Hydrocephalus

A key concept in evaluating children with suspected hydrocephalus is the correlation of imaging findings with an abnormally high rate of head growth that can be documented with serial measurements of head circumference. These patients also can present with headaches, papilledema, cranial nerve palsies, motor deficits and dysfunction of the hypothalamic-pituitary axis. Common causes of hydrocephalus in infants include meningitis, trauma, hemorrhage, Chiari II malformation, or aqueductal stenosis. Choroid plexus tumors and vein of Galen malformations are unusual culprits. In children over 2 years of age, posterior fossa tumors are the most frequent cause of new-onset hydrocephalus.

Hydrocephalus can be grouped into communicating and noncommunicating causes. In general, the communicating form is caused by extraventricular obstruction of CSF circulation or reduced resorption (Fig. 5). Noncommunicating hydrocephalus is characterized by intraventricular obstruction of CSF flow, usually by tumors, cysts, or scarring. The obstruction most commonly occurs at sites of narrowing within the ventricular system: the foramina of Monro, the aqueduct, or the fourth ventricular outflow foramina (Fig. 6). A third very rare subset of hydrocephalus results from CSF overproduction by tumors or hyperplasia of the choroid plexus.

The two most helpful imaging findings indicating hydrocephalus are enlargement of the anterior recess of the third ventricle and dilation of the temporal horns of the lateral ventricles in the setting of normal sized Sylvian fissures. Other signs include a rounded and widened configuration of the anterior and posterior horns of the lateral ventricles, and ventriculomegaly out of proportion to the size of the cerebral sulci. Atrophy can occasionally mimic the radiographic appearance of hydrocephalus but will not be seen in infants with concurrent macrocephaly or an excessively rapid increase in head size.

Figure 5. Communicating hydrocephalus following meningitis with enlargement of all ventricles. No intraventricular obstruction. (transaxial T2-WI)

Figure 6. Noncommunicating hydrocephalus, secondary to fourth ventricular medulloblastoma. Temporal horns are markedly enlarged. (transaxial CT)

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