Definition

 Hydrocephalus is not a specific disease; rather,

it is a group of conditions that result from
impaired circulation and absorption of CSF or,
in the rare circumstance, from increased
production CSF by a choroid plexus papilloma.
 CSF Physiology

Sources of CSF:
 Choroid plexus (75%) in Lateral, 3rd, and 4th
ventricles.
 Extrachoriodal (25%) capillary endothelium
within brain parenchyma.
 CSF Physiology

Volume of CSF
Infant: 50 ml

Adult: 150 ml

Rate of secretion: 20 ml/hour

 CSF Circulation

 CSF flow results from the pressure gradient that

exists between ventricular system (180 mm H2O)
and venous channels (90 mm H2O).
 CSF flows from lateral ventricle through
foramina of Monro into 3rd ventricle. The
through aqueduct of Sylvius to enter 4th
ventricle.
 CSF Circulation

 CSF exits the 4th ventricle through the paired lateral foramina of
Luschka and the midline foramen of Magendi into basal cisterns.

 CSF circulates from basal cisterns posteriorly through the cisterns

system and over the convexities of the cerebral hemisphere.

 CSF is absorbed primarily by the arachinoid villi endothelium. CSF is

absorbed to much lesser by the lymphatic channels directed to the
paranasal sinuses, along nerve root sleeves, and by the choroid plexus
itself.
CSF Circulation
 Causes

A- Obstructive (non Communicating): results from

obliteration to CSF flow in ventricular system.
* Aqueduct lesion:
1- Stenosis (mostly congenital)
2- Gliosis following neonatal meningitis or subarachinoid
haemorrahge in a premature infant.
* Posterior fossa lesions:
1- Tumors.
2- Malformations: Dandy Walker, Chiari type II.
 Causes

B- Non obstructive (Communicating): results from

obliteration of the subarachinoid cisterns or
malfunction of the arachinoid villi
 Subarachinoid hamorrhage.
 Tuberculous or pneumococcal meningitis.
 Intrauterine infections may also destroy the CSF
pathways.
 Leukaemic infiltrates in subarachinoid space.
 Causes

Dandy Walker:
 cystic expansion of the fourth ventricle due to mal
development of its roof during embryogenesis.

Chiari malformation II:

 Hdrocepalus + myelomenigiocele.
 Results from failure of pontine flexure during
embryogenesis which results in elongation of the
4th ventricle and kinking of brain stem.
 Clinical Manifestations

Variable and depends on many factors:

1- Age of onset.

2- Nature of the etiology.

3- Duration and rate of increase of ICP.

 Clinical Manifestations

Infants:
1- Progressive increase in HC.
2- Wide bulging anterior fontanel.
3- Dilated veins on the scalp.
4- Down word deviated eyes (sun set appearance) due to
impingement of tectum by dilated suprapineal recess.
 Clinical Manifestations

Infants:
5- Percussion of head gives crack pot “Mc Ewen sign”.

6- Neurologic symptoms e.g. brisk tendon reflexes and

spasticity due to stretching of corticospinal fibers
originating from leg motor cortex area.
 Clinical Manifestations

Older children:
manifestations of increased ICP??
 Investigations

 Plain x-ray:
- Infants:
Craniofacial disproportion.
- Children:
Separated sutures, erosion of posterior clenoid
process, increased convolutional markings (silver
beaten appearance).
 Investigations

 Trans Fontanelar US
 CT
 MRI
Plain X-ray
 Differential Diagnosis

1. Thickened cranium:
Chronic Hemolytic anemia, rickets, osteogenesis
imperfecta.
2. Chronic Subdural collections.
3. Megalocephaly due to storage disease e.g. Tay
Scahes; Gangliosidosis, muccopolysaccroidosis.
4. Hydranencephaly:
Absent cerebral hemispheres.
 Treatment

 Medical??
 Extra cranial shunts (ventriculoperitoneal
shunts)
 Prognosis

 Depends on the cause of dilated ventricles and not

on the size of cortical mantle at time of intervention.
 Increased risk of developmental disabilities e.g.
learning disability.
 Accelerated pubertal development in patients with
shunted hydrocephalus is relatively common due to
increased gonadotrophin secretion in response to
increased ICP.