Experimental feline hydrocephalus. The role of biomechanical changes in ventricular enlargement in cats.

In a craniectomy-durectomy model of kaolin-induced feline hydrocephalus, the pressure-volume index (PVI) technique of bolus manipulations of cerebrospinal fluid (CSF) was used to study the biomechanical changes associated with hydrocephalus. Steady-state intracranial pressure (ICP), PVI, and the resistance to the absorption of CSF were determined acutely and 3 to 5 weeks later in hydrocephalic cats and time-matched control cats. Steady-state ICP was 11.0 +/- 2.1 mm Hg (+/- standard deviation) in the hydrocephalic cats, compared to 10.8 +/- 2.2 mm Hg in the chronic control group (p greater than 0.1). The ICP in both the chronic hydrocephalic and chronic control groups was significantly higher (p less than 0.001) than after acute durectomy (mean ICP 8.5 +/- 1.2 mm Hg). Immediately after dural opening, the mean PVI was 3.6 +/- 0.2 ml (+/- standard error of the mean); over time, it decreased to 1.3 +/- 0.1 ml in the chronic control group (p less than 0.001), but remained elevated in the hydrocephalic group at 3.5 +/- 0.4 ml (p less than 0.001). Resistance to CSF absorption was 9.1 +/- 1.4 mm Hg/ml/min immediately after dural opening and increased to 28.8 +/- 4.5 mm Hg/ml/min (p less than 0.001) in the hydrocephalic cats; it increased even further in the chronic measurements in control cats, to 82.3 +/- 9.2 mm Hg/ml/min (p less than 0.001). Ventricular size was moderate to severely enlarged in all hydrocephalic cats, and normal in the control group. These results indicate that the biomechanical profile of the altered brain container model of kaolin-induced feline hydrocephalus resembles that described in hydrocephalic infants. As shown in the control subjects, an absorptive defect alone is not sufficient to cause progressive ventricular enlargement. Increased volume-buffering capacity coupled with a moderate increase of CSF absorption resistance facilitates volume storage in the ventricles.