Aqueductal Narrowing, Congenital and Acquired

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Abstract
Introduction Hydrocephalus secondary to narrowing of the Sylvian aqueduct was first reported in 1900 by Bourneville and Noir1 and Oppenheim.2 Many authors have described additional cases since then, often speculating whether they were congenital—the result of a developmental anomaly—or acquired. In some cases the narrowing was clearly acquired, as in gummatous3 or tuberculous4 occlusions; in others, such as hereditary aqueductal stenosis, the clinical, histologic, and genetic features proved it to be congenital.5 Aqueductal gliosis and forking are entities that are not easily classified, however. Although they have been defined many times, the criteria vary from author to author. How many glial cells and fibers constitute "gliosis" of the aqueduct is not certain; nor is it clear when division of the main channel is an inborn defect or due to glial partitioning. Different authors fail to agree on which changes are acquired, which congenital. We have