RESUMO
Thickening of the corpus callosum is an important feature of development, whereas thinning of the corpus callosum can be the result of a number of diseases that affect development or cause destruction of the corpus callosum. Corpus callosum thickness reflects the volume of the hemispheres and responds to changes through direct effects or through Wallerian degeneration. It is therefore not only important to evaluate the morphology of the corpus callosum for congenital anomalies but also to evaluate the thickness of specific components or the whole corpus callosum in association with other findings. The goal of this pictorial review is raise awareness that the thickness of the corpus callosum can be a useful feature of pathology in pediatric central nervous system disease and must be considered in the context of the stage of development of a child. Thinning of the corpus callosum can be primary or secondary, and generalized or focal. Primary thinning is caused by abnormal or failed myelination related to the hypomyelinating leukoencephalopathies, metabolic disorders affecting white matter, and microcephaly. Secondary thinning of the corpus callosum can be caused by diffuse injury such as hypoxic-ischemic encephalopathy, human immunodeficiency virus (HIV) encephalopathy, hydrocephalus, dysmyelinating conditions and demyelinating conditions. Focal disturbance of formation or focal injury also causes localized thinning, e.g., callosal dysgenesis, metabolic disorders with localized effects, hypoglycemia, white matter injury of prematurity, HIV-related atrophy, infarction and vasculitis, trauma and toxins. The corpus callosum might be too thick because of a primary disorder in which the corpus callosum finding is essential to diagnosis; abnormal thickening can also be secondary to inflammation, infection and trauma.