Pulsatility index

Object. In many cases communicating hydrocephalus is the result of impairme nts in cerebrospinal fluid absorption in the arachnoid villi at the cranial convexity. Reported methods of creating experimental hydrocephalus have no t sought to produce an arachnoidal adhesion in the cranial convexity. In th is study the authors investigate alterations in cerebral blood flow (CBF) i n experimental communicating hydrocephalus induced by the injection of kaol in into the subarachnoid space at the convexity in neonatal rats. Methods. In neonatal rats, kaolin was injected into the subarachnoid space at the cranial convexity. Assessment of CBF alterations was performed using transcranial Doppler ultrasonography preinjection and at 10 days, 4 weeks, and 8 weeks postinjection. Light microscopy examination was also performed at 4 weeks and 8 weeks postinjection. Conspicuous lateral ventricle enlargements of different dimensions were obs erved in kaolin-injected rats at 4 to 8 weeks postinjection. The third and fourth ventricles were dilated to a lesser extent. Resistance to CBF and in creased mean CBF velocity were apparent 8 weeks after kaolin injection. Fur ther, destruction and even loss of ependymal layers were more prominent at the chronic stage. Conclusions. The present model may be considered a progressive communicatin g hydrocephalus because of marked changes in blood flow dynamics and destru ction of the ependymal layer at the chronic stage.