Pediatric hydrocephalus

Understanding terminologies

  • Communicating hydrocephalus: extraventricular obstructive hydrocephalus
  • Noncommunicating hydrocephalus: intraventricular obstructive hydrocephalus


  • Imbalance between production and absorption
  • Produced by choroid plexus
  • Absorbed by brain and spinal cord, less extent arachnoid granulations
  • Net CSF flow from lateral to third to fourth ventricle due to cerebrovascular pulsations


  • Neonates, infants: post hemorrhage, post infection, Chiari II, Dandy-Walker, vein of Galen malformation
  • Older children: aqueduct stenosis, posterior fossa midline tumors, raised intracranial venous pressure (craniosynostosis)

Clinical presentation

  • Before fontanelle closure (2 years): progressive macrocephaly, frontal bossing, calvarial thinning, tense bulging anterior fontanelle, sutural diastasis, enlarged scalp veins, sunsetting eyes, lateral rectus palsy, leg spasticity
  • > 2 years: early morning headache, nausea, vomiting, papilledema, altered consciousness

Sites of narrowing in ventricular system

  • Foramen of Munro – superior extension of suprasellar tumors, arachnoid cysts, colloid cysts, giant cell astrocytoma
  • Aqueduct – tectal plate glioma, superior extension of midline posterior fossa mass like brain stem diffuse astrocytoma, inferior extension of pineal region tumors
  • Fourth ventricle outlet – displacement in Chiari II

Communicating hydrocephalus

  • Spinal cord tumors
  • Hemorrhage or exudates or pial dissemination of tumors

CSF diversion

  • Temporary – external drainage
  • Permanent – ventriculoperitoneal, ventriculoatrial or third ventriculostomy
  • Third ventriculostomy – puncture floor of third ventricle, CSF flows into suprasellar cistern

Imaging findings

  • Noncommunicating hydrocephalus: temporal horns disproportionately dilated to lateral ventricle body, dilated anterior and posterior recess of third ventricles, inferior bowing of floor of third ventricle, transependymal edema, bulging fontanelles. Sulci and cisterns small or obliterated. Some less consistent findings: widened radius of frontal horn, dorsum sella erosion, copper beaten skull
  • Communicating hydrocephalus: general ventriculomegaly to normal study

Sulcal spaces

  • < 2 years: benign enlargement of sulci is normal. Children can have prominent sulci without any underlying hydrocephalus. Concentrate on head size and cerebrum to rule out atrophy. Serial imaging helps to identify cause
  • Beyond 10 years, the sulci are less conspicuous, ventricles less prominent, this is normal. Basal cisterns SHOULD NOT be effaced.

Shunt dysfunction

  • Recurrence of hydrocephalus, fluid tracking along shunt tubing, calcification at either end of shunt due to fibrosis or inflammation, absence of T2 flow void across third ventriculostomy
  • Shunt infection – ventriculitis, cerebritis, possible fatal brain injury.