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✓ The reaction of the periventricular tissue of the lateral ventricle to silicone rubber shunt tubing was studied by scanning and transmission electron microscopy. Nonfunctioning shunt tubing was implanted bilaterally into the frontal horns of rabbits, which were then sacrificed at postoperative intervals of 3 days to 16 weeks. Colchicine was used to study mitotic activity at the 3-day to 4-week postimplantation intervals. Reactive changes that occurred in the periventricular tissue correlated with the degree of contact with the implant and also with the duration of the postoperative period. Ependymal cells underwent progressive attenuation and sloughed completely in the most severely affected areas. Prominent gliosis in the subependyma accompanied the ependymal changes. The ventricular surface directly adjacent to holes in the implant developed ependyma-covered glial evaginations which grew into the implant holes beginning 1 week postimplantation. In the region of the outgrowths, ependymal mitotic activity was significantly increased at 1 and 2 weeks postimplantation, and astroglial mitotic activity was increased at 3 days and 1 week. Proliferation of ependymal and glial cells in the area touching the shunt tubing and mechanical factors contributed to the development of cellular outgrowths which may be a factor in the pathogenesis of shunt obstruction in human hydrocephalus.

✓ Hydrocephalus was induced in rabbits by injection of silicone oil into the cisterna magna. At 1 and 8 weeks postinjection the rabbits were either sacrificed or treated by cerebrospinal fluid shunting for 1 week. Blood vessel profiles in the periventricular neuropil were examined by light microscopy. In the caudate nucleus, septal area, and corpus callosum, hydrocephalus caused a reduction in the number of capillaries but no changes were observed in the number of larger blood vessels. Shunting reduced the size of the ventricles to normal and the number of capillaries increased if hydrocephalus was present for 1 week prior to shunting. If hydrocephalus was present for 8 weeks prior to shunting, the number of capillaries did not increase. These observations support the concept that collapse of capillaries may account for the decreased cerebral blood flow that has been measured in hydrocephalic brains.

Object.The origin of chronic communicating hydrocephalus following subarachnoid hemorrhage (SAH) is not well understood. Fibrosis of the arachnoid villi has been suggested as the cause for obstruction of cerebrospinal fluid (CSF) flow, but this is not well supported in the literature. The goal of this study was to determine the relationship between blood, inflammation, and cellular proliferation in arachnoid villi after SAH.

Methods.Arachnoid villi from 50 adult patients were sampled at autopsy. All specimens were subjected to a variety of histochemical and immunohistochemical stains. The 23 cases of SAH consisted of patients in whom an autopsy was performed 12 hours to 34 years post-SAH. Fifteen cases were identified as moderate-to-severe SAH, with varying degrees of hydrocephalus. In comparison with 27 age-matched non-SAH controls, the authors observed blood and inflammation within the arachnoid villi during the 1st week after SAH. Greater mitotic activity was also noted among arachnoid cap cells. The patient with chronic SAH presented with ventriculomegaly 2 months post-SAH and exhibited remarkable arachnoid cap cell accumulation.

Conclusions.The authors postulate that proliferation of arachnoidal cells, triggered by the inflammatory reaction or blood clotting products, could result in obstruction of CSF flow through arachnoid villi into the venous sinuses. This does not exclude the possibility that SAH causes generalized fibrosis in the subarachnoid space.

Object.Hydrocephalus, a pathological dilation of the ventricles of the brain, causes damage to periventricular white matter, at least in part, through chronic ischemia. The authors tested the hypothesis that treatment with nimodipine, an L-type calcium channel-blocking agent with demonstrated efficacy in a range of cerebral ischemic disorders, would ameliorate the adverse effects of experimental hydrocephalus.

Methods.脑积水在质询大鼠诱导jection of kaolin into the cisterna magna. The rats were treated by continuous administration of nimodipine or control vehicle for 2 weeks, beginning 2 weeks after induction of hydrocephalus. During the treatment period, the animals underwent repeated tests of motor and cognitive behavior. At the end of the treatment period, the rat brains were analyzed by histopathological and biochemical means.

Nimodipine treatment prevented the declines in motor and cognitive behavior that were observed in untreated control rats. During the treatment period, ventricular enlargement, determined by magnetic resonance imaging, was equal in the two groups, although the corpus callosum was thicker in the treated rats. Myelin content in white matter and synaptophysin content in gray matter, an indicator of synapses, did not differ.

Conclusions.The protective effect of nimodipine is most likely based on improved blood flow, although prevention of calcium influx—mediated proteolytic processes in axons cannot be excluded. Adjunctive pharmacological therapy may be beneficial to patients with hydrocephalus.

✓ An infant of 43 weeks gestational age with severe congenital hydrocephalus was operated on for removal of a subependymal astrocytoma in the region of the foramen of Monro. A biopsy of periventricular tissue was taken from the lateral ventricle for examination by scanning and transmission electron microscopy. The ependyma was largely denuded, with glial cell processes forming most of the ventricular lining. Many of the attenuated ependymal cells, however, had intact junctional complexes at areas of contact with other ependymal cells. Club-shaped unipolar cells, believed to be a previously undescribed form of immature ependymal cells, were found in the ventricular lining. Cerebrospinal fluid edema was present in the neuropil up to 60µm from the ventricular lumen, but there was no obvious axonal pathology in the tissues examined.

Object.It can be inferred from data published in the literature that brain compression occurs in the early stages of acute hydrocephalus and that drainage of extracellular waste products is impaired. The authors hypothesized that compression of the cortex would alter water distribution and retard the diffusion of fluid in the hydrocephalic brain.

Methods.Proton diffusion, blood perfusion, and T₁and T₂弛豫时间确定在成人rat brain by using magnetic resonance imaging prior to, and 1 and 8 days after induction of hydrocephalus by kaolin injection. Five anatomical regions of interest were studied. The striatum, dorsal cortex, and lateral cortex exhibited decreased T₂and apparent diffusion coefficient (ADC) values but no change in perfusion. Examination of white matter revealed an initial decrease in ADC followed by a significant increase. The T₂relaxation times increased and perfusion decreased progressively between 1 and 8 days after induction of hydrocephalus.

Conclusions.Acute experimental hydrocephalus causes compression of gray matter, perhaps associated with reduction in total water, which impairs diffusion of water in the tissue. White matter compression and hypoperfusion precede the development of edema. These findings have importance for understanding the neurochemical changes that occur in hydrocephalic brains.