ANALYSIS OF INTRACRANIAL-PRESSURE PULSE-WAVE IN EXPERIMENTAL HYDROCEPHALUS

Much has been written about the relationship between the pulse pressur e (PP) of the intracranial pressure pulse wave (ICPPW) and ventricle d ilatation. Some data suggest that high PP is the cause of ventricle di latation, and other authors have reported that high PP results from de creased intracranial compliance. In order to clarify these points, the amplitude of PP and pressure-volume response (PVR: an indicator of in tracranial compliance) were measured in bilateral ventricles using Hoc hwald's hydrocephalic model (right-left difference in ventricle size i s clear due to hemicraniectomy). Hydrocephalus was induced by means of intracisternal injection of a kaolin powder solution to dogs. The mea n ICP, amplitude of the PP, PVR and ventricle size (estimated by MR im aging) were evaluated in pathologic conditions induced by the followin g procedures. Group A, control: kaolin-induced hydrocephalus without c raniectomy; group B: kaolin-induced hydrocephalus with right-sided cra niectomy; group C: kaolin-induced hydrocephalus with right-sided crani ectomy and dural resection; group D: kaolin-induced hydrocephalus with right-sided craniectomy, dura resection and temporal muscle resection . Using MR imaging, the same degree of symmetrical ventricle dilatatio n was identified in all groups except group D. Group D alone demonstra ted a difference in ventricular size (craniectomy side > non-craniecto my side). There was no appreciable difference in mean ICP between any two groups. However, the amplitude of PP and the PVR decreased stepwis e from group A to group D. The difference in the amplitude of the PP a nd PVR between the right and left ventricles was not significant in an y group. Even on the larger ventricle side (right) in group D, the amp litude of PP was the same as that of the left ventricle, and much smal ler than in other groups. The results of our research suggest that: (1 ) There was no relation between ventricle dilatation and the amplitude of PP. This means that the increased amplitude of PP was not the caus e of the ventricle dilatation in this model. (2) A high degree of corr elation exists between the amplitude of PP and the PVR. This means tha t PP can be a good parameter of intracranial compliance in this model