Kin H, Mizukami M, Araki G, Mihara H
No Shinkei Geka. 1976 Jan;4(1):33-41.
It is well recognized that the communicating hydrocephalus following the rupture of intracranial aneurysms is one of the factors which cause the disturbance of consciousness in acute stage and the impairment of mental functions in chronic stage. In this report we analyzed the surgical experience with this complication and discussed the mechanisms which cause the ventricular dilatation. 1. The communicating hydrocephalus following the rupture of intracranial aneurysms is devided into the acute form and the chronic form. 2. Acute communicating hydrocephalus may develop with 24 hours after the onset and the incidence is about 10% (6 out of 66 cases). 3. Intraventicular pressure is high in acute communicating hydrocephalus and becomes normal in chronic stage. 4. The incidence of the chronic communicating hydrocephalus is about 10% (6 out of 66 cases). 5. There are two types of chronic communicating hydrocephalus. One develops from acute form and another develops gradually after onset. Among 6 chronic communicating hydrocephalus, 3 developed from acute form, 2 showed slowly progressive ventricular dilatation and 1 admitted with hydrocephalus at chronic stage resepctively. 6. The intraventricular pressure of the acute form is high and the chronic form shows high pressure in acute stage, intermittent high pressure wave lasting 20-30 minutes in subacute stage and normal pressure in chronic stage when the ventricle is dilated. 7. The mechanisms of ventricular dilatation in normal pressure hydrocephalus are discussed on the basis of the continuous monitoring of intraventricular pressure in cases with rupture of intracranial aneurysm. 8. Indication of shunting procedures whould be determined by combination of clinical pictures, ventriculocranial index, findings of cisternography and EEG. Our operative criteria are presented.
