Hydrocephalus

Obstructive Hydrocephalus

The sites where the ventricular system is normally narrow (i.e., the foramina) are particularly vulnerable to obstruction.

Causes of intraventricular obstruction at the level of the foramen of Monro include: 1 colloid cyst of the third ventricle, 2 ependymoma, 3 teratoma, 4 congenital atresia, 5 involvement by adjacent glioma.

The posterior third ventricle may be obstructed by pinealomas and aneurysms of the vein of Galen. Aqueductal obstruction can also occur in association with aqueductal stenosis, periaqueductal gliomas, arteriovenous malformations, and cysts of the quadrigeminal region.

Communicating Hydrocephalus

Communicating hydrocephalus may result from previous infection such as meningitis or may be secondary to previous hemorrhage caused by trauma, surgery, or rupture of an aneurysm with subarachnoid hemorrhage. It is also seen in association with Arnold-Chiari malformation and in the presence of subarachnoid seeding of tumor (meningiocarcinomatosis).

A functional hydrocephalus in the presence of elevated CSF protein is seen in association with spinal cord tumors, typically ependymomas. Overproduction of CSF caused by choroid plexus papilloma or carcinoma may also result in hydrocephalus.

Normal-Pressure Hydrocephalus

An idiopathic form of communicating hydrocephalus, usually seen in older adults and known as normal-pressure hydrocephalus (NPH), was described originally by Adarns and Hakim and their colleag. These authors reported a clinical triad of gait impairment characterized as magnetic gait, dementia, and urinary incontinence. Symptoms can be relieved by ventricular shunting, with the most dramatic improvement usually seen in gait.

The typical patient with NPH who is likely to respond a shunt exhibits a mild cognitive impairment along with a significant gait disturbance.

Differentiating NPH from cerebral atrophy can be extremely difficult. Initial enthusiasm for the concept of NPH as a treatable cause of dementia and gait impairment resulted in shunt procedures in patients who either failed to respond or showed an initial improvement but subsequently continued to deteriorate. Because of these discouraging results, the number of shunt procedures for NPH in the elderly has significantly decreased. The failure of patients to respond to the shunt procedure probably resulted from erroneous diagnosis of hydrocephalus in patients who were suffering from degenerative brain disease such as cerebral atrophy associated with AD. This has led to more stringent criteria to identify potential shunt candidates.

These criteria include:

  • radioisotope cisternography,
  • continuous intracranial pressure recorlings spinal effusion,
  • CT cisternography with intrathecal iodinated contrast material.

Despite these criteria, a reliable study predicting shunt outcome has not been established.

In terms of MRI, two approaches can be used to differentiate NPH from cerebral atrophy: the anatomic approach and the functional approach. Anatomically, in patients with AD, volume loss of the hippocampus develops and resultant dilatation of the perihippocampal fissures ensues. Patients with NPH have dilation of the temporal horn.