Imaging description

Enlarged ventricles can be caused by hydrocephalus or parenchymal loss. Hydrocephalus is classified as non-communicating (obstructive) or communicating. It is important to try and distinguish among these different patterns, as this will direct further workup and management.

Non-communicating hydrocephalus results from obstruction of the ventricular outflow of cerebrospinal fluid (CSF). Frequent causes include neoplasms, aqueductal stenosis, and intraventricular hemorrhage. The site of obstruction can be implied by which ventricles are enlarged.

Communicating hydrocephalus usually results from obstruction of CSF resorption at the arachnoid granulations. Less common causes include overproduction of CSF and compromised venous outflow. Normal-pressure hydrocephalus (NPH) is a specific form of communicating hydrocephalus which is associated with the clinical triad of dementia, ataxia, and urinary incontinence.

Hydrocephalus may lead to transpendymal edema, caused by transpendymal resorption of CSF. This will produce a rim of decreased attenuation (CT) or high T2/FLAIR signal (MRI) around the lateral ventricles (Figure 6.1). This usually indicates an acute enlargement of the ventricles [1].

Some apparent cases of communicating hydrocephalus are caused by fourth ventricular outflow obstruction. An apparent obstructive lesion may not be evident; CT and conventional MRI may miss small webs which obstruct outflow at the foramina of Luschka and Magendie. The addition of 3D constructive interference in the steady state (CISS) images may allow for improved detection of small membranes at the suspected site of obstruction (Figure 6.2) [2].