Post-traumatic ventricular dilatation may have a wide range of aetiological factors: starting from neuronal loss due to head trauma and possible secondary ischaemic insults, to obstruction of CSF circulation resulting in hydrocephalus. It is important to differentiate between post-traumatic hydrocephalus and brain atrophy before considering placement of a shunt. Making this decision can be facilitated by measurement of the resistance to CSF outflow.1 However, the pattern of the CSF circulation may change dramatically after a cranioplasty resulting from a previous decompressive craniectomy for refractory intracranial hypertension after head injury. The effect of the skull and dura on CSF hydrodynamics has been explored experimentally: the resistance to CSF outflow after craniectomy decreases twofold and brain compliance (expressed using the pressure-volume index, PVI) increases.2 This problem is important clinically as the following case illustrates: