Morphological Analysis of Progressive Hydrocephalus and Shunt-Dependent Arrested Hydrocephalus

Abstract

This experimental study was performed to determine if surgically treated feline hydrocephalus could produce any morphological and physiological changes in the periventricular tissue. The result was analyzed with clinical outcome, comparing two differently prepared models in which the biomechanical characteristics of the container property of the brain were altered. Craniectomies were performed in adult mongrel cats and the dura mater was left untouched in group A, while the dura was incised in crucial fashion in groub B. Thirty-four animals underwent ventriculopleural shunt surgery 6–8 weeks after kaolin induction into the cisterna magna. In 19 animals, no shunt was implanted; they served as sham controls. These and 10 normal animals were subjected to transmission electron microscopic study or measurement of white matter water content. The regions studied were divided into three sections according to their depth from the ventricular surface (Wl, W2 and W3). Considering the efficacy of shunting, the increased water content observed in preshunt animals decreased and was almost identical to normal controls after effective diversion surgery. On the other hand, the animals with ineffective shunt failed to normalize the water content and the figures were similar to the time-matched sham animals. These trends were preserved in groups A and B, but water content was much higher in group B. On histological observation, the chronological profile of subependymal extracellular space (Wl, W2) in chronic condition did not correspond to the chronological changes in water content, while both changes observed after successful shunt were apparently linked. Subependymal glial proliferation was increased in volume as a function of time in all animals observed, but this was much more marked in group A than group B. Furthermore, gliosis was more evident in shunted animals than in the other group and was more prominent in cats with effective shunts than in those with ineffective shunts. These histological changes and clinical outcome were not closely related in this study. These results indicated that: (1) The shunting procedure itself could promote subependymal gliosis and this progresses unexpectedly even if CSF pressure is low enough after effective shunting. (2) This histological change is not necessarily a sufficient explanation for clinical improvement after successful shunting. (3) A biomechanical characteristic of the differently treated container property of the brain exerts an influence on the histological change and change in CSF dynamics in periependymal tissue mostly at an early stage of hydrocephalus rather than at a later stage. Therefore early treatment should be considered while avoiding an overindication for shunting.

Ventricular cerebrospinal fluid neurofilament protein levels decrease in parallel with white matter pathology after shunt surgery in normal pressure hydrocephalus

“…Hypothetically, the implantation of the ventricular catheter may cause a reactive gliosis and disruption of the BBB, either in general or at the site of the catheter. This view is supported by experimental studies showing general or subependymal gliosis after shunting [29,30].…”

Periventricular rigidity in long-term shunt-treated hydrocephalus

“…There is, however, strong evidence for the existence of periventricular gliosis that could result in a stiff ventricular wall. 4,6,7,21 Microscopic examinations of the ependymal wall in experimental hydrocephalus reveal severe ependymal damage and subependymal edema during the early stage of the evolution of hydrocephalus. 5,11 A massive loss of cilia along the ependymal surface occurs, and within 3 hours of the induction of hydrocephalus by balloon occlusion of the fourth ventricle, a noticeable increase in the subependymal astroglial activity is evident.…”

“…It is believed that this phenomenon represents an ongoing process of tissue injury related to abnormal stresses created by shunt-induced negative pressure within the ventricle. 21 From such dramatic periventricular gliosis and the resulting resistance to cannulation of the ventricle during shunt surgery it has been inferred that altered ventricular compliance is responsible for failure of the ventricles to dilate in shunt-dependent patients at the time of shunt malfunction. In this study there is no direct evidence of the existence of periventricular gliosis; however, the results provide compelling evidence that the ventric-ular wall is not stiff and is unlikely to restrict ventricular enlargement.…”

“…Such periventricular gliosis has been shown in shunt-treated experimental hydrocephalus models. 4,11,21 There is, however, no direct evidence that periventricular gliosis can or does restrict ventricular enlargement at the time of shunt malfunction in experimental or clinical hydrocephalus. 8 Moreover, at the time of a shunt malfunction following a recent shunt revision, enlarged dilated ventricles may develop in some patients.…”

Preservation of functional architecture in visual cortex of cats with experimentally induced hydrocephalus

“…Histological abnormalities have been observed in kaolin-induced hydrocephalus (Rubin et al, 1976a,b;Takei et al, 1987;Kriebel et al, 1993;Takei & Sato, 1995;Kriebel & McAllister, 2000). These studies have shown that the white matter in hydrocephalic animals is edematous and that myelination is delayed in both the periventricular region and the core of the cerebral gyri.…”