neurologic disorder that severely impairs social, language, and cognitive development. Whether autism involves maldevelopment of neuroanatomical structures is not known. The size of the cerebellar vermis in patients with autism was measured on magnetic resonance scans and compared with its size in controls. The neocerebellar vermal lobules VI and VII were found to be significantly smaller in the patients. This appeared to be a result of developmental hypoplasia rather than shrinkage or deterioration after full development had been achieved. In contrast, the adjacent vermal lobules I to V, which are ontogenetically, developmentally, and anatomically distinct from lobules VI and VII, were found to be of normal size. Maldevelopment of the vermal neocerebellum had occurred in both retarded and nonretarded patients with autism. This localized maldevelopment may serve as a temporal marker to identify the events that damage the brain in autism, as well as other neural structures that may be concomitantly damaged. Our findings suggest that in patients with autism, neocerebellar abnormality may directly impair cognitive functions that some investigators have attributed to the neocerebellum; may indirectly affect, through its connections to the brain stem, hypothalamus, and thalamus, the development and functioning of one or more systems involved in cognitive, sensory, autonomic, and motor activities; or may occur concomitantly with damage to other neural sites whose dysfunction directly underlies the cognitive deficits in autism.

Recent studies of infantile autism using computed tomographic scanning emphasized the importance of studying cases of classic autism (Kanner's syndrome) without complicating conditions such as mental retardation. Computed tomographic scan studies of such patients reported no evidence of anatomical abnormalities of cerebral hemispheres or of subcortical structures, which are defined by landmarks such as the lateral ventricles and lentiform nuclei. Examination of the cerebellum was not mentioned. The most recent postmortem neuropathologic study reported significant cerebellar abnormality, but the study was of a severely retarded autistic individual. Using magnetic resonance imaging, we have found in vivo evidence of a significant and unusual cerebellar malformation in a person with the classic form of autism uncomplicated by mental retardation (current nonverbal IQ = 112), epilepsy, history of drug use, postnatal trauma, or disease. The finding showed hypoplasia of the declive, folium, and tuber in posterior vermis, but not of the anterior vermis, and hypoplasia of only the medial aspect of each cerebellar hemisphere. The right posterior cerebral hemisphere also showed pathologic findings.