Obstructive hydrocephalus

Obstructive hydrocephalus encompasses both communicating and non-communicatingnoncommunicating forms, and merely refers to an underlying defect in the free circulation and absorption of CSF through the ventricular system and subarachnoid space. 

For a discussion of this terminology please refer to the more general article on hydrocephalus. 

Normal pressure hydrocephalus (NPH) is a poorly understood form of communicating hydrocephalus, and is also discussed separately. 

Epidemiology

The demographics of affected patients will depend on the underlying causes, which include:

• congenital aqueduct stenosis
• subarachnoid haemorrhage (SAH)
• meningitis
• obstructing tumour (e.g. tectal plate glioma)

Clinical presentation

As is the case with most mass effect conditions affecting the brain, presentation will vary dramatically depending on the speed of onset. 

In acute obstructive hydrocephalus, as is the case with a colloid cyst obstructing the foramina of Monro, sudden increase in intraventricular pressure can lead to rapid loss of consciousness and even death. 

In other patients where obstruction is incomplete or gradual (e.g. aqueduct stenosis) there may be almost no symptoms despite massive dilatation of the ventricles. 

Overall the presentation will depend on the presence of raised intracranial pressure which has the usual constellation of symptoms including headaches, made worse with stooping or straining, nausea and vomiting. Papilloedema may be evident ². 

In children whose cranial sutures have yet to fuse, rapid enlargement of the head circumference ². 

Radiographic features

Both CT and MRI (and ultrasound in the neonatal period) are able to demonstrate most of the features, although the underlying cause may be more or less easily discernible  (e.g. a web across the aqueduct causing aqueduct stenosis will only be visible on dedicated high resolution MRI images). 

Acute obstructive hydrocephalus

An important caveat to be aware of is that in acute obstructive hydrocephalus in young patients only minor ventriculomegaly may be visible despite significant elevation of intracranial pressure.

If previous films are available they are probably the most reliable way of identifying early hydrocephalus. Features which are helpful in making the diagnosis of acute obstructive hydrocephalus include ³:

• lateral ventricles
  • enlargement of the temporal horns (best indicator)
  • transependymal oedema, or periventricular oozing, may be visible as high T2 signal on MRI or low density change on CT around the margins of the ventricles, and should not be confused with white matter change of chronic small vessel ischaemia. It is also called as periventricular oozing.
• third ventricle
  • outward bowing of the lateral walls
  • inferior bowing of the floor
• fourth ventricle
  • poor indicator of hydrocephalus as the confined nature of the posterior fossa prevents significant enlargement
  • a prominent fourth ventricle suggests that the obstruction is either at the foramina of Luschka and Magendie or within the subarachnoid space

Chronic obstructive hydrocephalus

Changes of chronic obstructive hydrocephalus depend on whether or not it is communicating or non-communicating. 

Communicating obstructive hydrocephalus

Communicating obstructive hydrocephalus (usually referred to as merely 'communicating hydrocephalus') can be challenging to distinguish from non-obstructive hydrocephalus as seen in patients with ex vacuo dilatation of the ventricles due to parenchymal volume loss. Again the third ventricle and temporal horns of the lateral ventricles are key to the diagnosis, as even in patients with significant ex vacuo dilatation, these regions are usually relatively preserved ³.  

Additionally often there is crowding of the sulci at the vertex and disproportionate widening of the Sylvian cisterns. 

See also: hydrocephalus versus atrophy

Non-communicating obstructive hydrocephalus

Non-communicating obstructive hydrocephalus (often merely referred to as obstructive hydrocephalus) is usually a relatively simple diagnosis to make on imaging. Over time the portions of the ventricular system upstream from the obstruction gradually enlarge compressing and thinning the overlying cortex. 

Features of long standing non-communicating obstructive hydrocephalus (at the level of the aqueduct of Sylvius or below) include ^1-3:

• marked dilatation of the ventricles, especially the lateral and third ventricles
• thinned and elevated corpus callosum
• fenestration of the septum pellucidum
• depression of the fornices
• the floor of the 3^rd ventricle is displaced inferiorly, abutting the skull base, obliterating the suprasellar cistern
• outward bowing (ballooning) of the recesses of the third ventricle (infundibular, optic and pineal recesses)
• ballooning of the suprapineal recess

Treatment and prognosis

Treatment depends on the cause and location of the obstruction. In some patients with temporary obstruction (such as with subarachnoid haemorrhage) temporary CSF diversion is sufficient (e.g. via an external ventricular drain (EVD)). Similarly if the cause is mechanical, it may be possible to resect the mass (e.g. colloid cyst). 

In may cases obstruction is permanent or unable to be directly treated (e.g. most tectal gliomas), and as such permanent CSF diversion may be required. Treatment options include:

• shunting, most commonly with a VP shunt
• third ventriculostomy is useful in patients with non-communicating obstructive hydrocephalus at or below the level of the aqueduct of Sylvius.