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Object. In many cases communicating hydrocephalus is the result of impairments in cerebrospinal fluid absorption in the arachnoid villi at the cranial convexity. Reported methods of creating experimental hydrocephalus have not sought to produce an arachnoidal adhesion in the cranial convexity. In this study the authors investigate alterations in cerebral blood flow (CBF) in experimental communicating hydrocephalus induced by the injection of kaolin 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 by transcranial Doppler ultrasonography preinjection, and at 10 days, 4 weeks, and 8 weeks postinjection. Light microscopic examination was also performed at 4 and 8 weeks postinjection.
Conspicuous lateral ventricle enlargements of different dimensions were observed 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 increased mean cerebral blood velocity were apparent 8 weeks after kaolin injection. Further, destruction and even loss of ependymal layers were more prominent at the chronic stage.
Conclusions. The present model may be considered a progressive communicating hydrocephalus because of marked changes in blood flow dynamics and destruction of the ependymal layer at the chronic stage.
Experimental hydrocephalus can be induced by injection of kaolin into the cisterna magna. After removal of calvaria and opening of the dura in hydrocephalic animals, there is a clinical resemblance to infants with hydrocephalus in whom there are open calvarial sutures. If kaolin is injected into the cisterna magna, ventricular enlargement occurs as a result of the mechanical obstruction of CSF pathways in the fourth ventricle outlets. The spinal dural sac acts as a reservoir for normal CSF, and kaolin-reactive fibrosis can cause loss of CSF communication between the cranial and spinal subarachnoid compartments. Because kaolin injected into the cisterna magna induces nonprogressive hydrocephalus, deficiency in absorption of CSF has not been proven to be the cause of progressive ventricular enlargement, and, further, stabilization in ventricular enlargement at the chronic stage has been proven.
Transcranial Doppler ultrasonography is a noninvasive diagnostic method of measuring cerebral hemodynamic changes, and it can be used in the follow-up evaluation of clinical hydrocephalus and other intracranial diseases.
The purpose of the present paper is to investigate CBF dynamics and histopathological changes in a progressive communicating hydrocephalus model. To our knowledge, this report is the first to describe an injection of kaolin into the subarachnoid space at the neonatal calvarial convexity for the purpose of inducing progressive communicating hydrocephalus in rats. Transcranial Doppler measurements in this new experimental hydrocephalus model were obtained to determine whether the model could be clinically applicable.
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