Pediatric Hydrocephalus pp 1-25 | Cite as
Pathology of Pediatric Hydrocephalus
Abstract
This chapter focuses on the pathology of hydrocephalus in children. With respect to causes of hydrocephalus, an anatomical approach is used highlighting abnormalities that can impede cerebrospinal fluid movements at the interventricular foramina, the cerebral aqueduct, the fourth ventricular apertures, and the subarachnoid space. Inflammatory processes, some very subtle, secondary to infections or hemorrhage can damage the ependymal layer and allow fusion of adjacent brain surfaces or cause collagenous scarring in the subarachnoid space. Neoplasms and other lesions that can compress the cerebrospinal fluid pathways are briefly summarized. Several complex malformations of the posterior fossa (including Chiari type 2, Meckel-Gruber, Dandy-Walker) are also associated with hydrocephalus. Ventricular enlargement, when sufficiently severe or rapid, can cause secondary damage in the brain. Early-onset hydrocephalus (e.g., in fetuses or premature infants) might alter subsequent brain development. Periventricular axon damage, which is caused by a combination of mechanical distortion and blood flow alterations, is preventable by shunting but is not reversible. Most changes in the neuron cell body are secondary to the axonal damage. The histopathology of shunt obstruction is briefly reviewed. In conjunction with in vivo imaging and animal experimentation, there remains much to be learned from autopsies, explanted cerebrospinal fluid shunts, and possibly brain biopsies from hydrocephalic children.
Keywords
Autopsy Axon Ependyma Human Hydrocephalus MyelinReferences
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